Cardiology

Febuxostat (Uloric) emerged as noninferior to allopurinol regarding risk of cardiovascular death among people 60 years and older with gout and at least one additional cardiovascular risk factor, results of the Febuxostat versus Allopurinol Streamlined Trial (FAST) suggest.

This primary outcome of the FAST trial stands in contrast to results of the CARES trial in 2018. The CARES researchers previously reported a 4.3% increased risk of cardiovascular death associated with febuxostat, compared with a 3.2% rate with allopurinol, a statistically significant 34% increase in the relative risk.

“In contrast to previous studies, there was no evidence of increased mortality with febuxostat, and we believe the regulators should review febuxostat licensing restrictions,” senior author Thomas MacDonald, MD, of the University of Dundee (Scotland), said during a late-breaking abstract session at the virtual annual meeting of the American College of Rheumatology.

The results of the FAST trial were simultaneously published online in The Lancet.

Both febuxostat and allopurinol treat gout by lowering urate levels. Concerns about the cardiovascular safety of febuxostat led to two post-licensing studies: the Cardiovascular Safety of Febuxostat and Allopurinol in Participants with Gout and Cardiovascular Comorbidities (CARES) study, mandated by the U.S. Food and Drug Administration, and FAST, requested by the European Medicines Agency. In February 2019, the FDA added a warning about elevated cardiovascular death and death risk associated with febuxostat.

“When CARES was published, it was somewhat of a threat to our study,” Dr. MacDonald said. “After hearing from our data-monitoring committee, we were told we could continue the trial.”
 

Some switched from allopurinol to febuxostat

So Dr. MacDonald, lead author Isla Mackenzie, MBChB, and their colleagues enrolled 6,128 people with gout in the United Kingdom, Sweden, and Denmark between December 2011 and January 2018. They followed patients for a median of 4 years. Participants had a mean age of 71 years, 85% were men, and 33% had a history of cardiovascular disease. The investigators excluded anyone with a stroke or myocardial infarction in the previous 6 months.

All participants were being treated with allopurinol. The investigators titrated those not at target up to an ideal dose that achieved a serum urate concentration of less than 0.357 mmol/L (< 6 mg/dL). Next, they randomly assigned 3,065 people to continue allopurinol and another 3,063 to switch to 80-120 mg of febuxostat.

The primary outcome of the multicenter, prospective, randomized, open-label FAST trial was a composite of hospitalization for nonfatal MI or biomarker positive for acute coronary syndrome, nonfatal stroke, or cardiovascular death.
 

Key findings

“There was definitely a noninferior primary outcome,” Dr. MacDonald said. In the on-treatment analysis, 172 patients in the febuxostat group reached the composite endpoint versus 241 patients in the allopurinol group. There were 1.72 events per 100 patient-years in the febuxostat group versus 2.05 events in the allopurinol group (adjusted hazard ratio, 0.85; 95% confidence interval, 0.70-1.03). An intent-to-treat analysis also found that febuxostat was noninferior to allopurinol on this measure.

Urate levels were approximately 80 micromoles lower in the febuxostat group versus the allopurinol group each year of the study, Dr. MacDonald said.

At least one gout flare was experienced by 1,017 patients in the febuxostat group and by 1,044 participants in the allopurinol group. “However, there was no placebo group, so we don’t know the effectiveness of either of these agents at preventing flares” based on this research, he said.

Both the on-treatment and intention-to-treat (ITT) secondary analyses demonstrated the noninferiority of febuxostat, compared with allopurinol, for all-cause death, each individual component of the composite primary outcome – cardiovascular death, hospitalization for heart failure, and hospitalization for new, unstable, or worsening angina.

In contrast, the ITT analysis revealed a “nominally significant increase” in hospitalization for arrhythmia with no evidence of ischemia in the febuxostat group. The 0.583 events per 100 patient-years in this group versus 0.385 events in the allopurinol cohort generated an adjusted HR of 1.51 (95% CI, 1.05-2.17).

In terms of all-cause mortality, 222 participants (7.2%) in the febuxostat group died, compared with 263 people (8.6%) in the allopurinol group.

Adverse events and withdrawals

A total 1,720 participants (57.3%) in the febuxostat group experienced at least one serious adverse event, as did 1,812 participants (59.4%) in the allopurinol group. Less than 1% of serious adverse events in each group were considered treatment-related.

Dr. MacDonald said that 6.2% of the febuxostat patients and 5.5% of the allopurinol group withdrew from the study. “We had pretty good follow-up [94%],” Dr. MacDonald said. “I don’t want to criticize CARES, but 47% did drop out of that study, and they could not follow them anymore.”

Limitations of FAST include its open-label design and lack of a placebo group, although Dr. MacDonald pointed out that a placebo group would have been unethical. Strengths included its large randomized trial design and good external validity, he added. “This is what will happen in clinical practice if you switch people from allopurinol to febuxostat.”

When asked how he would treat people with gout now given the FAST findings, Dr. MacDonald said, “I’m not a rheumatologist, I’m a cardiovascular physician. But I would say from the evidence from the FAST trial, it appears to be safe to give patients febuxostat whether or not they have cardiovascular risk factors or prior cardiovascular disease.”

“The FAST study indicates that febuxostat is similar to allopurinol in terms of cardiovascular events during the treatment period. The strengths of this study are its large sample size, excellent follow-up rate, and the relatively long follow-up time,” session moderator Shervin Assassi, MD, said when asked for comment. Dr. Assassi, director of the division of rheumatology at the University of Texas Health Science Center at Houston, was not involved in the research.

Menarini, Ipsen, and Teijin Pharma funded the study. The University of Dundee receives research funds from Menarini. Dr. MacDonald disclosed that he received speaker or consultant fees from Menarini. Dr. Assassi had no relevant disclosures.

SOURCE: MacDonald T et al. Arthritis Rheumatol. 2020;72(suppl 10). ACR 2020, Abstract L08.

Febuxostat (Uloric) emerged as noninferior to allopurinol regarding risk of cardiovascular death among people 60 years and older with gout and at least one additional cardiovascular risk factor, results of the Febuxostat versus Allopurinol Streamlined Trial (FAST) suggest.

This primary outcome of the FAST trial stands in contrast to results of the CARES trial in 2018. The CARES researchers previously reported a 4.3% increased risk of cardiovascular death associated with febuxostat, compared with a 3.2% rate with allopurinol, a statistically significant 34% increase in the relative risk.

“In contrast to previous studies, there was no evidence of increased mortality with febuxostat, and we believe the regulators should review febuxostat licensing restrictions,” senior author Thomas MacDonald, MD, of the University of Dundee (Scotland), said during a late-breaking abstract session at the virtual annual meeting of the American College of Rheumatology.

The results of the FAST trial were simultaneously published online in The Lancet.

Both febuxostat and allopurinol treat gout by lowering urate levels. Concerns about the cardiovascular safety of febuxostat led to two post-licensing studies: the Cardiovascular Safety of Febuxostat and Allopurinol in Participants with Gout and Cardiovascular Comorbidities (CARES) study, mandated by the U.S. Food and Drug Administration, and FAST, requested by the European Medicines Agency. In February 2019, the FDA added a warning about elevated cardiovascular death and death risk associated with febuxostat.

“When CARES was published, it was somewhat of a threat to our study,” Dr. MacDonald said. “After hearing from our data-monitoring committee, we were told we could continue the trial.”
 

Some switched from allopurinol to febuxostat

So Dr. MacDonald, lead author Isla Mackenzie, MBChB, and their colleagues enrolled 6,128 people with gout in the United Kingdom, Sweden, and Denmark between December 2011 and January 2018. They followed patients for a median of 4 years. Participants had a mean age of 71 years, 85% were men, and 33% had a history of cardiovascular disease. The investigators excluded anyone with a stroke or myocardial infarction in the previous 6 months.

All participants were being treated with allopurinol. The investigators titrated those not at target up to an ideal dose that achieved a serum urate concentration of less than 0.357 mmol/L (< 6 mg/dL). Next, they randomly assigned 3,065 people to continue allopurinol and another 3,063 to switch to 80-120 mg of febuxostat.

The primary outcome of the multicenter, prospective, randomized, open-label FAST trial was a composite of hospitalization for nonfatal MI or biomarker positive for acute coronary syndrome, nonfatal stroke, or cardiovascular death.
 

Key findings

“There was definitely a noninferior primary outcome,” Dr. MacDonald said. In the on-treatment analysis, 172 patients in the febuxostat group reached the composite endpoint versus 241 patients in the allopurinol group. There were 1.72 events per 100 patient-years in the febuxostat group versus 2.05 events in the allopurinol group (adjusted hazard ratio, 0.85; 95% confidence interval, 0.70-1.03). An intent-to-treat analysis also found that febuxostat was noninferior to allopurinol on this measure.

Urate levels were approximately 80 micromoles lower in the febuxostat group versus the allopurinol group each year of the study, Dr. MacDonald said.

At least one gout flare was experienced by 1,017 patients in the febuxostat group and by 1,044 participants in the allopurinol group. “However, there was no placebo group, so we don’t know the effectiveness of either of these agents at preventing flares” based on this research, he said.

Both the on-treatment and intention-to-treat (ITT) secondary analyses demonstrated the noninferiority of febuxostat, compared with allopurinol, for all-cause death, each individual component of the composite primary outcome – cardiovascular death, hospitalization for heart failure, and hospitalization for new, unstable, or worsening angina.

In contrast, the ITT analysis revealed a “nominally significant increase” in hospitalization for arrhythmia with no evidence of ischemia in the febuxostat group. The 0.583 events per 100 patient-years in this group versus 0.385 events in the allopurinol cohort generated an adjusted HR of 1.51 (95% CI, 1.05-2.17).

In terms of all-cause mortality, 222 participants (7.2%) in the febuxostat group died, compared with 263 people (8.6%) in the allopurinol group.

Adverse events and withdrawals

A total 1,720 participants (57.3%) in the febuxostat group experienced at least one serious adverse event, as did 1,812 participants (59.4%) in the allopurinol group. Less than 1% of serious adverse events in each group were considered treatment-related.

Dr. MacDonald said that 6.2% of the febuxostat patients and 5.5% of the allopurinol group withdrew from the study. “We had pretty good follow-up [94%],” Dr. MacDonald said. “I don’t want to criticize CARES, but 47% did drop out of that study, and they could not follow them anymore.”

Limitations of FAST include its open-label design and lack of a placebo group, although Dr. MacDonald pointed out that a placebo group would have been unethical. Strengths included its large randomized trial design and good external validity, he added. “This is what will happen in clinical practice if you switch people from allopurinol to febuxostat.”

When asked how he would treat people with gout now given the FAST findings, Dr. MacDonald said, “I’m not a rheumatologist, I’m a cardiovascular physician. But I would say from the evidence from the FAST trial, it appears to be safe to give patients febuxostat whether or not they have cardiovascular risk factors or prior cardiovascular disease.”

“The FAST study indicates that febuxostat is similar to allopurinol in terms of cardiovascular events during the treatment period. The strengths of this study are its large sample size, excellent follow-up rate, and the relatively long follow-up time,” session moderator Shervin Assassi, MD, said when asked for comment. Dr. Assassi, director of the division of rheumatology at the University of Texas Health Science Center at Houston, was not involved in the research.

Menarini, Ipsen, and Teijin Pharma funded the study. The University of Dundee receives research funds from Menarini. Dr. MacDonald disclosed that he received speaker or consultant fees from Menarini. Dr. Assassi had no relevant disclosures.

SOURCE: MacDonald T et al. Arthritis Rheumatol. 2020;72(suppl 10). ACR 2020, Abstract L08.

Febuxostat (Uloric) emerged as noninferior to allopurinol regarding risk of cardiovascular death among people 60 years and older with gout and at least one additional cardiovascular risk factor, results of the Febuxostat versus Allopurinol Streamlined Trial (FAST) suggest.

This primary outcome of the FAST trial stands in contrast to results of the CARES trial in 2018. The CARES researchers previously reported a 4.3% increased risk of cardiovascular death associated with febuxostat, compared with a 3.2% rate with allopurinol, a statistically significant 34% increase in the relative risk.

“In contrast to previous studies, there was no evidence of increased mortality with febuxostat, and we believe the regulators should review febuxostat licensing restrictions,” senior author Thomas MacDonald, MD, of the University of Dundee (Scotland), said during a late-breaking abstract session at the virtual annual meeting of the American College of Rheumatology.

The results of the FAST trial were simultaneously published online in The Lancet.

Both febuxostat and allopurinol treat gout by lowering urate levels. Concerns about the cardiovascular safety of febuxostat led to two post-licensing studies: the Cardiovascular Safety of Febuxostat and Allopurinol in Participants with Gout and Cardiovascular Comorbidities (CARES) study, mandated by the U.S. Food and Drug Administration, and FAST, requested by the European Medicines Agency. In February 2019, the FDA added a warning about elevated cardiovascular death and death risk associated with febuxostat.

“When CARES was published, it was somewhat of a threat to our study,” Dr. MacDonald said. “After hearing from our data-monitoring committee, we were told we could continue the trial.”
 

Some switched from allopurinol to febuxostat

So Dr. MacDonald, lead author Isla Mackenzie, MBChB, and their colleagues enrolled 6,128 people with gout in the United Kingdom, Sweden, and Denmark between December 2011 and January 2018. They followed patients for a median of 4 years. Participants had a mean age of 71 years, 85% were men, and 33% had a history of cardiovascular disease. The investigators excluded anyone with a stroke or myocardial infarction in the previous 6 months.

All participants were being treated with allopurinol. The investigators titrated those not at target up to an ideal dose that achieved a serum urate concentration of less than 0.357 mmol/L (< 6 mg/dL). Next, they randomly assigned 3,065 people to continue allopurinol and another 3,063 to switch to 80-120 mg of febuxostat.

The primary outcome of the multicenter, prospective, randomized, open-label FAST trial was a composite of hospitalization for nonfatal MI or biomarker positive for acute coronary syndrome, nonfatal stroke, or cardiovascular death.
 

Key findings

“There was definitely a noninferior primary outcome,” Dr. MacDonald said. In the on-treatment analysis, 172 patients in the febuxostat group reached the composite endpoint versus 241 patients in the allopurinol group. There were 1.72 events per 100 patient-years in the febuxostat group versus 2.05 events in the allopurinol group (adjusted hazard ratio, 0.85; 95% confidence interval, 0.70-1.03). An intent-to-treat analysis also found that febuxostat was noninferior to allopurinol on this measure.

Urate levels were approximately 80 micromoles lower in the febuxostat group versus the allopurinol group each year of the study, Dr. MacDonald said.

At least one gout flare was experienced by 1,017 patients in the febuxostat group and by 1,044 participants in the allopurinol group. “However, there was no placebo group, so we don’t know the effectiveness of either of these agents at preventing flares” based on this research, he said.

Both the on-treatment and intention-to-treat (ITT) secondary analyses demonstrated the noninferiority of febuxostat, compared with allopurinol, for all-cause death, each individual component of the composite primary outcome – cardiovascular death, hospitalization for heart failure, and hospitalization for new, unstable, or worsening angina.

In contrast, the ITT analysis revealed a “nominally significant increase” in hospitalization for arrhythmia with no evidence of ischemia in the febuxostat group. The 0.583 events per 100 patient-years in this group versus 0.385 events in the allopurinol cohort generated an adjusted HR of 1.51 (95% CI, 1.05-2.17).

In terms of all-cause mortality, 222 participants (7.2%) in the febuxostat group died, compared with 263 people (8.6%) in the allopurinol group.

Adverse events and withdrawals

A total 1,720 participants (57.3%) in the febuxostat group experienced at least one serious adverse event, as did 1,812 participants (59.4%) in the allopurinol group. Less than 1% of serious adverse events in each group were considered treatment-related.

Dr. MacDonald said that 6.2% of the febuxostat patients and 5.5% of the allopurinol group withdrew from the study. “We had pretty good follow-up [94%],” Dr. MacDonald said. “I don’t want to criticize CARES, but 47% did drop out of that study, and they could not follow them anymore.”

Limitations of FAST include its open-label design and lack of a placebo group, although Dr. MacDonald pointed out that a placebo group would have been unethical. Strengths included its large randomized trial design and good external validity, he added. “This is what will happen in clinical practice if you switch people from allopurinol to febuxostat.”

When asked how he would treat people with gout now given the FAST findings, Dr. MacDonald said, “I’m not a rheumatologist, I’m a cardiovascular physician. But I would say from the evidence from the FAST trial, it appears to be safe to give patients febuxostat whether or not they have cardiovascular risk factors or prior cardiovascular disease.”

“The FAST study indicates that febuxostat is similar to allopurinol in terms of cardiovascular events during the treatment period. The strengths of this study are its large sample size, excellent follow-up rate, and the relatively long follow-up time,” session moderator Shervin Assassi, MD, said when asked for comment. Dr. Assassi, director of the division of rheumatology at the University of Texas Health Science Center at Houston, was not involved in the research.

Menarini, Ipsen, and Teijin Pharma funded the study. The University of Dundee receives research funds from Menarini. Dr. MacDonald disclosed that he received speaker or consultant fees from Menarini. Dr. Assassi had no relevant disclosures.

SOURCE: MacDonald T et al. Arthritis Rheumatol. 2020;72(suppl 10). ACR 2020, Abstract L08.

Dietary patterns with higher inflammatory potential were significantly associated with a higher incidence of cardiovascular disease (CVD) and stroke in a new pooled analysis of three prospective cohort studies.

The analysis included 210,145 U.S. women and men followed for up to 32 years in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study.

After adjustment for use of anti-inflammatory medications and CVD risk factors, those whose dietary pattern ranked in the highest quintile of inflammatory potential had a 38% higher risk of CVD (hazard ratio comparing highest with lowest quintiles, 1.38), a 46% higher risk of coronary heart disease (HR, 1.46), and a 28% higher risk of stroke (HR, 1.28) (all P for trend < .001).

Jun Li, MD, PhD, and colleagues at Harvard School of Public Health and Harvard Medical School, Boston, published the findings of their study in the Nov. 10 issue of the Journal of the American College of Cardiology.

The inflammatory potential of a diet was assessed using a food-based, dietary index called the “empirical dietary inflammatory pattern” or EDIP.

In an interview, Dr. Li explained that the EDIP was developed 4 years ago by many of the same authors involved with this study, including nutrition heavyweights Walter C. Willett, MD, DrPH, and Frank B. Hu, MD, PhD, both from Harvard.

“We summarized all the foods people eat into 39 defined food groups and did a reduced-rank regression analysis that looked at these 39 food groups and three inflammatory markers – interleukin-6, C-reactive protein, and tumor necrosis factor–alpha receptor 2. We found 18 food groups that are most predictive of these biomarkers, and the EDIP was calculated as the weighted sum of these 18 food groups.”

Individuals who had higher intakes of green-leafy vegetables (kale, spinach, arugula), dark-yellow vegetables (pumpkin, yellow peppers, carrots), whole grains, fruits, tea, coffee and wine had lower long-term CVD risk than those with higher intakes of red meat, processed meat, organ meat, refined carbohydrates, and sweetened beverages. 

The associations were consistent across cohorts and between sexes and remained significant in multiple sensitivity analysis that adjusted for alcohol consumption, smoking pack-years, use of lipid-lowering and antihypertensive medications, sodium intake, and blood pressure.

In a secondary analysis, diets with higher inflammatory potential were also associated with significantly higher biomarker levels indicative of more systemic, vascular, and metabolic inflammation, as well as less favorable lipid profiles.

“We wanted to be able to provide guidance on dietary patterns and food combinations,” said Dr. Li. “If you tell people to eat more polyunsaturated fats instead of saturated fat or trans fat, most people don’t know what foods are higher and lower in those nutrients. Also, many foods have different nutrients – some of which are good and some of which are bad – so we wanted to help people find the foods with the higher proportion of healthy nutrients rather than point out specific nutrients to avoid.”

Researchers used prospectively gathered data from the Nurses’ Health Studies I and II starting from 1984 and from the Health Professionals Follow-up Study. After excluding participants with missing diet information or previously diagnosed heart disease, stroke or cancer, over 210,000 participants were included in the analysis. Participants completed a survey every 4 years to ascertain dietary intake. 
 

Prevention, not treatment

In an editorial comment, Ramon Estruch, MD, PhD, from the Hospital Clinic in Barcelona, and colleagues suggested that it might be time for better dietary guidelines.

“A better knowledge of health protection provided by different foods and dietary patterns, mainly their anti-inflammatory properties, should provide the basis for designing even healthier dietary patterns to protect against heart disease,” the editorialists wrote.

They added extra-virgin olive oil, fatty fish, and tomatoes to the list of foods with “established anti-inflammatory activity.”

In a comment, Dr. Estruch said the findings of this new study are confirmatory of the PREDIMED trial, which showed a reduction in risk of major CV events in individuals at high cardiovascular risk assigned to an anti-inflammatory Mediterranean diet pattern supplemented with extra-virgin olive oil or nuts as compared with those assigned to a reduced-fat diet. 

“The study of Jun Li et al. confirms that an anti-inflammatory diet is useful to prevent cardiovascular events and, more important, that healthy dietary patterns may be even healthier if subjects increase consumption of foods with the highest anti-inflammatory potential,” he said, adding that “mechanistic explanations add plausibility to the results of observational studies.”

Dr. Estruch was the principal investigator of PREDIMED. This trial was originally published in 2013 and then retracted and republished in 2018, with some required corrections, but the results had not materially changed.

Dr. Li is supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases and Boston Nutrition Obesity Research Center. Dr. Estruch disclosed no financial relationships relevant to the contents of this article.  

A version of this article originally appeared on Medscape.com.

Dietary patterns with higher inflammatory potential were significantly associated with a higher incidence of cardiovascular disease (CVD) and stroke in a new pooled analysis of three prospective cohort studies.

The analysis included 210,145 U.S. women and men followed for up to 32 years in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study.

After adjustment for use of anti-inflammatory medications and CVD risk factors, those whose dietary pattern ranked in the highest quintile of inflammatory potential had a 38% higher risk of CVD (hazard ratio comparing highest with lowest quintiles, 1.38), a 46% higher risk of coronary heart disease (HR, 1.46), and a 28% higher risk of stroke (HR, 1.28) (all P for trend < .001).

Jun Li, MD, PhD, and colleagues at Harvard School of Public Health and Harvard Medical School, Boston, published the findings of their study in the Nov. 10 issue of the Journal of the American College of Cardiology.

The inflammatory potential of a diet was assessed using a food-based, dietary index called the “empirical dietary inflammatory pattern” or EDIP.

In an interview, Dr. Li explained that the EDIP was developed 4 years ago by many of the same authors involved with this study, including nutrition heavyweights Walter C. Willett, MD, DrPH, and Frank B. Hu, MD, PhD, both from Harvard.

“We summarized all the foods people eat into 39 defined food groups and did a reduced-rank regression analysis that looked at these 39 food groups and three inflammatory markers – interleukin-6, C-reactive protein, and tumor necrosis factor–alpha receptor 2. We found 18 food groups that are most predictive of these biomarkers, and the EDIP was calculated as the weighted sum of these 18 food groups.”

Individuals who had higher intakes of green-leafy vegetables (kale, spinach, arugula), dark-yellow vegetables (pumpkin, yellow peppers, carrots), whole grains, fruits, tea, coffee and wine had lower long-term CVD risk than those with higher intakes of red meat, processed meat, organ meat, refined carbohydrates, and sweetened beverages. 

The associations were consistent across cohorts and between sexes and remained significant in multiple sensitivity analysis that adjusted for alcohol consumption, smoking pack-years, use of lipid-lowering and antihypertensive medications, sodium intake, and blood pressure.

In a secondary analysis, diets with higher inflammatory potential were also associated with significantly higher biomarker levels indicative of more systemic, vascular, and metabolic inflammation, as well as less favorable lipid profiles.

“We wanted to be able to provide guidance on dietary patterns and food combinations,” said Dr. Li. “If you tell people to eat more polyunsaturated fats instead of saturated fat or trans fat, most people don’t know what foods are higher and lower in those nutrients. Also, many foods have different nutrients – some of which are good and some of which are bad – so we wanted to help people find the foods with the higher proportion of healthy nutrients rather than point out specific nutrients to avoid.”

Researchers used prospectively gathered data from the Nurses’ Health Studies I and II starting from 1984 and from the Health Professionals Follow-up Study. After excluding participants with missing diet information or previously diagnosed heart disease, stroke or cancer, over 210,000 participants were included in the analysis. Participants completed a survey every 4 years to ascertain dietary intake. 
 

Prevention, not treatment

In an editorial comment, Ramon Estruch, MD, PhD, from the Hospital Clinic in Barcelona, and colleagues suggested that it might be time for better dietary guidelines.

“A better knowledge of health protection provided by different foods and dietary patterns, mainly their anti-inflammatory properties, should provide the basis for designing even healthier dietary patterns to protect against heart disease,” the editorialists wrote.

They added extra-virgin olive oil, fatty fish, and tomatoes to the list of foods with “established anti-inflammatory activity.”

In a comment, Dr. Estruch said the findings of this new study are confirmatory of the PREDIMED trial, which showed a reduction in risk of major CV events in individuals at high cardiovascular risk assigned to an anti-inflammatory Mediterranean diet pattern supplemented with extra-virgin olive oil or nuts as compared with those assigned to a reduced-fat diet. 

“The study of Jun Li et al. confirms that an anti-inflammatory diet is useful to prevent cardiovascular events and, more important, that healthy dietary patterns may be even healthier if subjects increase consumption of foods with the highest anti-inflammatory potential,” he said, adding that “mechanistic explanations add plausibility to the results of observational studies.”

Dr. Estruch was the principal investigator of PREDIMED. This trial was originally published in 2013 and then retracted and republished in 2018, with some required corrections, but the results had not materially changed.

Dr. Li is supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases and Boston Nutrition Obesity Research Center. Dr. Estruch disclosed no financial relationships relevant to the contents of this article.  

A version of this article originally appeared on Medscape.com.

Dietary patterns with higher inflammatory potential were significantly associated with a higher incidence of cardiovascular disease (CVD) and stroke in a new pooled analysis of three prospective cohort studies.

The analysis included 210,145 U.S. women and men followed for up to 32 years in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study.

After adjustment for use of anti-inflammatory medications and CVD risk factors, those whose dietary pattern ranked in the highest quintile of inflammatory potential had a 38% higher risk of CVD (hazard ratio comparing highest with lowest quintiles, 1.38), a 46% higher risk of coronary heart disease (HR, 1.46), and a 28% higher risk of stroke (HR, 1.28) (all P for trend < .001).

Jun Li, MD, PhD, and colleagues at Harvard School of Public Health and Harvard Medical School, Boston, published the findings of their study in the Nov. 10 issue of the Journal of the American College of Cardiology.

The inflammatory potential of a diet was assessed using a food-based, dietary index called the “empirical dietary inflammatory pattern” or EDIP.

In an interview, Dr. Li explained that the EDIP was developed 4 years ago by many of the same authors involved with this study, including nutrition heavyweights Walter C. Willett, MD, DrPH, and Frank B. Hu, MD, PhD, both from Harvard.

“We summarized all the foods people eat into 39 defined food groups and did a reduced-rank regression analysis that looked at these 39 food groups and three inflammatory markers – interleukin-6, C-reactive protein, and tumor necrosis factor–alpha receptor 2. We found 18 food groups that are most predictive of these biomarkers, and the EDIP was calculated as the weighted sum of these 18 food groups.”

Individuals who had higher intakes of green-leafy vegetables (kale, spinach, arugula), dark-yellow vegetables (pumpkin, yellow peppers, carrots), whole grains, fruits, tea, coffee and wine had lower long-term CVD risk than those with higher intakes of red meat, processed meat, organ meat, refined carbohydrates, and sweetened beverages. 

The associations were consistent across cohorts and between sexes and remained significant in multiple sensitivity analysis that adjusted for alcohol consumption, smoking pack-years, use of lipid-lowering and antihypertensive medications, sodium intake, and blood pressure.

In a secondary analysis, diets with higher inflammatory potential were also associated with significantly higher biomarker levels indicative of more systemic, vascular, and metabolic inflammation, as well as less favorable lipid profiles.

“We wanted to be able to provide guidance on dietary patterns and food combinations,” said Dr. Li. “If you tell people to eat more polyunsaturated fats instead of saturated fat or trans fat, most people don’t know what foods are higher and lower in those nutrients. Also, many foods have different nutrients – some of which are good and some of which are bad – so we wanted to help people find the foods with the higher proportion of healthy nutrients rather than point out specific nutrients to avoid.”

Researchers used prospectively gathered data from the Nurses’ Health Studies I and II starting from 1984 and from the Health Professionals Follow-up Study. After excluding participants with missing diet information or previously diagnosed heart disease, stroke or cancer, over 210,000 participants were included in the analysis. Participants completed a survey every 4 years to ascertain dietary intake. 
 

Prevention, not treatment

In an editorial comment, Ramon Estruch, MD, PhD, from the Hospital Clinic in Barcelona, and colleagues suggested that it might be time for better dietary guidelines.

“A better knowledge of health protection provided by different foods and dietary patterns, mainly their anti-inflammatory properties, should provide the basis for designing even healthier dietary patterns to protect against heart disease,” the editorialists wrote.

They added extra-virgin olive oil, fatty fish, and tomatoes to the list of foods with “established anti-inflammatory activity.”

In a comment, Dr. Estruch said the findings of this new study are confirmatory of the PREDIMED trial, which showed a reduction in risk of major CV events in individuals at high cardiovascular risk assigned to an anti-inflammatory Mediterranean diet pattern supplemented with extra-virgin olive oil or nuts as compared with those assigned to a reduced-fat diet. 

“The study of Jun Li et al. confirms that an anti-inflammatory diet is useful to prevent cardiovascular events and, more important, that healthy dietary patterns may be even healthier if subjects increase consumption of foods with the highest anti-inflammatory potential,” he said, adding that “mechanistic explanations add plausibility to the results of observational studies.”

Dr. Estruch was the principal investigator of PREDIMED. This trial was originally published in 2013 and then retracted and republished in 2018, with some required corrections, but the results had not materially changed.

Dr. Li is supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases and Boston Nutrition Obesity Research Center. Dr. Estruch disclosed no financial relationships relevant to the contents of this article.  

A version of this article originally appeared on Medscape.com.

Thyroid dysfunction had virtually no independent impact on survival in a retrospective study of nearly 5,000 English patients with chronic heart failure, adding to evidence that subclinical thyroid disorders in these patients requires no special management beyond ongoing monitoring.

Sebastian Kaulitzki/Fotolia

“Although thyroid dysfunction is related to outcome in patients with chronic heart failure, the association disappears when adjustment is made for established prognostic variables, such as age, NT-proBNP [N-terminal of the prohormone brain natriuretic peptide], and [New York Heart Association] class,” wrote Nathan A. Samuel, MBChB, and coauthors in the American Journal of Cardiology.

Results from several earlier studies had shown evidence for reduced survival in heart failure patients with thyroid dysfunction, but in analyses that did not adjust for heart failure severity, such as a 2013 report that used data from the Sudden Cardiac Death in Heart Failure Trial SCD-HeFT. Other studies that adjusted for heart failure severity based on serum level of natriuretic peptides did not show significant associations between thyroid function and mortality, and when those results couple with the new report they together minimize the immediate risk from subclinical thyroid dysfunction faced by heart failure patients, wrote the authors of the new report.

Don’t treat subclinical thyroid dysfunction

“Our results suggest that subclinical thyroid disease has little impact on outcomes, and that we should not treat subclinical hypothyroidism in the expectation of improving outlook,” said Andrew L. Clark, MD, senior author on the new report and professor and head of the department of academic cardiology at Hull (England) York Medical School.

“Both hyper-and hypothyroidism can cause heart failure, so thyroid function should always be checked in patients when they present with heart failure. A small proportion of patients have heart failure that is potentially reversible” with thyroid-directed treatment, Dr. Clark said in an interview.

But “subclinical disease should probably not be treated, although we have not conducted a clinical trial that proves this assertion. We speculate, based on our findings, that such a trial is unlikely to be positive.”

Patients with subclinical thyroid disorders, particularly subclinical hypothyroidism, “need to be followed and treated should they develop clinical disease,” he maintained. “Except in extreme circumstances, such as the handful of patients who might have gross myxedema and may be near coma, thyroid replacement therapy for those [with heart failure] who have clinical hypothyroidism should follow standard lines.”

It is important to monitor thyroid function,” agreed Dr. Samuel, a researcher in the department of academic cardiology at Hull York Medical School. “We found that thyroxine use was most common among patients with hyperthyroidism, suggesting that they were previously hypothyroid and had received inappropriate treatment.”

Confounder adjustment mitigates the thyroid link

The new analysis used data collected from 6,782 consecutive heart failure patients enrolled during 2000-2018 at a community heart failure clinic that serves patients in the region of Hull, England. The researchers identified 4,992 of these patients with confirmed heart failure and adequate data for their analyses, including 2,997 (60%) with heart failure with reduced ejection fraction (HFrEF) and 1,995 (40%) with heart failure with normal ejection fraction (HFnEF, the term used by the authors but often called heart failure with preserved ejection fraction).

Thyroid hormone levels showed that 90% of these patients were euthyroid, 6% were hyperthyroid, and 4% were hypothyroid, rates consistent with prior reports for both the general population and heart failure patients. Only 12 patients (0.2%) had overt hypothyroidism, and fewer that 1% (about 45 patients) had overt hyperthyroidism. Patients averaged about 73 years of age, and during a median 4.6 years of follow-up 58% died.

Both the hypo- and hyperthyroid patients showed significantly higher mortality rates than euthyroid patients in a univariate analysis. But the patients with thyroid dysfunction also had more comorbidities, more severe heart failure symptoms measured by NYHA functional class, and more severe heart failure measured as higher serum levels of NT-proBNP.

In a multivariate analysis that adjusted for these factors, the significant differences disappeared among the entire group of heart failure patients for the outcomes of all-cause mortality, and mortality or hospitalization with heart failure. The multivariate analysis also showed no significant association between higher levels of thyroid-stimulating hormone (TSH) and all-cause death or death plus heart failure hospitalization among the patients with HFrEF.

Among patients with HFnEF, the multivariate adjusted analysis showed a small increase in both mortality and mortality plus hospitalization for heart failure, a 2% rise for each of these two endpoints for each 1 mIU/L increase in TSH, the authors reported. Although the P value for each of these two significant differences among patients with HFnEF was .02, the 95% confidence interval included 1.00 and ranged from 1.00 to 1.04.

The multivariate analysis identified three variables with the strongest associations with all-cause mortality: older age, higher levels of NT-proBNP, and higher NYHA class indicating greater functional impairment.

The results support the hypothesis that “worsening heart failure can lead to down-regulation of thyroid hormone signaling,” the authors suggested. Their study is also “the first to examine the prognostic significance of thyroid dysfunction in a large population of patients with HFnEF.” This analysis showed a “weak but significant association between increasing TSH and both mortality and the composite endpoint in patients with HFnEF.”

“HFnEF is a heterogeneous group of conditions that are difficult to diagnose in many cases. Therefore, future studies are needed to provide further clarity on the effect of thyroid dysfunction in these patients,” Dr. Samuel said.

The study received no commercial funding. Dr. Samuel and Dr. Clark had no disclosures.

[email protected]

SOURCE: Samuel NA et al. Am J Cardiol. 2020 Oct 24. doi: 10.1016/j.amjcard.2020.10.034.

Thyroid dysfunction had virtually no independent impact on survival in a retrospective study of nearly 5,000 English patients with chronic heart failure, adding to evidence that subclinical thyroid disorders in these patients requires no special management beyond ongoing monitoring.

Sebastian Kaulitzki/Fotolia

“Although thyroid dysfunction is related to outcome in patients with chronic heart failure, the association disappears when adjustment is made for established prognostic variables, such as age, NT-proBNP [N-terminal of the prohormone brain natriuretic peptide], and [New York Heart Association] class,” wrote Nathan A. Samuel, MBChB, and coauthors in the American Journal of Cardiology.

Results from several earlier studies had shown evidence for reduced survival in heart failure patients with thyroid dysfunction, but in analyses that did not adjust for heart failure severity, such as a 2013 report that used data from the Sudden Cardiac Death in Heart Failure Trial SCD-HeFT. Other studies that adjusted for heart failure severity based on serum level of natriuretic peptides did not show significant associations between thyroid function and mortality, and when those results couple with the new report they together minimize the immediate risk from subclinical thyroid dysfunction faced by heart failure patients, wrote the authors of the new report.

Don’t treat subclinical thyroid dysfunction

“Our results suggest that subclinical thyroid disease has little impact on outcomes, and that we should not treat subclinical hypothyroidism in the expectation of improving outlook,” said Andrew L. Clark, MD, senior author on the new report and professor and head of the department of academic cardiology at Hull (England) York Medical School.

“Both hyper-and hypothyroidism can cause heart failure, so thyroid function should always be checked in patients when they present with heart failure. A small proportion of patients have heart failure that is potentially reversible” with thyroid-directed treatment, Dr. Clark said in an interview.

But “subclinical disease should probably not be treated, although we have not conducted a clinical trial that proves this assertion. We speculate, based on our findings, that such a trial is unlikely to be positive.”

Patients with subclinical thyroid disorders, particularly subclinical hypothyroidism, “need to be followed and treated should they develop clinical disease,” he maintained. “Except in extreme circumstances, such as the handful of patients who might have gross myxedema and may be near coma, thyroid replacement therapy for those [with heart failure] who have clinical hypothyroidism should follow standard lines.”

It is important to monitor thyroid function,” agreed Dr. Samuel, a researcher in the department of academic cardiology at Hull York Medical School. “We found that thyroxine use was most common among patients with hyperthyroidism, suggesting that they were previously hypothyroid and had received inappropriate treatment.”

Confounder adjustment mitigates the thyroid link

The new analysis used data collected from 6,782 consecutive heart failure patients enrolled during 2000-2018 at a community heart failure clinic that serves patients in the region of Hull, England. The researchers identified 4,992 of these patients with confirmed heart failure and adequate data for their analyses, including 2,997 (60%) with heart failure with reduced ejection fraction (HFrEF) and 1,995 (40%) with heart failure with normal ejection fraction (HFnEF, the term used by the authors but often called heart failure with preserved ejection fraction).

Thyroid hormone levels showed that 90% of these patients were euthyroid, 6% were hyperthyroid, and 4% were hypothyroid, rates consistent with prior reports for both the general population and heart failure patients. Only 12 patients (0.2%) had overt hypothyroidism, and fewer that 1% (about 45 patients) had overt hyperthyroidism. Patients averaged about 73 years of age, and during a median 4.6 years of follow-up 58% died.

Both the hypo- and hyperthyroid patients showed significantly higher mortality rates than euthyroid patients in a univariate analysis. But the patients with thyroid dysfunction also had more comorbidities, more severe heart failure symptoms measured by NYHA functional class, and more severe heart failure measured as higher serum levels of NT-proBNP.

In a multivariate analysis that adjusted for these factors, the significant differences disappeared among the entire group of heart failure patients for the outcomes of all-cause mortality, and mortality or hospitalization with heart failure. The multivariate analysis also showed no significant association between higher levels of thyroid-stimulating hormone (TSH) and all-cause death or death plus heart failure hospitalization among the patients with HFrEF.

Among patients with HFnEF, the multivariate adjusted analysis showed a small increase in both mortality and mortality plus hospitalization for heart failure, a 2% rise for each of these two endpoints for each 1 mIU/L increase in TSH, the authors reported. Although the P value for each of these two significant differences among patients with HFnEF was .02, the 95% confidence interval included 1.00 and ranged from 1.00 to 1.04.

The multivariate analysis identified three variables with the strongest associations with all-cause mortality: older age, higher levels of NT-proBNP, and higher NYHA class indicating greater functional impairment.

The results support the hypothesis that “worsening heart failure can lead to down-regulation of thyroid hormone signaling,” the authors suggested. Their study is also “the first to examine the prognostic significance of thyroid dysfunction in a large population of patients with HFnEF.” This analysis showed a “weak but significant association between increasing TSH and both mortality and the composite endpoint in patients with HFnEF.”

“HFnEF is a heterogeneous group of conditions that are difficult to diagnose in many cases. Therefore, future studies are needed to provide further clarity on the effect of thyroid dysfunction in these patients,” Dr. Samuel said.

The study received no commercial funding. Dr. Samuel and Dr. Clark had no disclosures.

[email protected]

SOURCE: Samuel NA et al. Am J Cardiol. 2020 Oct 24. doi: 10.1016/j.amjcard.2020.10.034.

Thyroid dysfunction had virtually no independent impact on survival in a retrospective study of nearly 5,000 English patients with chronic heart failure, adding to evidence that subclinical thyroid disorders in these patients requires no special management beyond ongoing monitoring.

Sebastian Kaulitzki/Fotolia

“Although thyroid dysfunction is related to outcome in patients with chronic heart failure, the association disappears when adjustment is made for established prognostic variables, such as age, NT-proBNP [N-terminal of the prohormone brain natriuretic peptide], and [New York Heart Association] class,” wrote Nathan A. Samuel, MBChB, and coauthors in the American Journal of Cardiology.

Results from several earlier studies had shown evidence for reduced survival in heart failure patients with thyroid dysfunction, but in analyses that did not adjust for heart failure severity, such as a 2013 report that used data from the Sudden Cardiac Death in Heart Failure Trial SCD-HeFT. Other studies that adjusted for heart failure severity based on serum level of natriuretic peptides did not show significant associations between thyroid function and mortality, and when those results couple with the new report they together minimize the immediate risk from subclinical thyroid dysfunction faced by heart failure patients, wrote the authors of the new report.

Don’t treat subclinical thyroid dysfunction

“Our results suggest that subclinical thyroid disease has little impact on outcomes, and that we should not treat subclinical hypothyroidism in the expectation of improving outlook,” said Andrew L. Clark, MD, senior author on the new report and professor and head of the department of academic cardiology at Hull (England) York Medical School.

“Both hyper-and hypothyroidism can cause heart failure, so thyroid function should always be checked in patients when they present with heart failure. A small proportion of patients have heart failure that is potentially reversible” with thyroid-directed treatment, Dr. Clark said in an interview.

But “subclinical disease should probably not be treated, although we have not conducted a clinical trial that proves this assertion. We speculate, based on our findings, that such a trial is unlikely to be positive.”

Patients with subclinical thyroid disorders, particularly subclinical hypothyroidism, “need to be followed and treated should they develop clinical disease,” he maintained. “Except in extreme circumstances, such as the handful of patients who might have gross myxedema and may be near coma, thyroid replacement therapy for those [with heart failure] who have clinical hypothyroidism should follow standard lines.”

It is important to monitor thyroid function,” agreed Dr. Samuel, a researcher in the department of academic cardiology at Hull York Medical School. “We found that thyroxine use was most common among patients with hyperthyroidism, suggesting that they were previously hypothyroid and had received inappropriate treatment.”

Confounder adjustment mitigates the thyroid link

The new analysis used data collected from 6,782 consecutive heart failure patients enrolled during 2000-2018 at a community heart failure clinic that serves patients in the region of Hull, England. The researchers identified 4,992 of these patients with confirmed heart failure and adequate data for their analyses, including 2,997 (60%) with heart failure with reduced ejection fraction (HFrEF) and 1,995 (40%) with heart failure with normal ejection fraction (HFnEF, the term used by the authors but often called heart failure with preserved ejection fraction).

Thyroid hormone levels showed that 90% of these patients were euthyroid, 6% were hyperthyroid, and 4% were hypothyroid, rates consistent with prior reports for both the general population and heart failure patients. Only 12 patients (0.2%) had overt hypothyroidism, and fewer that 1% (about 45 patients) had overt hyperthyroidism. Patients averaged about 73 years of age, and during a median 4.6 years of follow-up 58% died.

Both the hypo- and hyperthyroid patients showed significantly higher mortality rates than euthyroid patients in a univariate analysis. But the patients with thyroid dysfunction also had more comorbidities, more severe heart failure symptoms measured by NYHA functional class, and more severe heart failure measured as higher serum levels of NT-proBNP.

In a multivariate analysis that adjusted for these factors, the significant differences disappeared among the entire group of heart failure patients for the outcomes of all-cause mortality, and mortality or hospitalization with heart failure. The multivariate analysis also showed no significant association between higher levels of thyroid-stimulating hormone (TSH) and all-cause death or death plus heart failure hospitalization among the patients with HFrEF.

Among patients with HFnEF, the multivariate adjusted analysis showed a small increase in both mortality and mortality plus hospitalization for heart failure, a 2% rise for each of these two endpoints for each 1 mIU/L increase in TSH, the authors reported. Although the P value for each of these two significant differences among patients with HFnEF was .02, the 95% confidence interval included 1.00 and ranged from 1.00 to 1.04.

The multivariate analysis identified three variables with the strongest associations with all-cause mortality: older age, higher levels of NT-proBNP, and higher NYHA class indicating greater functional impairment.

The results support the hypothesis that “worsening heart failure can lead to down-regulation of thyroid hormone signaling,” the authors suggested. Their study is also “the first to examine the prognostic significance of thyroid dysfunction in a large population of patients with HFnEF.” This analysis showed a “weak but significant association between increasing TSH and both mortality and the composite endpoint in patients with HFnEF.”

“HFnEF is a heterogeneous group of conditions that are difficult to diagnose in many cases. Therefore, future studies are needed to provide further clarity on the effect of thyroid dysfunction in these patients,” Dr. Samuel said.

The study received no commercial funding. Dr. Samuel and Dr. Clark had no disclosures.

[email protected]

SOURCE: Samuel NA et al. Am J Cardiol. 2020 Oct 24. doi: 10.1016/j.amjcard.2020.10.034.

In order for percutaneous coronary intervention (PCI) to shine, compared with meds alone in patients with type-2 diabetes and stable coronary disease (CAD), it needs help from aggressive control of LDL cholesterol (LDL-C) levels, suggests a patient-level meta-analysis of three major randomized trials.

Performing PCI in such patients with diabetes conferred further benefit over optimal medical therapy (OMT) for major adverse cardiac or cerebrovascular events (MACCE) only among those whose LDL-C levels had been pushed below the guidelines-specified threshold of 70 mg/dL within 1 year.

At that level of LDL-C control, PCI, compared with the meds-alone strategy, was followed by a nearly 40% drop in 4-year risk for the composite endpoint, which consisted of death from any cause or nonfatal myocardial infarction (MI) or stroke.

Also for patients reaching a 1-year LDL-C of <70 mg/dL, the risk of MACCE was similar for those who had been assigned to coronary bypass surgery (CABG), compared with PCI. But that risk was significantly lower for the CABG group among those reaching LDL-C levels above that threshold.

“The strategy of revascularization with the LDL lowering, that’s the combination that seems to be a winner” in such patients with diabetes and stable CAD, lead author Michael E. Farkouh, MD, MSc, said in an interview.

If their LDL-C “stays above 70 mg/dL, they don’t really enjoy any benefit of PCI. It’s a message to our interventional community to really drive that LDL down,” said Dr. Farkouh, of the University of Toronto. “Not only with statins, but perhaps with PCSK9 inhibitors, ezetimibe, and other therapies to lower that LDL-C.”

The analysis, published Nov. 2 in the Journal of the American College of Cardiology, pooled more than 4,000 patients with diabetes and stable CAD randomized in the BARI 2D, FREEDOM, and COURAGE trials.

The new study adds a twist to an ongoing theme throughout some meta-analyses and clinical trials like ISCHEMIA since the results of COURAGE were unveiled 13 years ago. The latter trial famously saw no significant difference in death, MI, or stroke in patients with stable CAD assigned to OMT with or without PCI. That set off years of controversy about the relative merits of the revascularization and meds-only strategies in stable CAD that persists today.

But, Dr. Farkouh proposed, whether PCI improves clinical outcomes, compared with meds alone, at least in patients with diabetes, may be tied to the success of LDL-C-lowering therapies in reaching that goal, which in the current study was below 70 mg/dL.

“In this analysis of pooled data from the three major trials, we demonstrate that attaining that level of LDL-C at 1 year portends a better outcome for PCI” in patients with diabetes and stable CAD, he said.

The findings “probably need to be studied further, but it is compelling to think that if we can drive the LDL-C down by one year after the procedure, we have better outcomes with PCI,” compared with a meds-only strategy in patients with diabetes and stable CAD. “That really vindicates a lot of those who believe in PCI,” Dr. Farkouh said.

“What’s surprising to me is, if the patient has an LDL less than 70, why is it that there is a benefit of PCI, compared to medical therapy alone? Because they’re already so aggressively managed, you would think there shouldn’t be a benefit,” Sripal Bangalore, MD, MHA, New York University, said in an interview. “For me, that part is difficult to understand.”

The finding somewhat contradicts the results of ISCHEMIA, in which OMT – including LDL-C-lowering therapy – was considered more aggressive than usually managed in practice, Bangalore said. Yet the trial saw no outcomes difference between PCI and the more conservative approach, leading some to speculate that PCI may be a better choice when, for whatever reason, medical therapy isn’t optimal.

The observed superiority of PCI over meds-only at the lowest LDL-C levels is, according to Dr. Banagalore, “more likely because of residual confounding, given the fact that they’re combining three different trials, which are aimed to address different sets of questions.” He was an investigator with the FREEDOM and ISCHEMIA trials but isn’t associated with the current report.

The main message from this observational analysis is that “of course, we want to get the LDL as low as possible in these patients with demonstrated cardiovascular disease and diabetes,” Donald M. Lloyd-Jones, MD, ScM, Northwestern University, Chicago, said in an interview. “Every one of these patients should be shooting for as low an LDL as possible.”

Regardless of revascularization strategy, he said, “we have to get people on a high-intensity statin, or at least their maximally targeted dose, and have a careful and thoughtful conversation about whether they need additional lowering with, perhaps, ezetimibe, if they’re not below the thresholds we’d like to see them at, in this case, 70 mg/dL.”

Still, the current findings that the relative effects of PCI and CABG in these patients may vary by degree of LDL-C reduction “are interesting, but would have to be tested a little bit more directly,” said Dr. Lloyd-Jones, who is not affiliated with the analysis.

An accompanying editorial, which also acknowledges the study’s limitations, says its results “are relevant for clinical practice and may pave the way toward the generation of novel personalized medicine models that can optimize care of patients with type-2 diabetes.” 

They “support the concept of an individualized treatment strategy that accounts for a patient’s LDL-C level to estimate clinical outcomes and expected treatment effects after therapeutic interventions,” say the authors, led by Eliano P. Navarese, MD, PhD, Nicolaus Copernicus University, Bydgoszcz, Poland.

“For daily practice, these results also underscore the importance of follow-up LDL-C measurements, both as a risk stratifier and as an indicator for therapy adjustments,” they write, noting that “current guidelines provide no formal recommendation on when to check LDL-C after PCI.”

The meta-analysis followed a total of 4050 patients with diabetes and stable CAD from the three randomized trials, those with evaluable baseline and follow-up LDL-C measurements, for a median of 4 years after the 1-year LDL-C assessment. At that time, at least 90% of patients in each of the trials had statin prescriptions, the group reported.

At one year, 34.5% of the total cohort had an LDL-C <70 mg/dL; their mean was 55.8 mg/dL.

And 42.2% had an LDL-C from 70 mg/dL to <100 mg/dL; their mean was 83.4 mg/dL. Compared with patients with an LDL-C <70 mg/dL, their adjusted hazard ratio for the composite endpoint was not elevated at 1.07 (95% CI, 0.86-1.32, P = .54).

Finally, 23.2% had an LDL-C ≥100 mg/dL; the mean was 123.0 mg/dL. Compared with the group with the lowest 1-year LDL-C, their adjusted HR for MACCE was increased at 1.46 (95% CI, 1.15 - 1.85, P = .002).

That HR among the 42.3% of patients in the PCI cohort, compared with the 33.3% assigned to meds only, climbed significantly only among those in the lowest 1-year LDL-C stratum: HR, 0.61 (95% CI, 0.40-0.91, P = .016). Corresponding HRs in the mid-range and highest 1-year LDL strata were close to unity and nonsignificant at P = .71 and P = .98, respectively.

On the other hand, the 24.4% of patients assigned to CABG showed better MACCE outcomes than those in the meds-only group across all three 1-year LDL-C strata.

The risk of MACCE wasn’t significantly altered by CABG, compared with PCI among patients achieving a 1-year LDL-C less than 70 mg/dL. However, it fell by about one-half for CABG vs. PCI in both the mid-range and highest 1-year LDL-C strata, P = .003 and P = .022, respectively.

Dr. Bangalore said he’s entirely behind the results of the study’s comparison of PCI and CABG. “It’s exactly the hypothesis that I’ve been putting forward, that if you want to achieve results as good as CABG, do PCI with aggressive medical therapy.” That means second-generation drug-eluting stents for the target lesions, “and aggressive medical therapy to address all of the nontarget lesions, specifically in diabetics.”

It’s possible, Dr. Lloyd-Jones said, that there is “no longer a dichotomy between revascularization strategies,” with respect to clinical outcomes, in such patients who maintain an LDL less than 70 mg/dL, as the study suggests.

“But I wonder, if it had continued for another 4 years of follow-up, whether we would see the CABG patients start to have more events,” such that the CABG advantage goes away at higher LDL-C levels, he proposed.

Or, Dr. Lloyd-Jones speculated, if all patients had achieved LDL-C below 70 mg/dL, “would there be such a difference between the PCI and CABG groups? My bet would be that it would be small or abolished.”

Dr. Farkouh discloses receiving research grants from Amgen, Novo Nordisk, and Novartis. Disclosures for the other study authors can be found with the original article. Editorialist Dr. Navarese discloses receiving consulting fees or honoraria from Abbott, AstraZeneca, Amgen, Bayer, Sanofi, and Pfizer; and grants from Abbott and Amgen. Dr. Lloyd-Jones has disclosed no relevant financial relationships.

This article first appeared on Medscape.com.

In order for percutaneous coronary intervention (PCI) to shine, compared with meds alone in patients with type-2 diabetes and stable coronary disease (CAD), it needs help from aggressive control of LDL cholesterol (LDL-C) levels, suggests a patient-level meta-analysis of three major randomized trials.

Performing PCI in such patients with diabetes conferred further benefit over optimal medical therapy (OMT) for major adverse cardiac or cerebrovascular events (MACCE) only among those whose LDL-C levels had been pushed below the guidelines-specified threshold of 70 mg/dL within 1 year.

At that level of LDL-C control, PCI, compared with the meds-alone strategy, was followed by a nearly 40% drop in 4-year risk for the composite endpoint, which consisted of death from any cause or nonfatal myocardial infarction (MI) or stroke.

Also for patients reaching a 1-year LDL-C of <70 mg/dL, the risk of MACCE was similar for those who had been assigned to coronary bypass surgery (CABG), compared with PCI. But that risk was significantly lower for the CABG group among those reaching LDL-C levels above that threshold.

“The strategy of revascularization with the LDL lowering, that’s the combination that seems to be a winner” in such patients with diabetes and stable CAD, lead author Michael E. Farkouh, MD, MSc, said in an interview.

If their LDL-C “stays above 70 mg/dL, they don’t really enjoy any benefit of PCI. It’s a message to our interventional community to really drive that LDL down,” said Dr. Farkouh, of the University of Toronto. “Not only with statins, but perhaps with PCSK9 inhibitors, ezetimibe, and other therapies to lower that LDL-C.”

The analysis, published Nov. 2 in the Journal of the American College of Cardiology, pooled more than 4,000 patients with diabetes and stable CAD randomized in the BARI 2D, FREEDOM, and COURAGE trials.

The new study adds a twist to an ongoing theme throughout some meta-analyses and clinical trials like ISCHEMIA since the results of COURAGE were unveiled 13 years ago. The latter trial famously saw no significant difference in death, MI, or stroke in patients with stable CAD assigned to OMT with or without PCI. That set off years of controversy about the relative merits of the revascularization and meds-only strategies in stable CAD that persists today.

But, Dr. Farkouh proposed, whether PCI improves clinical outcomes, compared with meds alone, at least in patients with diabetes, may be tied to the success of LDL-C-lowering therapies in reaching that goal, which in the current study was below 70 mg/dL.

“In this analysis of pooled data from the three major trials, we demonstrate that attaining that level of LDL-C at 1 year portends a better outcome for PCI” in patients with diabetes and stable CAD, he said.

The findings “probably need to be studied further, but it is compelling to think that if we can drive the LDL-C down by one year after the procedure, we have better outcomes with PCI,” compared with a meds-only strategy in patients with diabetes and stable CAD. “That really vindicates a lot of those who believe in PCI,” Dr. Farkouh said.

“What’s surprising to me is, if the patient has an LDL less than 70, why is it that there is a benefit of PCI, compared to medical therapy alone? Because they’re already so aggressively managed, you would think there shouldn’t be a benefit,” Sripal Bangalore, MD, MHA, New York University, said in an interview. “For me, that part is difficult to understand.”

The finding somewhat contradicts the results of ISCHEMIA, in which OMT – including LDL-C-lowering therapy – was considered more aggressive than usually managed in practice, Bangalore said. Yet the trial saw no outcomes difference between PCI and the more conservative approach, leading some to speculate that PCI may be a better choice when, for whatever reason, medical therapy isn’t optimal.

The observed superiority of PCI over meds-only at the lowest LDL-C levels is, according to Dr. Banagalore, “more likely because of residual confounding, given the fact that they’re combining three different trials, which are aimed to address different sets of questions.” He was an investigator with the FREEDOM and ISCHEMIA trials but isn’t associated with the current report.

The main message from this observational analysis is that “of course, we want to get the LDL as low as possible in these patients with demonstrated cardiovascular disease and diabetes,” Donald M. Lloyd-Jones, MD, ScM, Northwestern University, Chicago, said in an interview. “Every one of these patients should be shooting for as low an LDL as possible.”

Regardless of revascularization strategy, he said, “we have to get people on a high-intensity statin, or at least their maximally targeted dose, and have a careful and thoughtful conversation about whether they need additional lowering with, perhaps, ezetimibe, if they’re not below the thresholds we’d like to see them at, in this case, 70 mg/dL.”

Still, the current findings that the relative effects of PCI and CABG in these patients may vary by degree of LDL-C reduction “are interesting, but would have to be tested a little bit more directly,” said Dr. Lloyd-Jones, who is not affiliated with the analysis.

An accompanying editorial, which also acknowledges the study’s limitations, says its results “are relevant for clinical practice and may pave the way toward the generation of novel personalized medicine models that can optimize care of patients with type-2 diabetes.” 

They “support the concept of an individualized treatment strategy that accounts for a patient’s LDL-C level to estimate clinical outcomes and expected treatment effects after therapeutic interventions,” say the authors, led by Eliano P. Navarese, MD, PhD, Nicolaus Copernicus University, Bydgoszcz, Poland.

“For daily practice, these results also underscore the importance of follow-up LDL-C measurements, both as a risk stratifier and as an indicator for therapy adjustments,” they write, noting that “current guidelines provide no formal recommendation on when to check LDL-C after PCI.”

The meta-analysis followed a total of 4050 patients with diabetes and stable CAD from the three randomized trials, those with evaluable baseline and follow-up LDL-C measurements, for a median of 4 years after the 1-year LDL-C assessment. At that time, at least 90% of patients in each of the trials had statin prescriptions, the group reported.

At one year, 34.5% of the total cohort had an LDL-C <70 mg/dL; their mean was 55.8 mg/dL.

And 42.2% had an LDL-C from 70 mg/dL to <100 mg/dL; their mean was 83.4 mg/dL. Compared with patients with an LDL-C <70 mg/dL, their adjusted hazard ratio for the composite endpoint was not elevated at 1.07 (95% CI, 0.86-1.32, P = .54).

Finally, 23.2% had an LDL-C ≥100 mg/dL; the mean was 123.0 mg/dL. Compared with the group with the lowest 1-year LDL-C, their adjusted HR for MACCE was increased at 1.46 (95% CI, 1.15 - 1.85, P = .002).

That HR among the 42.3% of patients in the PCI cohort, compared with the 33.3% assigned to meds only, climbed significantly only among those in the lowest 1-year LDL-C stratum: HR, 0.61 (95% CI, 0.40-0.91, P = .016). Corresponding HRs in the mid-range and highest 1-year LDL strata were close to unity and nonsignificant at P = .71 and P = .98, respectively.

On the other hand, the 24.4% of patients assigned to CABG showed better MACCE outcomes than those in the meds-only group across all three 1-year LDL-C strata.

The risk of MACCE wasn’t significantly altered by CABG, compared with PCI among patients achieving a 1-year LDL-C less than 70 mg/dL. However, it fell by about one-half for CABG vs. PCI in both the mid-range and highest 1-year LDL-C strata, P = .003 and P = .022, respectively.

Dr. Bangalore said he’s entirely behind the results of the study’s comparison of PCI and CABG. “It’s exactly the hypothesis that I’ve been putting forward, that if you want to achieve results as good as CABG, do PCI with aggressive medical therapy.” That means second-generation drug-eluting stents for the target lesions, “and aggressive medical therapy to address all of the nontarget lesions, specifically in diabetics.”

It’s possible, Dr. Lloyd-Jones said, that there is “no longer a dichotomy between revascularization strategies,” with respect to clinical outcomes, in such patients who maintain an LDL less than 70 mg/dL, as the study suggests.

“But I wonder, if it had continued for another 4 years of follow-up, whether we would see the CABG patients start to have more events,” such that the CABG advantage goes away at higher LDL-C levels, he proposed.

Or, Dr. Lloyd-Jones speculated, if all patients had achieved LDL-C below 70 mg/dL, “would there be such a difference between the PCI and CABG groups? My bet would be that it would be small or abolished.”

Dr. Farkouh discloses receiving research grants from Amgen, Novo Nordisk, and Novartis. Disclosures for the other study authors can be found with the original article. Editorialist Dr. Navarese discloses receiving consulting fees or honoraria from Abbott, AstraZeneca, Amgen, Bayer, Sanofi, and Pfizer; and grants from Abbott and Amgen. Dr. Lloyd-Jones has disclosed no relevant financial relationships.

This article first appeared on Medscape.com.

In order for percutaneous coronary intervention (PCI) to shine, compared with meds alone in patients with type-2 diabetes and stable coronary disease (CAD), it needs help from aggressive control of LDL cholesterol (LDL-C) levels, suggests a patient-level meta-analysis of three major randomized trials.

Performing PCI in such patients with diabetes conferred further benefit over optimal medical therapy (OMT) for major adverse cardiac or cerebrovascular events (MACCE) only among those whose LDL-C levels had been pushed below the guidelines-specified threshold of 70 mg/dL within 1 year.

At that level of LDL-C control, PCI, compared with the meds-alone strategy, was followed by a nearly 40% drop in 4-year risk for the composite endpoint, which consisted of death from any cause or nonfatal myocardial infarction (MI) or stroke.

Also for patients reaching a 1-year LDL-C of <70 mg/dL, the risk of MACCE was similar for those who had been assigned to coronary bypass surgery (CABG), compared with PCI. But that risk was significantly lower for the CABG group among those reaching LDL-C levels above that threshold.

“The strategy of revascularization with the LDL lowering, that’s the combination that seems to be a winner” in such patients with diabetes and stable CAD, lead author Michael E. Farkouh, MD, MSc, said in an interview.

If their LDL-C “stays above 70 mg/dL, they don’t really enjoy any benefit of PCI. It’s a message to our interventional community to really drive that LDL down,” said Dr. Farkouh, of the University of Toronto. “Not only with statins, but perhaps with PCSK9 inhibitors, ezetimibe, and other therapies to lower that LDL-C.”

The analysis, published Nov. 2 in the Journal of the American College of Cardiology, pooled more than 4,000 patients with diabetes and stable CAD randomized in the BARI 2D, FREEDOM, and COURAGE trials.

The new study adds a twist to an ongoing theme throughout some meta-analyses and clinical trials like ISCHEMIA since the results of COURAGE were unveiled 13 years ago. The latter trial famously saw no significant difference in death, MI, or stroke in patients with stable CAD assigned to OMT with or without PCI. That set off years of controversy about the relative merits of the revascularization and meds-only strategies in stable CAD that persists today.

But, Dr. Farkouh proposed, whether PCI improves clinical outcomes, compared with meds alone, at least in patients with diabetes, may be tied to the success of LDL-C-lowering therapies in reaching that goal, which in the current study was below 70 mg/dL.

“In this analysis of pooled data from the three major trials, we demonstrate that attaining that level of LDL-C at 1 year portends a better outcome for PCI” in patients with diabetes and stable CAD, he said.

The findings “probably need to be studied further, but it is compelling to think that if we can drive the LDL-C down by one year after the procedure, we have better outcomes with PCI,” compared with a meds-only strategy in patients with diabetes and stable CAD. “That really vindicates a lot of those who believe in PCI,” Dr. Farkouh said.

“What’s surprising to me is, if the patient has an LDL less than 70, why is it that there is a benefit of PCI, compared to medical therapy alone? Because they’re already so aggressively managed, you would think there shouldn’t be a benefit,” Sripal Bangalore, MD, MHA, New York University, said in an interview. “For me, that part is difficult to understand.”

The finding somewhat contradicts the results of ISCHEMIA, in which OMT – including LDL-C-lowering therapy – was considered more aggressive than usually managed in practice, Bangalore said. Yet the trial saw no outcomes difference between PCI and the more conservative approach, leading some to speculate that PCI may be a better choice when, for whatever reason, medical therapy isn’t optimal.

The observed superiority of PCI over meds-only at the lowest LDL-C levels is, according to Dr. Banagalore, “more likely because of residual confounding, given the fact that they’re combining three different trials, which are aimed to address different sets of questions.” He was an investigator with the FREEDOM and ISCHEMIA trials but isn’t associated with the current report.

The main message from this observational analysis is that “of course, we want to get the LDL as low as possible in these patients with demonstrated cardiovascular disease and diabetes,” Donald M. Lloyd-Jones, MD, ScM, Northwestern University, Chicago, said in an interview. “Every one of these patients should be shooting for as low an LDL as possible.”

Regardless of revascularization strategy, he said, “we have to get people on a high-intensity statin, or at least their maximally targeted dose, and have a careful and thoughtful conversation about whether they need additional lowering with, perhaps, ezetimibe, if they’re not below the thresholds we’d like to see them at, in this case, 70 mg/dL.”

Still, the current findings that the relative effects of PCI and CABG in these patients may vary by degree of LDL-C reduction “are interesting, but would have to be tested a little bit more directly,” said Dr. Lloyd-Jones, who is not affiliated with the analysis.

An accompanying editorial, which also acknowledges the study’s limitations, says its results “are relevant for clinical practice and may pave the way toward the generation of novel personalized medicine models that can optimize care of patients with type-2 diabetes.” 

They “support the concept of an individualized treatment strategy that accounts for a patient’s LDL-C level to estimate clinical outcomes and expected treatment effects after therapeutic interventions,” say the authors, led by Eliano P. Navarese, MD, PhD, Nicolaus Copernicus University, Bydgoszcz, Poland.

“For daily practice, these results also underscore the importance of follow-up LDL-C measurements, both as a risk stratifier and as an indicator for therapy adjustments,” they write, noting that “current guidelines provide no formal recommendation on when to check LDL-C after PCI.”

The meta-analysis followed a total of 4050 patients with diabetes and stable CAD from the three randomized trials, those with evaluable baseline and follow-up LDL-C measurements, for a median of 4 years after the 1-year LDL-C assessment. At that time, at least 90% of patients in each of the trials had statin prescriptions, the group reported.

At one year, 34.5% of the total cohort had an LDL-C <70 mg/dL; their mean was 55.8 mg/dL.

And 42.2% had an LDL-C from 70 mg/dL to <100 mg/dL; their mean was 83.4 mg/dL. Compared with patients with an LDL-C <70 mg/dL, their adjusted hazard ratio for the composite endpoint was not elevated at 1.07 (95% CI, 0.86-1.32, P = .54).

Finally, 23.2% had an LDL-C ≥100 mg/dL; the mean was 123.0 mg/dL. Compared with the group with the lowest 1-year LDL-C, their adjusted HR for MACCE was increased at 1.46 (95% CI, 1.15 - 1.85, P = .002).

That HR among the 42.3% of patients in the PCI cohort, compared with the 33.3% assigned to meds only, climbed significantly only among those in the lowest 1-year LDL-C stratum: HR, 0.61 (95% CI, 0.40-0.91, P = .016). Corresponding HRs in the mid-range and highest 1-year LDL strata were close to unity and nonsignificant at P = .71 and P = .98, respectively.

On the other hand, the 24.4% of patients assigned to CABG showed better MACCE outcomes than those in the meds-only group across all three 1-year LDL-C strata.

The risk of MACCE wasn’t significantly altered by CABG, compared with PCI among patients achieving a 1-year LDL-C less than 70 mg/dL. However, it fell by about one-half for CABG vs. PCI in both the mid-range and highest 1-year LDL-C strata, P = .003 and P = .022, respectively.

Dr. Bangalore said he’s entirely behind the results of the study’s comparison of PCI and CABG. “It’s exactly the hypothesis that I’ve been putting forward, that if you want to achieve results as good as CABG, do PCI with aggressive medical therapy.” That means second-generation drug-eluting stents for the target lesions, “and aggressive medical therapy to address all of the nontarget lesions, specifically in diabetics.”

It’s possible, Dr. Lloyd-Jones said, that there is “no longer a dichotomy between revascularization strategies,” with respect to clinical outcomes, in such patients who maintain an LDL less than 70 mg/dL, as the study suggests.

“But I wonder, if it had continued for another 4 years of follow-up, whether we would see the CABG patients start to have more events,” such that the CABG advantage goes away at higher LDL-C levels, he proposed.

Or, Dr. Lloyd-Jones speculated, if all patients had achieved LDL-C below 70 mg/dL, “would there be such a difference between the PCI and CABG groups? My bet would be that it would be small or abolished.”

Dr. Farkouh discloses receiving research grants from Amgen, Novo Nordisk, and Novartis. Disclosures for the other study authors can be found with the original article. Editorialist Dr. Navarese discloses receiving consulting fees or honoraria from Abbott, AstraZeneca, Amgen, Bayer, Sanofi, and Pfizer; and grants from Abbott and Amgen. Dr. Lloyd-Jones has disclosed no relevant financial relationships.

This article first appeared on Medscape.com.

Five common therapies and practices related to children’s heart health may be unnecessary, and physicians and parents should be careful about using them, the American Academy of Pediatrics explained in guidance released Nov. 2.

The AAP Section on Cardiology and Cardiac Surgery developed the recommendations as part of the Choosing Wisely campaign after reviewing evidence pertaining to practices common during pediatric visits, such as routinely ordering an electrocardiogram (ECG) as part of a sports exam.

The guidance lets physicians know what is not necessary or not indicated, with noted exceptions, Christopher S. Snyder, MD, chair of the section, said in an interview.

In all cases, family history is key, said Dr. Snyder, who is also chief of the division of pediatric cardiology at University Hospitals Cleveland Medical Center. That means taking the time necessary to ask about aunts, uncles, and all first-degree relatives, not just asking the single question of whether a patient has a family history of cardiac problems.

The following are the targeted practices and the AAP’s guidance on each.
 

ECG for sports participation

A screening ECG should not be ordered as part of a routine sports entry examination in otherwise healthy patients who have no symptoms and no personal or family history of cardiac disease, the committee says.

Some medical societies argue that all children who participate in sports should have an ECG, but, Dr. Snyder said, “Currently there are no data that support that, especially in the United States.”

ECGs often yield false positive findings, he noted: “About 10% of them will say the child is a little abnormal.”

That can be a particular problem in places with few or no pediatric cardiologists because kids can become sidelined from sports without access to experts who could clear them.

“In the U.S.,” he said, “we believe that the preparticipation physical exam and screening, which is routine for all high school athletes for sure and most athletes who compete in sports, is currently good enough.”

However, he warned, patients with a family history of heart disease need to see a pediatric cardiologist and “those patients need an ECG.”

The test is not perfect, though, he noted: “You could get your screening, go home, get a fever, COVID, something like that, and come back and have myocarditis and drop dead.”
 

ECG before ADHD therapy

Similarly, a screening ECG is not routinely needed before initiating therapy for ADHD in asymptomatic, otherwise healthy children who have no personal or family history of cardiac disease, according to the new guidance.

Dr. Snyder said that it has become routine for children to undergo an ECG before ADHD therapy, but evidence doesn’t support the practice, and with the rise in the number of ADHD diagnoses, the tests have increasingly become a burden.

Twenty years ago, the prevalence of ADHD was 3%-4%, Dr. Snyder said. It is now almost threefold higher.

The AAP committee points out that, when ECG abnormalities are identified, they rarely lead to a change in ADHD therapy. Additionally, the typical stimulants used to treat ADHD “have never shown any major effect on the heart,” Dr. Snyder said.

“Black box warnings have been put on these medications, but nothing has been found in the very routine stimulants in normal, routine doses to warrant an ECG,” he said.
 

Echocardiogram for syncope

The committee says routine use of echocardiograms for children with syncope is unnecessary unless a child has a concerning history or ECG abnormalities.

Most patient who have true syncope or are passing out or fainting are diagnosed through thorough family history, Dr. Snyder said.

“The vast majority of those need an ECG to rule out one other cause that can do this and a physical exam. If those things are normal, there really is no indication to do an echocardiogram,” he said.

“If the patient passes out while they’re running, they pass out doing strenuous exercise, or they pass out for 10-15 minutes as opposed to 20 seconds – those are the ones that need a thorough cardiac workup. But routine passing out, waking up in seconds, those do not.”
 

Echocardiogram for chest pain

Children with chest pain do not need an echocardiogram unless an ECG is abnormal or the patient has a concerning history, according to the new recommendations.

Too often, Dr. Snyder said, providers treat kids as they would adults.

“Often it comes down to what you learn in medical school,” Dr. Snyder said. “In medical school, we have 6 weeks of cardiology and we had 1 hour of pediatric cardiology.”

That younger patients will clog their arteries with fatty foods and high lipids “is really exceptionally rare,” Dr. Snyder said.

Chest pain “rarely, if ever” means heart attack in younger children, he added.

A thorough history and complete physical exam are critical, “without jumping immediately to an echocardiogram, which 99.9% of the time is going to be normal,” he said.
 

Troponins for chest pain

In addition, a typical workup for pediatric chest pain need not include evaluating troponins unless there is a concerning history or ECG abnormalities.

Snyder notes that kids with chest pain are often brought to emergency departments that are not pediatric specific, and thus clinicians turn to the standard treatment for adults with chest pain: ECG and troponin.

“The reason we in pediatric cardiology don’t love this is that troponins tend not to be specific just for heart in kids,” Dr. Snyder said. “If someone has anginal chest pain – shortness of breath, chest pain doing anything and everything, [chest pain that] occurs when they’re exercising, feels like an elephant standing on their chest – then we do encourage troponins on those patients.”

The guidance discourages ordering troponins without careful consideration of the patient’s age and condition, he said.

This list was developed by faculty in Pediatric Cardiology at University Hospitals in Cleveland. It was revised and approved by the AAP Section on Cardiology and Cardiac Surgery and the AAP Executive Committee.
 

A version of this article originally appeared on Medscape.com.

Five common therapies and practices related to children’s heart health may be unnecessary, and physicians and parents should be careful about using them, the American Academy of Pediatrics explained in guidance released Nov. 2.

The AAP Section on Cardiology and Cardiac Surgery developed the recommendations as part of the Choosing Wisely campaign after reviewing evidence pertaining to practices common during pediatric visits, such as routinely ordering an electrocardiogram (ECG) as part of a sports exam.

The guidance lets physicians know what is not necessary or not indicated, with noted exceptions, Christopher S. Snyder, MD, chair of the section, said in an interview.

In all cases, family history is key, said Dr. Snyder, who is also chief of the division of pediatric cardiology at University Hospitals Cleveland Medical Center. That means taking the time necessary to ask about aunts, uncles, and all first-degree relatives, not just asking the single question of whether a patient has a family history of cardiac problems.

The following are the targeted practices and the AAP’s guidance on each.
 

ECG for sports participation

A screening ECG should not be ordered as part of a routine sports entry examination in otherwise healthy patients who have no symptoms and no personal or family history of cardiac disease, the committee says.

Some medical societies argue that all children who participate in sports should have an ECG, but, Dr. Snyder said, “Currently there are no data that support that, especially in the United States.”

ECGs often yield false positive findings, he noted: “About 10% of them will say the child is a little abnormal.”

That can be a particular problem in places with few or no pediatric cardiologists because kids can become sidelined from sports without access to experts who could clear them.

“In the U.S.,” he said, “we believe that the preparticipation physical exam and screening, which is routine for all high school athletes for sure and most athletes who compete in sports, is currently good enough.”

However, he warned, patients with a family history of heart disease need to see a pediatric cardiologist and “those patients need an ECG.”

The test is not perfect, though, he noted: “You could get your screening, go home, get a fever, COVID, something like that, and come back and have myocarditis and drop dead.”
 

ECG before ADHD therapy

Similarly, a screening ECG is not routinely needed before initiating therapy for ADHD in asymptomatic, otherwise healthy children who have no personal or family history of cardiac disease, according to the new guidance.

Dr. Snyder said that it has become routine for children to undergo an ECG before ADHD therapy, but evidence doesn’t support the practice, and with the rise in the number of ADHD diagnoses, the tests have increasingly become a burden.

Twenty years ago, the prevalence of ADHD was 3%-4%, Dr. Snyder said. It is now almost threefold higher.

The AAP committee points out that, when ECG abnormalities are identified, they rarely lead to a change in ADHD therapy. Additionally, the typical stimulants used to treat ADHD “have never shown any major effect on the heart,” Dr. Snyder said.

“Black box warnings have been put on these medications, but nothing has been found in the very routine stimulants in normal, routine doses to warrant an ECG,” he said.
 

Echocardiogram for syncope

The committee says routine use of echocardiograms for children with syncope is unnecessary unless a child has a concerning history or ECG abnormalities.

Most patient who have true syncope or are passing out or fainting are diagnosed through thorough family history, Dr. Snyder said.

“The vast majority of those need an ECG to rule out one other cause that can do this and a physical exam. If those things are normal, there really is no indication to do an echocardiogram,” he said.

“If the patient passes out while they’re running, they pass out doing strenuous exercise, or they pass out for 10-15 minutes as opposed to 20 seconds – those are the ones that need a thorough cardiac workup. But routine passing out, waking up in seconds, those do not.”
 

Echocardiogram for chest pain

Children with chest pain do not need an echocardiogram unless an ECG is abnormal or the patient has a concerning history, according to the new recommendations.

Too often, Dr. Snyder said, providers treat kids as they would adults.

“Often it comes down to what you learn in medical school,” Dr. Snyder said. “In medical school, we have 6 weeks of cardiology and we had 1 hour of pediatric cardiology.”

That younger patients will clog their arteries with fatty foods and high lipids “is really exceptionally rare,” Dr. Snyder said.

Chest pain “rarely, if ever” means heart attack in younger children, he added.

A thorough history and complete physical exam are critical, “without jumping immediately to an echocardiogram, which 99.9% of the time is going to be normal,” he said.
 

Troponins for chest pain

In addition, a typical workup for pediatric chest pain need not include evaluating troponins unless there is a concerning history or ECG abnormalities.

Snyder notes that kids with chest pain are often brought to emergency departments that are not pediatric specific, and thus clinicians turn to the standard treatment for adults with chest pain: ECG and troponin.

“The reason we in pediatric cardiology don’t love this is that troponins tend not to be specific just for heart in kids,” Dr. Snyder said. “If someone has anginal chest pain – shortness of breath, chest pain doing anything and everything, [chest pain that] occurs when they’re exercising, feels like an elephant standing on their chest – then we do encourage troponins on those patients.”

The guidance discourages ordering troponins without careful consideration of the patient’s age and condition, he said.

This list was developed by faculty in Pediatric Cardiology at University Hospitals in Cleveland. It was revised and approved by the AAP Section on Cardiology and Cardiac Surgery and the AAP Executive Committee.
 

A version of this article originally appeared on Medscape.com.

Five common therapies and practices related to children’s heart health may be unnecessary, and physicians and parents should be careful about using them, the American Academy of Pediatrics explained in guidance released Nov. 2.

The AAP Section on Cardiology and Cardiac Surgery developed the recommendations as part of the Choosing Wisely campaign after reviewing evidence pertaining to practices common during pediatric visits, such as routinely ordering an electrocardiogram (ECG) as part of a sports exam.

The guidance lets physicians know what is not necessary or not indicated, with noted exceptions, Christopher S. Snyder, MD, chair of the section, said in an interview.

In all cases, family history is key, said Dr. Snyder, who is also chief of the division of pediatric cardiology at University Hospitals Cleveland Medical Center. That means taking the time necessary to ask about aunts, uncles, and all first-degree relatives, not just asking the single question of whether a patient has a family history of cardiac problems.

The following are the targeted practices and the AAP’s guidance on each.
 

ECG for sports participation

A screening ECG should not be ordered as part of a routine sports entry examination in otherwise healthy patients who have no symptoms and no personal or family history of cardiac disease, the committee says.

Some medical societies argue that all children who participate in sports should have an ECG, but, Dr. Snyder said, “Currently there are no data that support that, especially in the United States.”

ECGs often yield false positive findings, he noted: “About 10% of them will say the child is a little abnormal.”

That can be a particular problem in places with few or no pediatric cardiologists because kids can become sidelined from sports without access to experts who could clear them.

“In the U.S.,” he said, “we believe that the preparticipation physical exam and screening, which is routine for all high school athletes for sure and most athletes who compete in sports, is currently good enough.”

However, he warned, patients with a family history of heart disease need to see a pediatric cardiologist and “those patients need an ECG.”

The test is not perfect, though, he noted: “You could get your screening, go home, get a fever, COVID, something like that, and come back and have myocarditis and drop dead.”
 

ECG before ADHD therapy

Similarly, a screening ECG is not routinely needed before initiating therapy for ADHD in asymptomatic, otherwise healthy children who have no personal or family history of cardiac disease, according to the new guidance.

Dr. Snyder said that it has become routine for children to undergo an ECG before ADHD therapy, but evidence doesn’t support the practice, and with the rise in the number of ADHD diagnoses, the tests have increasingly become a burden.

Twenty years ago, the prevalence of ADHD was 3%-4%, Dr. Snyder said. It is now almost threefold higher.

The AAP committee points out that, when ECG abnormalities are identified, they rarely lead to a change in ADHD therapy. Additionally, the typical stimulants used to treat ADHD “have never shown any major effect on the heart,” Dr. Snyder said.

“Black box warnings have been put on these medications, but nothing has been found in the very routine stimulants in normal, routine doses to warrant an ECG,” he said.
 

Echocardiogram for syncope

The committee says routine use of echocardiograms for children with syncope is unnecessary unless a child has a concerning history or ECG abnormalities.

Most patient who have true syncope or are passing out or fainting are diagnosed through thorough family history, Dr. Snyder said.

“The vast majority of those need an ECG to rule out one other cause that can do this and a physical exam. If those things are normal, there really is no indication to do an echocardiogram,” he said.

“If the patient passes out while they’re running, they pass out doing strenuous exercise, or they pass out for 10-15 minutes as opposed to 20 seconds – those are the ones that need a thorough cardiac workup. But routine passing out, waking up in seconds, those do not.”
 

Echocardiogram for chest pain

Children with chest pain do not need an echocardiogram unless an ECG is abnormal or the patient has a concerning history, according to the new recommendations.

Too often, Dr. Snyder said, providers treat kids as they would adults.

“Often it comes down to what you learn in medical school,” Dr. Snyder said. “In medical school, we have 6 weeks of cardiology and we had 1 hour of pediatric cardiology.”

That younger patients will clog their arteries with fatty foods and high lipids “is really exceptionally rare,” Dr. Snyder said.

Chest pain “rarely, if ever” means heart attack in younger children, he added.

A thorough history and complete physical exam are critical, “without jumping immediately to an echocardiogram, which 99.9% of the time is going to be normal,” he said.
 

Troponins for chest pain

In addition, a typical workup for pediatric chest pain need not include evaluating troponins unless there is a concerning history or ECG abnormalities.

Snyder notes that kids with chest pain are often brought to emergency departments that are not pediatric specific, and thus clinicians turn to the standard treatment for adults with chest pain: ECG and troponin.

“The reason we in pediatric cardiology don’t love this is that troponins tend not to be specific just for heart in kids,” Dr. Snyder said. “If someone has anginal chest pain – shortness of breath, chest pain doing anything and everything, [chest pain that] occurs when they’re exercising, feels like an elephant standing on their chest – then we do encourage troponins on those patients.”

The guidance discourages ordering troponins without careful consideration of the patient’s age and condition, he said.

This list was developed by faculty in Pediatric Cardiology at University Hospitals in Cleveland. It was revised and approved by the AAP Section on Cardiology and Cardiac Surgery and the AAP Executive Committee.
 

A version of this article originally appeared on Medscape.com.

Survivors of Kawasaki disease remain at a higher long-term risk for cardiovascular events into young adulthood, including myocardial infarction, compared to people without the disease, new evidence reveals. The elevated risks emerged in survivors both with and without cardiovascular involvement at the time of initial diagnosis.

Overall risk of cardiovascular events was highest in the first year following Kawasaki disease diagnosis, and about 10 times greater than in healthy children, Cal Robinson, MD, said during a press conference at the virtual annual meeting of the American College of Rheumatology.

“The risk gradually decreased over time. However, even 10 years after diagnosis of their illness, they still had a 39% higher risk,” said study author Dr. Robinson, a PGY4 pediatric nephrology fellow at The Hospital for Sick Children in Toronto.

Dr. Robinson also put the numbers in perspective. “We fully acknowledged these are very rare events in children, especially healthy children, which is why we needed such a large cohort to study this. Interpret the numbers cautiously.”

In terms of patient and family counseling, “I would say children with Kawasaki disease have a higher risk of myocardial infarction, but the absolute risk is still low,” he added. For example, 16 Kawasaki disease survivors experienced a heart attack during follow-up, or 0.4% of the affected study population, compared to a rate of 0.1% among matched controls.

“These families are often very frightened after the initial Kawasaki disease diagnosis,” Dr. Robinson said. “We have to balance some discussion with what we know about Kawasaki disease without overly scaring or terrifying these families, who are already anxious.”

To quantify the incidence and timing of cardiovascular events and cardiac disease following diagnosis, Dr. Robinson and colleagues assessed large databases representing approximately 3 million children. They focused on children hospitalized with a Kawasaki disease diagnosis between 1995 and 2018. These children had a median length of stay of 3 days and 2.5% were admitted to critical care. The investigators matched his population 1:100 to unaffected children in Ontario.

Follow-up was up to 24 years (median, 11 years) in this retrospective, population-based cohort study.

Risks raised over a decade and beyond

Compared to matched controls, Kawasaki disease survivors had a higher risk for a cardiac event in the first year following diagnosis (adjusted hazard ratio, 11.65; 95% confidence interval, 10.34-13.13). The 1- to 5-year risk was lower (aHR, 3.35), a trend that continued between 5 and 10 years (aHR, 1.87) and as well as after more than 10 years (aHR, 1.39).

The risk of major adverse cardiac events (MACE, a composite of myocardial infarction, stroke, or cardiovascular death) was likewise highest in the first year after diagnosis (aHR, 3.27), followed by a 51% greater risk at 1-5 years, a 113% increased risk at 5-10 years, and a 17% elevated risk after 10 years.

The investigators compared the 144 Kawasaki disease survivors who experienced a coronary artery aneurysm (CAA) within 90 days of hospital admission to the 4,453 others who did not have a CAA. The risk for a composite cardiovascular event was elevated at each time point among those with a history of CAA, especially in the first year. The adjusted HR was 33.12 in the CAA group versus 10.44 in the non-CAA group.

“The most interesting finding of this study was that children with Kawasaki syndrome are at higher risk for composite cardiovascular events and major adverse cardiac events even if they were not diagnosed with coronary artery aneurysm,” session comoderator Shervin Assassi, MD, professor of medicine and director of division of rheumatology at the University of Texas Health Science Center at Houston, said when asked to comment.

Dr. Robinson and colleagues also looked at outcomes based on presence or absence of coronary involvement at the time of Kawasaki disease diagnosis. For example, among those with initial coronary involvement, 15% later experienced a cardiovascular event and 10% experienced a major cardiovascular event.

“However, we were specifically interested in looking at children without initial coronary involvement. In this group, we also found these children were at increased risk for cardiovascular events compared to children without Kawasaki disease,” Dr. Robinson said. He said the distinction is important because approximately 95% of children diagnosed with Kawasaki disease do not feature initial coronary involvement.

In terms of clinical care, “our data provides an early signal that Kawasaki disease survivors – including those without initial coronary involvement – may be at higher risk of cardiovascular events into early adulthood.”
 

A call for closer monitoring

“Based on our results, we find that Kawasaki disease survivors may benefit from additional follow-up and surveillance for cardiovascular disease risk factors, such as obesity, high blood pressure, and high cholesterol,” Dr. Robinson said. Early identification of heightened risk could allow physicians to more closely monitor this subgroup and emphasize potentially beneficial lifestyle modifications, including increasing physical activity, implementing a heart healthy diet, and avoiding smoking.

Mortality was not significantly different between groups. “Despite the risk of cardiac events we found, death was uncommon,” Dr. Robinson said. Among children with Kawasaki disease, 1 in 500 died during follow-up, so “the risk of death was actually lower than for children without Kawasaki disease.”

Similar findings of lower mortality have been reported in research out of Japan, he added during a plenary presentation at ACR 2020. Future research is warranted to evaluate this finding further, Dr. Robinson said.
 

Future plans

Going forward, the investigators plan to evaluate noncardiovascular outcomes in this patient population. They would also like to examine health care utilization following a diagnosis of Kawasaki disease “to better understand what kind of follow-up is happening now in Ontario,” Dr. Robinson said.

Another unanswered question is whether the cardiovascular events observed in the study stem from atherosclerotic disease or a different mechanism among survivors of Kawasaki disease.

The research was supported by a McMaster University Resident Research Grant, a Hamilton Health Sciences New Investigator Award, and Ontario’s Institute for Clinical Evaluative Sciences. Dr. Robinson had no relevant financial disclosures.

SOURCE: Robinson C et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 0937.

Survivors of Kawasaki disease remain at a higher long-term risk for cardiovascular events into young adulthood, including myocardial infarction, compared to people without the disease, new evidence reveals. The elevated risks emerged in survivors both with and without cardiovascular involvement at the time of initial diagnosis.

Overall risk of cardiovascular events was highest in the first year following Kawasaki disease diagnosis, and about 10 times greater than in healthy children, Cal Robinson, MD, said during a press conference at the virtual annual meeting of the American College of Rheumatology.

“The risk gradually decreased over time. However, even 10 years after diagnosis of their illness, they still had a 39% higher risk,” said study author Dr. Robinson, a PGY4 pediatric nephrology fellow at The Hospital for Sick Children in Toronto.

Dr. Robinson also put the numbers in perspective. “We fully acknowledged these are very rare events in children, especially healthy children, which is why we needed such a large cohort to study this. Interpret the numbers cautiously.”

In terms of patient and family counseling, “I would say children with Kawasaki disease have a higher risk of myocardial infarction, but the absolute risk is still low,” he added. For example, 16 Kawasaki disease survivors experienced a heart attack during follow-up, or 0.4% of the affected study population, compared to a rate of 0.1% among matched controls.

“These families are often very frightened after the initial Kawasaki disease diagnosis,” Dr. Robinson said. “We have to balance some discussion with what we know about Kawasaki disease without overly scaring or terrifying these families, who are already anxious.”

To quantify the incidence and timing of cardiovascular events and cardiac disease following diagnosis, Dr. Robinson and colleagues assessed large databases representing approximately 3 million children. They focused on children hospitalized with a Kawasaki disease diagnosis between 1995 and 2018. These children had a median length of stay of 3 days and 2.5% were admitted to critical care. The investigators matched his population 1:100 to unaffected children in Ontario.

Follow-up was up to 24 years (median, 11 years) in this retrospective, population-based cohort study.

Risks raised over a decade and beyond

Compared to matched controls, Kawasaki disease survivors had a higher risk for a cardiac event in the first year following diagnosis (adjusted hazard ratio, 11.65; 95% confidence interval, 10.34-13.13). The 1- to 5-year risk was lower (aHR, 3.35), a trend that continued between 5 and 10 years (aHR, 1.87) and as well as after more than 10 years (aHR, 1.39).

The risk of major adverse cardiac events (MACE, a composite of myocardial infarction, stroke, or cardiovascular death) was likewise highest in the first year after diagnosis (aHR, 3.27), followed by a 51% greater risk at 1-5 years, a 113% increased risk at 5-10 years, and a 17% elevated risk after 10 years.

The investigators compared the 144 Kawasaki disease survivors who experienced a coronary artery aneurysm (CAA) within 90 days of hospital admission to the 4,453 others who did not have a CAA. The risk for a composite cardiovascular event was elevated at each time point among those with a history of CAA, especially in the first year. The adjusted HR was 33.12 in the CAA group versus 10.44 in the non-CAA group.

“The most interesting finding of this study was that children with Kawasaki syndrome are at higher risk for composite cardiovascular events and major adverse cardiac events even if they were not diagnosed with coronary artery aneurysm,” session comoderator Shervin Assassi, MD, professor of medicine and director of division of rheumatology at the University of Texas Health Science Center at Houston, said when asked to comment.

Dr. Robinson and colleagues also looked at outcomes based on presence or absence of coronary involvement at the time of Kawasaki disease diagnosis. For example, among those with initial coronary involvement, 15% later experienced a cardiovascular event and 10% experienced a major cardiovascular event.

“However, we were specifically interested in looking at children without initial coronary involvement. In this group, we also found these children were at increased risk for cardiovascular events compared to children without Kawasaki disease,” Dr. Robinson said. He said the distinction is important because approximately 95% of children diagnosed with Kawasaki disease do not feature initial coronary involvement.

In terms of clinical care, “our data provides an early signal that Kawasaki disease survivors – including those without initial coronary involvement – may be at higher risk of cardiovascular events into early adulthood.”
 

A call for closer monitoring

“Based on our results, we find that Kawasaki disease survivors may benefit from additional follow-up and surveillance for cardiovascular disease risk factors, such as obesity, high blood pressure, and high cholesterol,” Dr. Robinson said. Early identification of heightened risk could allow physicians to more closely monitor this subgroup and emphasize potentially beneficial lifestyle modifications, including increasing physical activity, implementing a heart healthy diet, and avoiding smoking.

Mortality was not significantly different between groups. “Despite the risk of cardiac events we found, death was uncommon,” Dr. Robinson said. Among children with Kawasaki disease, 1 in 500 died during follow-up, so “the risk of death was actually lower than for children without Kawasaki disease.”

Similar findings of lower mortality have been reported in research out of Japan, he added during a plenary presentation at ACR 2020. Future research is warranted to evaluate this finding further, Dr. Robinson said.
 

Future plans

Going forward, the investigators plan to evaluate noncardiovascular outcomes in this patient population. They would also like to examine health care utilization following a diagnosis of Kawasaki disease “to better understand what kind of follow-up is happening now in Ontario,” Dr. Robinson said.

Another unanswered question is whether the cardiovascular events observed in the study stem from atherosclerotic disease or a different mechanism among survivors of Kawasaki disease.

The research was supported by a McMaster University Resident Research Grant, a Hamilton Health Sciences New Investigator Award, and Ontario’s Institute for Clinical Evaluative Sciences. Dr. Robinson had no relevant financial disclosures.

SOURCE: Robinson C et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 0937.

Survivors of Kawasaki disease remain at a higher long-term risk for cardiovascular events into young adulthood, including myocardial infarction, compared to people without the disease, new evidence reveals. The elevated risks emerged in survivors both with and without cardiovascular involvement at the time of initial diagnosis.

Overall risk of cardiovascular events was highest in the first year following Kawasaki disease diagnosis, and about 10 times greater than in healthy children, Cal Robinson, MD, said during a press conference at the virtual annual meeting of the American College of Rheumatology.

“The risk gradually decreased over time. However, even 10 years after diagnosis of their illness, they still had a 39% higher risk,” said study author Dr. Robinson, a PGY4 pediatric nephrology fellow at The Hospital for Sick Children in Toronto.

Dr. Robinson also put the numbers in perspective. “We fully acknowledged these are very rare events in children, especially healthy children, which is why we needed such a large cohort to study this. Interpret the numbers cautiously.”

In terms of patient and family counseling, “I would say children with Kawasaki disease have a higher risk of myocardial infarction, but the absolute risk is still low,” he added. For example, 16 Kawasaki disease survivors experienced a heart attack during follow-up, or 0.4% of the affected study population, compared to a rate of 0.1% among matched controls.

“These families are often very frightened after the initial Kawasaki disease diagnosis,” Dr. Robinson said. “We have to balance some discussion with what we know about Kawasaki disease without overly scaring or terrifying these families, who are already anxious.”

To quantify the incidence and timing of cardiovascular events and cardiac disease following diagnosis, Dr. Robinson and colleagues assessed large databases representing approximately 3 million children. They focused on children hospitalized with a Kawasaki disease diagnosis between 1995 and 2018. These children had a median length of stay of 3 days and 2.5% were admitted to critical care. The investigators matched his population 1:100 to unaffected children in Ontario.

Follow-up was up to 24 years (median, 11 years) in this retrospective, population-based cohort study.

Risks raised over a decade and beyond

Compared to matched controls, Kawasaki disease survivors had a higher risk for a cardiac event in the first year following diagnosis (adjusted hazard ratio, 11.65; 95% confidence interval, 10.34-13.13). The 1- to 5-year risk was lower (aHR, 3.35), a trend that continued between 5 and 10 years (aHR, 1.87) and as well as after more than 10 years (aHR, 1.39).

The risk of major adverse cardiac events (MACE, a composite of myocardial infarction, stroke, or cardiovascular death) was likewise highest in the first year after diagnosis (aHR, 3.27), followed by a 51% greater risk at 1-5 years, a 113% increased risk at 5-10 years, and a 17% elevated risk after 10 years.

The investigators compared the 144 Kawasaki disease survivors who experienced a coronary artery aneurysm (CAA) within 90 days of hospital admission to the 4,453 others who did not have a CAA. The risk for a composite cardiovascular event was elevated at each time point among those with a history of CAA, especially in the first year. The adjusted HR was 33.12 in the CAA group versus 10.44 in the non-CAA group.

“The most interesting finding of this study was that children with Kawasaki syndrome are at higher risk for composite cardiovascular events and major adverse cardiac events even if they were not diagnosed with coronary artery aneurysm,” session comoderator Shervin Assassi, MD, professor of medicine and director of division of rheumatology at the University of Texas Health Science Center at Houston, said when asked to comment.

Dr. Robinson and colleagues also looked at outcomes based on presence or absence of coronary involvement at the time of Kawasaki disease diagnosis. For example, among those with initial coronary involvement, 15% later experienced a cardiovascular event and 10% experienced a major cardiovascular event.

“However, we were specifically interested in looking at children without initial coronary involvement. In this group, we also found these children were at increased risk for cardiovascular events compared to children without Kawasaki disease,” Dr. Robinson said. He said the distinction is important because approximately 95% of children diagnosed with Kawasaki disease do not feature initial coronary involvement.

In terms of clinical care, “our data provides an early signal that Kawasaki disease survivors – including those without initial coronary involvement – may be at higher risk of cardiovascular events into early adulthood.”
 

A call for closer monitoring

“Based on our results, we find that Kawasaki disease survivors may benefit from additional follow-up and surveillance for cardiovascular disease risk factors, such as obesity, high blood pressure, and high cholesterol,” Dr. Robinson said. Early identification of heightened risk could allow physicians to more closely monitor this subgroup and emphasize potentially beneficial lifestyle modifications, including increasing physical activity, implementing a heart healthy diet, and avoiding smoking.

Mortality was not significantly different between groups. “Despite the risk of cardiac events we found, death was uncommon,” Dr. Robinson said. Among children with Kawasaki disease, 1 in 500 died during follow-up, so “the risk of death was actually lower than for children without Kawasaki disease.”

Similar findings of lower mortality have been reported in research out of Japan, he added during a plenary presentation at ACR 2020. Future research is warranted to evaluate this finding further, Dr. Robinson said.
 

Future plans

Going forward, the investigators plan to evaluate noncardiovascular outcomes in this patient population. They would also like to examine health care utilization following a diagnosis of Kawasaki disease “to better understand what kind of follow-up is happening now in Ontario,” Dr. Robinson said.

Another unanswered question is whether the cardiovascular events observed in the study stem from atherosclerotic disease or a different mechanism among survivors of Kawasaki disease.

The research was supported by a McMaster University Resident Research Grant, a Hamilton Health Sciences New Investigator Award, and Ontario’s Institute for Clinical Evaluative Sciences. Dr. Robinson had no relevant financial disclosures.

SOURCE: Robinson C et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 0937.

Patients who take the vitamin K antagonist warfarin to prevent thromboembolic events are significantly more likely to require knee or hip replacement surgery – a surrogate endpoint for end-stage osteoarthritis – than are patients who take direct oral anticoagulants (DOACs), results of a U.K.-based study showed.

In a nested case-control study, warfarin use was associated with a 1.5-fold risk for knee and hip replacement, compared with use of DOACs.

The findings provide additional evidence for the role of vitamin K and vitamin K–dependent proteins for limiting osteoarthritis progression, said lead author Priyanka Ballal, MD, a rheumatology fellow at Boston University.

“Given the prevalence and impact of osteoarthritis, our data, along with the existing literature, support the need for a well-powered, randomized, controlled trial for evaluating vitamin K supplementation in osteoarthritis. Our study also raises the consideration of using DOACs over warfarin when indicated in people with or at risk of osteoarthritis,“ she said in a plenary session at the virtual annual meeting of the American College of Rheumatology.

Warfarin targets vitamin K for its role in coagulation, but vitamin K is also an essential co-factor for vitamin K-dependent proteins in bone and cartilage, Dr. Ballal said,

Inadequate vitamin K levels are associated with abnormal joint tissue mineralization, and with increased incidence and prevalence of osteoarthritis. In a randomized, controlled trial, vitamin K supplementation was associated with trends toward less osteoarthritis progression among patients with vitamin K deficiency, she said.

To see whether warfarin therapy has biologic effects similar to that seen in patients with vitamin K deficiency, Dr. Ballal and colleagues conducted a nested, case-control study using data from The Health Improvement Network (THIN), an electronic medical record database of patients enrolled with general practitioners in the United Kingdom.

The sample included adults aged 40-80 years with atrial fibrillation who had received one or more prescriptions for warfarin or a DOAC beginning in 2009, a year after DOACs were first marketed in the United Kingdom, and within 1 year of the index date (date of joint replacement surgery). The researchers excluded patients with knee or hip replacements before 2014, severe comorbidities that would limit joint replacement, or who had used either warfarin or a DOAC prior to study entry. Each case was matched by age, gender, and index date with up to four control patients (those who did not have surgery).

A total of 913 cases and 3,652 controls were included. The groups had similar characteristics (sex, age, cancer, renal disease, chronic lung disease, hypertension, and incidence of venous thromboembolism [VTE]), except for somewhat higher rates of diabetes and heart failure among controls, and a higher rate of obesity among cases.

The investigators first looked at warfarin use among all knee and/or hip replacement cases and controls and calculated an odds ratio of 1.57 (95% confidence interval [CI], 1.30-1.89) for knee and hip replacement with warfarin after adjustment for body mass index, factors influencing choice of anticoagulant, comorbidities, other medications, general practitioner visits, and hospitalizations.

The association between warfarin and joint replacement held up in an analysis restricted to knee replacement only, with an adjusted OR of 1.48 (95% CI, 1.16-1.89).

There was also a clear association between duration of warfarin use and risk of knee and hip replacement.

“This abstract suggests the role of adequate vitamin K may be important in decreasing progression of osteoarthritis, which would then favor patients with OA who are on warfarin to consider changing to a DOAC; however, further studies are needed to confirm this finding and consider its impact on VTE and wound healing postop,” said Minna Kohler, MD, director of the rheumatology musculoskeletal ultrasound program at Massachusetts General Hospital in Boston. Dr. Kohler, who was not involved in the study, replied to an email request for comment.

The study was supported by grants from the National Institutes of Health. Dr. Ballal and Dr. Kohler reported having no conflicts of interest to disclose.

SOURCE: Ballal P et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 0934.

Patients who take the vitamin K antagonist warfarin to prevent thromboembolic events are significantly more likely to require knee or hip replacement surgery – a surrogate endpoint for end-stage osteoarthritis – than are patients who take direct oral anticoagulants (DOACs), results of a U.K.-based study showed.

In a nested case-control study, warfarin use was associated with a 1.5-fold risk for knee and hip replacement, compared with use of DOACs.

The findings provide additional evidence for the role of vitamin K and vitamin K–dependent proteins for limiting osteoarthritis progression, said lead author Priyanka Ballal, MD, a rheumatology fellow at Boston University.

“Given the prevalence and impact of osteoarthritis, our data, along with the existing literature, support the need for a well-powered, randomized, controlled trial for evaluating vitamin K supplementation in osteoarthritis. Our study also raises the consideration of using DOACs over warfarin when indicated in people with or at risk of osteoarthritis,“ she said in a plenary session at the virtual annual meeting of the American College of Rheumatology.

Warfarin targets vitamin K for its role in coagulation, but vitamin K is also an essential co-factor for vitamin K-dependent proteins in bone and cartilage, Dr. Ballal said,

Inadequate vitamin K levels are associated with abnormal joint tissue mineralization, and with increased incidence and prevalence of osteoarthritis. In a randomized, controlled trial, vitamin K supplementation was associated with trends toward less osteoarthritis progression among patients with vitamin K deficiency, she said.

To see whether warfarin therapy has biologic effects similar to that seen in patients with vitamin K deficiency, Dr. Ballal and colleagues conducted a nested, case-control study using data from The Health Improvement Network (THIN), an electronic medical record database of patients enrolled with general practitioners in the United Kingdom.

The sample included adults aged 40-80 years with atrial fibrillation who had received one or more prescriptions for warfarin or a DOAC beginning in 2009, a year after DOACs were first marketed in the United Kingdom, and within 1 year of the index date (date of joint replacement surgery). The researchers excluded patients with knee or hip replacements before 2014, severe comorbidities that would limit joint replacement, or who had used either warfarin or a DOAC prior to study entry. Each case was matched by age, gender, and index date with up to four control patients (those who did not have surgery).

A total of 913 cases and 3,652 controls were included. The groups had similar characteristics (sex, age, cancer, renal disease, chronic lung disease, hypertension, and incidence of venous thromboembolism [VTE]), except for somewhat higher rates of diabetes and heart failure among controls, and a higher rate of obesity among cases.

The investigators first looked at warfarin use among all knee and/or hip replacement cases and controls and calculated an odds ratio of 1.57 (95% confidence interval [CI], 1.30-1.89) for knee and hip replacement with warfarin after adjustment for body mass index, factors influencing choice of anticoagulant, comorbidities, other medications, general practitioner visits, and hospitalizations.

The association between warfarin and joint replacement held up in an analysis restricted to knee replacement only, with an adjusted OR of 1.48 (95% CI, 1.16-1.89).

There was also a clear association between duration of warfarin use and risk of knee and hip replacement.

“This abstract suggests the role of adequate vitamin K may be important in decreasing progression of osteoarthritis, which would then favor patients with OA who are on warfarin to consider changing to a DOAC; however, further studies are needed to confirm this finding and consider its impact on VTE and wound healing postop,” said Minna Kohler, MD, director of the rheumatology musculoskeletal ultrasound program at Massachusetts General Hospital in Boston. Dr. Kohler, who was not involved in the study, replied to an email request for comment.

The study was supported by grants from the National Institutes of Health. Dr. Ballal and Dr. Kohler reported having no conflicts of interest to disclose.

SOURCE: Ballal P et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 0934.

Patients who take the vitamin K antagonist warfarin to prevent thromboembolic events are significantly more likely to require knee or hip replacement surgery – a surrogate endpoint for end-stage osteoarthritis – than are patients who take direct oral anticoagulants (DOACs), results of a U.K.-based study showed.

In a nested case-control study, warfarin use was associated with a 1.5-fold risk for knee and hip replacement, compared with use of DOACs.

The findings provide additional evidence for the role of vitamin K and vitamin K–dependent proteins for limiting osteoarthritis progression, said lead author Priyanka Ballal, MD, a rheumatology fellow at Boston University.

“Given the prevalence and impact of osteoarthritis, our data, along with the existing literature, support the need for a well-powered, randomized, controlled trial for evaluating vitamin K supplementation in osteoarthritis. Our study also raises the consideration of using DOACs over warfarin when indicated in people with or at risk of osteoarthritis,“ she said in a plenary session at the virtual annual meeting of the American College of Rheumatology.

Warfarin targets vitamin K for its role in coagulation, but vitamin K is also an essential co-factor for vitamin K-dependent proteins in bone and cartilage, Dr. Ballal said,

Inadequate vitamin K levels are associated with abnormal joint tissue mineralization, and with increased incidence and prevalence of osteoarthritis. In a randomized, controlled trial, vitamin K supplementation was associated with trends toward less osteoarthritis progression among patients with vitamin K deficiency, she said.

To see whether warfarin therapy has biologic effects similar to that seen in patients with vitamin K deficiency, Dr. Ballal and colleagues conducted a nested, case-control study using data from The Health Improvement Network (THIN), an electronic medical record database of patients enrolled with general practitioners in the United Kingdom.

The sample included adults aged 40-80 years with atrial fibrillation who had received one or more prescriptions for warfarin or a DOAC beginning in 2009, a year after DOACs were first marketed in the United Kingdom, and within 1 year of the index date (date of joint replacement surgery). The researchers excluded patients with knee or hip replacements before 2014, severe comorbidities that would limit joint replacement, or who had used either warfarin or a DOAC prior to study entry. Each case was matched by age, gender, and index date with up to four control patients (those who did not have surgery).

A total of 913 cases and 3,652 controls were included. The groups had similar characteristics (sex, age, cancer, renal disease, chronic lung disease, hypertension, and incidence of venous thromboembolism [VTE]), except for somewhat higher rates of diabetes and heart failure among controls, and a higher rate of obesity among cases.

The investigators first looked at warfarin use among all knee and/or hip replacement cases and controls and calculated an odds ratio of 1.57 (95% confidence interval [CI], 1.30-1.89) for knee and hip replacement with warfarin after adjustment for body mass index, factors influencing choice of anticoagulant, comorbidities, other medications, general practitioner visits, and hospitalizations.

The association between warfarin and joint replacement held up in an analysis restricted to knee replacement only, with an adjusted OR of 1.48 (95% CI, 1.16-1.89).

There was also a clear association between duration of warfarin use and risk of knee and hip replacement.

“This abstract suggests the role of adequate vitamin K may be important in decreasing progression of osteoarthritis, which would then favor patients with OA who are on warfarin to consider changing to a DOAC; however, further studies are needed to confirm this finding and consider its impact on VTE and wound healing postop,” said Minna Kohler, MD, director of the rheumatology musculoskeletal ultrasound program at Massachusetts General Hospital in Boston. Dr. Kohler, who was not involved in the study, replied to an email request for comment.

The study was supported by grants from the National Institutes of Health. Dr. Ballal and Dr. Kohler reported having no conflicts of interest to disclose.

SOURCE: Ballal P et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 0934.

Black patients with systemic lupus erythematosus (SLE) are known to have significantly elevated risk for stroke and ischemic heart disease (IHD), compared with non-Black patients with SLE.

Now a team of investigators has identified SLE-specific predictors for major cardiovascular complications in Black patients, pointing to potential prevention strategies in this high-risk population.

Among Black patients in a study of 336 patients with incident SLE, discoid rash at the time of SLE diagnosis predicted a fivefold higher risk for stroke, and renal disorder at the time of diagnosis was associated with a twofold higher risk, compared with non-Black patients, but neither of these symptoms predicted elevated risk of IHD.

In contrast, neurologic disorders, including prior psychosis or seizure, were associated with a fourfold higher risk for IHD, and immunologic disorders including anti-DNA, anti-Smith, or antiphospholipid antibodies were associated with a nearly fivefold greater risk for IHD in Black patients, but neither of these comorbidities predicted strokes, reported Shivani Garg, MD, assistant professor of medicine at the University of Wisconsin in Madison.

“Our study was one of the first to highlight racial disparities in CVD subtypes, with a threefold higher stroke risk and 24-fold higher ischemic heart disease risk in Black patients with lupus. Compared to previous studies in Black populations, our study highlights different peak timing of early stroke and ischemic heart disease in our cohort,“ she said at a plenary session during the virtual annual meeting of the American College of Rheumatology.

The study is one of the first to identify specific and unique SLE disease-related predictors of stroke and ischemic heart disease, she said.

Georgia Lupus Registry data

Dr. Garg and colleagues at the University of Wisconsin and Emory University in Atlanta drew on data from the Georgia Lupus Registry, a population-based registry of SLE patients from the Atlanta area. They identified patients diagnosed from 2002 through 2004 who had four or more ACR criteria for SLE, or three or more criteria plus a final diagnosis of SLE made by their board-certified rheumatologists.

The patients were matched to the Georgia Hospital Discharge Database and National Death Index from 2000 through 2013, with stroke- and IHD-related hospitalizations and deaths classified by the first three admission codes or cause-of-death codes.

Patients with transient ischemic attacks were included in the stroke category, and those with myocardial infarction and angina were included in the IHD category.

They identified 336 patients, 87% of whom were female, and 75% of whom were Black. The mean age at SLE diagnosis was 40 years. Among this cohort, there were 38 stroke-related events or deaths and 25 IHD-related events or deaths recorded from the period 2 years before through 14 years after an SLE diagnosis.
 

Early stroke, late IHD

The investigators first looked at the timing of stroke vs. IHD and found that a disproportionately high percentage of stroke events occurred in the second year after SLE diagnosis, whereas the peak of IHD-related events occurred in the 14^th year after diagnosis.

They then performed a race-stratified Cox proportional hazard analysis, and found a threefold higher risk for stroke in Black patients versus non-Black patients (P = .007) and a 24-fold higher risk for IHD (P < .0001).

In multivariate analysis, significant predictors of stroke were Black race with a hazard ratio (HR) of 3.4 (P = .028), discoid rash (HR, 4.6; P = .0028), and renal disorder (HR, 2.4; P = .04). However, stroke was not predicted by age, sex, immunologic disorder, serositis, hematologic disorder, or ACR criteria total greater than four.

Significant predictors of IHD included age 65 and older (HR, 61; P = .0007), Black race (HR, 24; P = .004), neurologic disorder (HR, 4.0; P = .018), and immunologic disorder (HR, 4.7; P = .02). But IHD could not be predicted by oral ulcers, discoid rash, or ACR criteria more than four.

“In future studies, we will examine mechanisms that drive the different timing and predictors of CVD subtypes and disparities. We will also examine the impact of timely prevention in high-risk SLE subsets,” Dr. Garg said.
 

Managing CVD risk

Angus Worthing, MD, from Arthritis & Rheumatism Associates in Chevy Chase, Md., and Washington, D.C., who moderated a press briefing where Dr. Garg discussed her data, routinely treats patients of different racial backgrounds with lupus. When asked how he manages patients with SLE and suspected cardiovascular complications, Dr. Worthing said, “I tend to, in my practice – and these kinds of studies may change what I do – watch for symptoms that might reflect coronary artery disease or cerebrovascular disease, potentially looking at the smaller arteries in the hands and feet as clues, and I will refer promptly to a vascular surgery expert or cardiologist for screening,” he said.

Dr. Garg added that in her practice, she and colleagues treat high-risk subsets of patients, such as those with lupus nephritis or multiple comorbidities, with aggressive blood pressure control and monitoring, as well as smoking cessation recommendations and lipid monitoring. They also try to limit or, if possible, decrease steroid doses to reduce risk for cardiovascular side effects.

Support for the study came in part from the U.S. Centers for Disease Control and Prevention. Dr. Garg and Dr. Worthing reported having no relevant disclosures.

SOURCE: Garg S et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 433 .

Black patients with systemic lupus erythematosus (SLE) are known to have significantly elevated risk for stroke and ischemic heart disease (IHD), compared with non-Black patients with SLE.

Now a team of investigators has identified SLE-specific predictors for major cardiovascular complications in Black patients, pointing to potential prevention strategies in this high-risk population.

Among Black patients in a study of 336 patients with incident SLE, discoid rash at the time of SLE diagnosis predicted a fivefold higher risk for stroke, and renal disorder at the time of diagnosis was associated with a twofold higher risk, compared with non-Black patients, but neither of these symptoms predicted elevated risk of IHD.

In contrast, neurologic disorders, including prior psychosis or seizure, were associated with a fourfold higher risk for IHD, and immunologic disorders including anti-DNA, anti-Smith, or antiphospholipid antibodies were associated with a nearly fivefold greater risk for IHD in Black patients, but neither of these comorbidities predicted strokes, reported Shivani Garg, MD, assistant professor of medicine at the University of Wisconsin in Madison.

“Our study was one of the first to highlight racial disparities in CVD subtypes, with a threefold higher stroke risk and 24-fold higher ischemic heart disease risk in Black patients with lupus. Compared to previous studies in Black populations, our study highlights different peak timing of early stroke and ischemic heart disease in our cohort,“ she said at a plenary session during the virtual annual meeting of the American College of Rheumatology.

The study is one of the first to identify specific and unique SLE disease-related predictors of stroke and ischemic heart disease, she said.

Georgia Lupus Registry data

Dr. Garg and colleagues at the University of Wisconsin and Emory University in Atlanta drew on data from the Georgia Lupus Registry, a population-based registry of SLE patients from the Atlanta area. They identified patients diagnosed from 2002 through 2004 who had four or more ACR criteria for SLE, or three or more criteria plus a final diagnosis of SLE made by their board-certified rheumatologists.

The patients were matched to the Georgia Hospital Discharge Database and National Death Index from 2000 through 2013, with stroke- and IHD-related hospitalizations and deaths classified by the first three admission codes or cause-of-death codes.

Patients with transient ischemic attacks were included in the stroke category, and those with myocardial infarction and angina were included in the IHD category.

They identified 336 patients, 87% of whom were female, and 75% of whom were Black. The mean age at SLE diagnosis was 40 years. Among this cohort, there were 38 stroke-related events or deaths and 25 IHD-related events or deaths recorded from the period 2 years before through 14 years after an SLE diagnosis.
 

Early stroke, late IHD

The investigators first looked at the timing of stroke vs. IHD and found that a disproportionately high percentage of stroke events occurred in the second year after SLE diagnosis, whereas the peak of IHD-related events occurred in the 14^th year after diagnosis.

They then performed a race-stratified Cox proportional hazard analysis, and found a threefold higher risk for stroke in Black patients versus non-Black patients (P = .007) and a 24-fold higher risk for IHD (P < .0001).

In multivariate analysis, significant predictors of stroke were Black race with a hazard ratio (HR) of 3.4 (P = .028), discoid rash (HR, 4.6; P = .0028), and renal disorder (HR, 2.4; P = .04). However, stroke was not predicted by age, sex, immunologic disorder, serositis, hematologic disorder, or ACR criteria total greater than four.

Significant predictors of IHD included age 65 and older (HR, 61; P = .0007), Black race (HR, 24; P = .004), neurologic disorder (HR, 4.0; P = .018), and immunologic disorder (HR, 4.7; P = .02). But IHD could not be predicted by oral ulcers, discoid rash, or ACR criteria more than four.

“In future studies, we will examine mechanisms that drive the different timing and predictors of CVD subtypes and disparities. We will also examine the impact of timely prevention in high-risk SLE subsets,” Dr. Garg said.
 

Managing CVD risk

Angus Worthing, MD, from Arthritis & Rheumatism Associates in Chevy Chase, Md., and Washington, D.C., who moderated a press briefing where Dr. Garg discussed her data, routinely treats patients of different racial backgrounds with lupus. When asked how he manages patients with SLE and suspected cardiovascular complications, Dr. Worthing said, “I tend to, in my practice – and these kinds of studies may change what I do – watch for symptoms that might reflect coronary artery disease or cerebrovascular disease, potentially looking at the smaller arteries in the hands and feet as clues, and I will refer promptly to a vascular surgery expert or cardiologist for screening,” he said.

Dr. Garg added that in her practice, she and colleagues treat high-risk subsets of patients, such as those with lupus nephritis or multiple comorbidities, with aggressive blood pressure control and monitoring, as well as smoking cessation recommendations and lipid monitoring. They also try to limit or, if possible, decrease steroid doses to reduce risk for cardiovascular side effects.

Support for the study came in part from the U.S. Centers for Disease Control and Prevention. Dr. Garg and Dr. Worthing reported having no relevant disclosures.

SOURCE: Garg S et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 433 .

Black patients with systemic lupus erythematosus (SLE) are known to have significantly elevated risk for stroke and ischemic heart disease (IHD), compared with non-Black patients with SLE.

Now a team of investigators has identified SLE-specific predictors for major cardiovascular complications in Black patients, pointing to potential prevention strategies in this high-risk population.

Among Black patients in a study of 336 patients with incident SLE, discoid rash at the time of SLE diagnosis predicted a fivefold higher risk for stroke, and renal disorder at the time of diagnosis was associated with a twofold higher risk, compared with non-Black patients, but neither of these symptoms predicted elevated risk of IHD.

In contrast, neurologic disorders, including prior psychosis or seizure, were associated with a fourfold higher risk for IHD, and immunologic disorders including anti-DNA, anti-Smith, or antiphospholipid antibodies were associated with a nearly fivefold greater risk for IHD in Black patients, but neither of these comorbidities predicted strokes, reported Shivani Garg, MD, assistant professor of medicine at the University of Wisconsin in Madison.

“Our study was one of the first to highlight racial disparities in CVD subtypes, with a threefold higher stroke risk and 24-fold higher ischemic heart disease risk in Black patients with lupus. Compared to previous studies in Black populations, our study highlights different peak timing of early stroke and ischemic heart disease in our cohort,“ she said at a plenary session during the virtual annual meeting of the American College of Rheumatology.

The study is one of the first to identify specific and unique SLE disease-related predictors of stroke and ischemic heart disease, she said.

Georgia Lupus Registry data

Dr. Garg and colleagues at the University of Wisconsin and Emory University in Atlanta drew on data from the Georgia Lupus Registry, a population-based registry of SLE patients from the Atlanta area. They identified patients diagnosed from 2002 through 2004 who had four or more ACR criteria for SLE, or three or more criteria plus a final diagnosis of SLE made by their board-certified rheumatologists.

The patients were matched to the Georgia Hospital Discharge Database and National Death Index from 2000 through 2013, with stroke- and IHD-related hospitalizations and deaths classified by the first three admission codes or cause-of-death codes.

Patients with transient ischemic attacks were included in the stroke category, and those with myocardial infarction and angina were included in the IHD category.

They identified 336 patients, 87% of whom were female, and 75% of whom were Black. The mean age at SLE diagnosis was 40 years. Among this cohort, there were 38 stroke-related events or deaths and 25 IHD-related events or deaths recorded from the period 2 years before through 14 years after an SLE diagnosis.
 

Early stroke, late IHD

The investigators first looked at the timing of stroke vs. IHD and found that a disproportionately high percentage of stroke events occurred in the second year after SLE diagnosis, whereas the peak of IHD-related events occurred in the 14^th year after diagnosis.

They then performed a race-stratified Cox proportional hazard analysis, and found a threefold higher risk for stroke in Black patients versus non-Black patients (P = .007) and a 24-fold higher risk for IHD (P < .0001).

In multivariate analysis, significant predictors of stroke were Black race with a hazard ratio (HR) of 3.4 (P = .028), discoid rash (HR, 4.6; P = .0028), and renal disorder (HR, 2.4; P = .04). However, stroke was not predicted by age, sex, immunologic disorder, serositis, hematologic disorder, or ACR criteria total greater than four.

Significant predictors of IHD included age 65 and older (HR, 61; P = .0007), Black race (HR, 24; P = .004), neurologic disorder (HR, 4.0; P = .018), and immunologic disorder (HR, 4.7; P = .02). But IHD could not be predicted by oral ulcers, discoid rash, or ACR criteria more than four.

“In future studies, we will examine mechanisms that drive the different timing and predictors of CVD subtypes and disparities. We will also examine the impact of timely prevention in high-risk SLE subsets,” Dr. Garg said.
 

Managing CVD risk

Angus Worthing, MD, from Arthritis & Rheumatism Associates in Chevy Chase, Md., and Washington, D.C., who moderated a press briefing where Dr. Garg discussed her data, routinely treats patients of different racial backgrounds with lupus. When asked how he manages patients with SLE and suspected cardiovascular complications, Dr. Worthing said, “I tend to, in my practice – and these kinds of studies may change what I do – watch for symptoms that might reflect coronary artery disease or cerebrovascular disease, potentially looking at the smaller arteries in the hands and feet as clues, and I will refer promptly to a vascular surgery expert or cardiologist for screening,” he said.

Dr. Garg added that in her practice, she and colleagues treat high-risk subsets of patients, such as those with lupus nephritis or multiple comorbidities, with aggressive blood pressure control and monitoring, as well as smoking cessation recommendations and lipid monitoring. They also try to limit or, if possible, decrease steroid doses to reduce risk for cardiovascular side effects.

Support for the study came in part from the U.S. Centers for Disease Control and Prevention. Dr. Garg and Dr. Worthing reported having no relevant disclosures.

SOURCE: Garg S et al. Arthritis Rheumatol. 2020;72(suppl 10): Abstract 433 .

A smartphone app that combines passively collected physiologic data from wearable devices, such as fitness trackers, and self-reported symptoms can discriminate between COVID-19–positive and –negative individuals among those who report symptoms, new data suggest.

LDProd/Getty Images

After analyzing data from more than 30,000 participants, researchers from the Digital Engagement and Tracking for Early Control and Treatment (DETECT) study concluded that adding individual changes in sensor data improves models based on symptoms alone for differentiating symptomatic persons who are COVID-19 positive and symptomatic persons who are COVID-19 negative.

The combination can potentially identify infection clusters before wider community spread occurs, Giorgio Quer, PhD, and colleagues report in an article published online Oct. 29 in Nature Medicine. DETECT investigators note that marrying participant-reported symptoms with personal sensor data, such as deviation from normal sleep duration and resting heart rate, resulted in an area under the curve (AUC) of 0.80 (interquartile range [IQR], 0.73-0.86) for differentiating between symptomatic individuals who were positive and those who were negative for COVID-19.

“By better characterizing each individual’s unique baseline, you can then identify changes that may indicate that someone has a viral illness,” said Dr. Quer, director of artificial intelligence at Scripps Research Translational Institute in La Jolla, Calif. “In previous research, we found that the proportion of individuals with elevated resting heart rate and sleep duration compared with their normal could significantly improve real-time detection of influenza-like illness rates at the state level,” he said in an interview.

Thus, continuous passively captured data may be a useful adjunct to bricks-and-mortar site testing, which is generally a one-off or infrequent sampling assay and is not always easily accessible, he added. Furthermore, traditional screening with temperature and symptom reporting is inadequate. An elevation in temperature is not as common as frequently believed for people who test positive for COVID-19, Dr. Quer continued. “Early identification via sensor variables of those who are presymptomatic or even asymptomatic would be especially valuable, as people may potentially be infectious during this period, and early detection is the ultimate goal,” Dr. Quer said.

According to his group, adding these physiologic changes from baseline values significantly outperformed detection (P < .01) using a British model described in an earlier study by by Cristina Menni, PhD, and associates. That method, in which symptoms were considered alone, yielded an AUC of 0.71 (IQR, 0.63-0.79).

According to Dr. Quer, one in five Americans currently wear an electronic device. “If we could enroll even a small percentage of these individuals, we’d be able to potentially identify clusters before they have the opportunity to spread,” he said.
 

DETECT study details

During the period March 15 to June 7, 2020, the study enrolled 30,529 participants from all 50 states. They ranged in age from younger than 35 years (23.1%) to older than 65 years (12.8%); the majority (63.5%) were aged 35-65 years, and 62% were women. Sensor devices in use by the cohort included Fitbit activity trackers (78.4%) and Apple HealthKit (31.2%).

Participants downloaded an app called MyDataHelps, which collects smartwatch and activity tracker information, including self-reported symptoms and diagnostic testing results. The app also monitors changes from baseline in resting heart rate, sleep duration, and physical activity, as measured by steps.

Overall, 3,811 participants reported having at least one symptom of some kind (e.g., fatigue, cough, dyspnea, loss of taste or smell). Of these, 54 reported testing positive for COVID-19, and 279 reported testing negative.

Sleep and activity were significantly different for the positive and negative groups, with an AUC of 0.68 (IQR, 0.57-0.79) for the sleep metric and 0.69 (IQR, 0.61-0.77) for the activity metric, suggesting that these parameters were more affected in COVID-19–positive participants.

When the investigators combined resting heart rate, sleep, and activity into a single metric, predictive performance improved to an AUC of 0.72 (IQR, 0.64-0.80).

The next step, Dr. Quer said, is to include an alert to notify users of possible infection.
 

Alerting users to possible COVID-19 infection

In a similar study, an alert feature was already incorporated. The study, led by Michael P. Snyder, PhD, director of the Center for Genomics and Personalized Medicine at Stanford (Calif.) University, will soon be published online in Nature Biomedical Engineering. In that study, presymptomatic detection of COVID-19 was achieved in more than 80% of participants using resting heart rate.

“The median is 4 days prior to symptom formation,” Dr. Snyder said in an interview. “We have an alarm system to notify people when their heart rate is elevated. So a positive signal from a smartwatch can be used to follow up by polymerase chain reaction [testing].”

Dr. Snyder said these approaches offer a roadmap to containing widespread infections. “Public health authorities need to be open to these technologies and begin incorporating them into their tracking,” he said. “Right now, people do temperature checks, which are of limited value. Resting heart rate is much better information.”

Although the DETECT researchers have not yet received feedback on their results, they believe public health authorities could recommend the use of such apps. “These are devices that people routinely wear for tracking their fitness and sleep, so it would be relatively easy to use the data for viral illness tracking,” said co–lead author Jennifer Radin, PhD, an epidemiologist at Scripps. “Testing resources are still limited and don’t allow for routine serial testing of individuals who may be asymptomatic or presymptomatic. Wearables can offer a different way to routinely monitor and screen people for changes in their data that may indicate COVID-19.”

The marshaling of data through consumer digital platforms to fight the coronavirus is gaining ground. New York State and New Jersey are already embracing smartphone apps to alert individuals to possible exposure to the virus.

More than 710,000 New Yorkers have downloaded the COVID NY Alert app, launched in October to help protect individuals and communities from COVID-19 by sending alerts without compromising privacy or personal information. “Upon receiving a notification about a potential exposure, users are then able to self-quarantine, get tested, and reduce the potential exposure risk to family, friends, coworkers, and others,” Jonah Bruno, a spokesperson for the New York State Department of Health, said in an interview.

And recently the Mayo Clinic and Safe Health Systems launched a platform to store COVID-19 testing and vaccination data.

Both the Scripps and Stanford platforms are part of a global technologic response to the COVID-19 pandemic. Prospective studies, led by device manufacturers and academic institutions, allow individuals to voluntarily share sensor and clinical data to address the crisis. Similar approaches have been used to track COVID-19 in large populations in Germany via the Corona Data Donation app.

The study by Dr. Quer and colleagues was funded by a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. One coauthor reported grants from Janssen and personal fees from Otsuka and Livongo outside of the submitted work. The other authors have disclosed no relevant financial relationships. Dr. Snyder has ties to Personalis, Qbio, January, SensOmics, Protos, Mirvie, and Oralome.
 

A version of this article originally appeared on Medscape.com.

A smartphone app that combines passively collected physiologic data from wearable devices, such as fitness trackers, and self-reported symptoms can discriminate between COVID-19–positive and –negative individuals among those who report symptoms, new data suggest.

LDProd/Getty Images

After analyzing data from more than 30,000 participants, researchers from the Digital Engagement and Tracking for Early Control and Treatment (DETECT) study concluded that adding individual changes in sensor data improves models based on symptoms alone for differentiating symptomatic persons who are COVID-19 positive and symptomatic persons who are COVID-19 negative.

The combination can potentially identify infection clusters before wider community spread occurs, Giorgio Quer, PhD, and colleagues report in an article published online Oct. 29 in Nature Medicine. DETECT investigators note that marrying participant-reported symptoms with personal sensor data, such as deviation from normal sleep duration and resting heart rate, resulted in an area under the curve (AUC) of 0.80 (interquartile range [IQR], 0.73-0.86) for differentiating between symptomatic individuals who were positive and those who were negative for COVID-19.

“By better characterizing each individual’s unique baseline, you can then identify changes that may indicate that someone has a viral illness,” said Dr. Quer, director of artificial intelligence at Scripps Research Translational Institute in La Jolla, Calif. “In previous research, we found that the proportion of individuals with elevated resting heart rate and sleep duration compared with their normal could significantly improve real-time detection of influenza-like illness rates at the state level,” he said in an interview.

Thus, continuous passively captured data may be a useful adjunct to bricks-and-mortar site testing, which is generally a one-off or infrequent sampling assay and is not always easily accessible, he added. Furthermore, traditional screening with temperature and symptom reporting is inadequate. An elevation in temperature is not as common as frequently believed for people who test positive for COVID-19, Dr. Quer continued. “Early identification via sensor variables of those who are presymptomatic or even asymptomatic would be especially valuable, as people may potentially be infectious during this period, and early detection is the ultimate goal,” Dr. Quer said.

According to his group, adding these physiologic changes from baseline values significantly outperformed detection (P < .01) using a British model described in an earlier study by by Cristina Menni, PhD, and associates. That method, in which symptoms were considered alone, yielded an AUC of 0.71 (IQR, 0.63-0.79).

According to Dr. Quer, one in five Americans currently wear an electronic device. “If we could enroll even a small percentage of these individuals, we’d be able to potentially identify clusters before they have the opportunity to spread,” he said.
 

DETECT study details

During the period March 15 to June 7, 2020, the study enrolled 30,529 participants from all 50 states. They ranged in age from younger than 35 years (23.1%) to older than 65 years (12.8%); the majority (63.5%) were aged 35-65 years, and 62% were women. Sensor devices in use by the cohort included Fitbit activity trackers (78.4%) and Apple HealthKit (31.2%).

Participants downloaded an app called MyDataHelps, which collects smartwatch and activity tracker information, including self-reported symptoms and diagnostic testing results. The app also monitors changes from baseline in resting heart rate, sleep duration, and physical activity, as measured by steps.

Overall, 3,811 participants reported having at least one symptom of some kind (e.g., fatigue, cough, dyspnea, loss of taste or smell). Of these, 54 reported testing positive for COVID-19, and 279 reported testing negative.

Sleep and activity were significantly different for the positive and negative groups, with an AUC of 0.68 (IQR, 0.57-0.79) for the sleep metric and 0.69 (IQR, 0.61-0.77) for the activity metric, suggesting that these parameters were more affected in COVID-19–positive participants.

When the investigators combined resting heart rate, sleep, and activity into a single metric, predictive performance improved to an AUC of 0.72 (IQR, 0.64-0.80).

The next step, Dr. Quer said, is to include an alert to notify users of possible infection.
 

Alerting users to possible COVID-19 infection

In a similar study, an alert feature was already incorporated. The study, led by Michael P. Snyder, PhD, director of the Center for Genomics and Personalized Medicine at Stanford (Calif.) University, will soon be published online in Nature Biomedical Engineering. In that study, presymptomatic detection of COVID-19 was achieved in more than 80% of participants using resting heart rate.

“The median is 4 days prior to symptom formation,” Dr. Snyder said in an interview. “We have an alarm system to notify people when their heart rate is elevated. So a positive signal from a smartwatch can be used to follow up by polymerase chain reaction [testing].”

Dr. Snyder said these approaches offer a roadmap to containing widespread infections. “Public health authorities need to be open to these technologies and begin incorporating them into their tracking,” he said. “Right now, people do temperature checks, which are of limited value. Resting heart rate is much better information.”

Although the DETECT researchers have not yet received feedback on their results, they believe public health authorities could recommend the use of such apps. “These are devices that people routinely wear for tracking their fitness and sleep, so it would be relatively easy to use the data for viral illness tracking,” said co–lead author Jennifer Radin, PhD, an epidemiologist at Scripps. “Testing resources are still limited and don’t allow for routine serial testing of individuals who may be asymptomatic or presymptomatic. Wearables can offer a different way to routinely monitor and screen people for changes in their data that may indicate COVID-19.”

The marshaling of data through consumer digital platforms to fight the coronavirus is gaining ground. New York State and New Jersey are already embracing smartphone apps to alert individuals to possible exposure to the virus.

More than 710,000 New Yorkers have downloaded the COVID NY Alert app, launched in October to help protect individuals and communities from COVID-19 by sending alerts without compromising privacy or personal information. “Upon receiving a notification about a potential exposure, users are then able to self-quarantine, get tested, and reduce the potential exposure risk to family, friends, coworkers, and others,” Jonah Bruno, a spokesperson for the New York State Department of Health, said in an interview.

And recently the Mayo Clinic and Safe Health Systems launched a platform to store COVID-19 testing and vaccination data.

Both the Scripps and Stanford platforms are part of a global technologic response to the COVID-19 pandemic. Prospective studies, led by device manufacturers and academic institutions, allow individuals to voluntarily share sensor and clinical data to address the crisis. Similar approaches have been used to track COVID-19 in large populations in Germany via the Corona Data Donation app.

The study by Dr. Quer and colleagues was funded by a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. One coauthor reported grants from Janssen and personal fees from Otsuka and Livongo outside of the submitted work. The other authors have disclosed no relevant financial relationships. Dr. Snyder has ties to Personalis, Qbio, January, SensOmics, Protos, Mirvie, and Oralome.
 

A version of this article originally appeared on Medscape.com.

A smartphone app that combines passively collected physiologic data from wearable devices, such as fitness trackers, and self-reported symptoms can discriminate between COVID-19–positive and –negative individuals among those who report symptoms, new data suggest.

LDProd/Getty Images

After analyzing data from more than 30,000 participants, researchers from the Digital Engagement and Tracking for Early Control and Treatment (DETECT) study concluded that adding individual changes in sensor data improves models based on symptoms alone for differentiating symptomatic persons who are COVID-19 positive and symptomatic persons who are COVID-19 negative.

The combination can potentially identify infection clusters before wider community spread occurs, Giorgio Quer, PhD, and colleagues report in an article published online Oct. 29 in Nature Medicine. DETECT investigators note that marrying participant-reported symptoms with personal sensor data, such as deviation from normal sleep duration and resting heart rate, resulted in an area under the curve (AUC) of 0.80 (interquartile range [IQR], 0.73-0.86) for differentiating between symptomatic individuals who were positive and those who were negative for COVID-19.

“By better characterizing each individual’s unique baseline, you can then identify changes that may indicate that someone has a viral illness,” said Dr. Quer, director of artificial intelligence at Scripps Research Translational Institute in La Jolla, Calif. “In previous research, we found that the proportion of individuals with elevated resting heart rate and sleep duration compared with their normal could significantly improve real-time detection of influenza-like illness rates at the state level,” he said in an interview.

Thus, continuous passively captured data may be a useful adjunct to bricks-and-mortar site testing, which is generally a one-off or infrequent sampling assay and is not always easily accessible, he added. Furthermore, traditional screening with temperature and symptom reporting is inadequate. An elevation in temperature is not as common as frequently believed for people who test positive for COVID-19, Dr. Quer continued. “Early identification via sensor variables of those who are presymptomatic or even asymptomatic would be especially valuable, as people may potentially be infectious during this period, and early detection is the ultimate goal,” Dr. Quer said.

According to his group, adding these physiologic changes from baseline values significantly outperformed detection (P < .01) using a British model described in an earlier study by by Cristina Menni, PhD, and associates. That method, in which symptoms were considered alone, yielded an AUC of 0.71 (IQR, 0.63-0.79).

According to Dr. Quer, one in five Americans currently wear an electronic device. “If we could enroll even a small percentage of these individuals, we’d be able to potentially identify clusters before they have the opportunity to spread,” he said.
 

DETECT study details

During the period March 15 to June 7, 2020, the study enrolled 30,529 participants from all 50 states. They ranged in age from younger than 35 years (23.1%) to older than 65 years (12.8%); the majority (63.5%) were aged 35-65 years, and 62% were women. Sensor devices in use by the cohort included Fitbit activity trackers (78.4%) and Apple HealthKit (31.2%).

Participants downloaded an app called MyDataHelps, which collects smartwatch and activity tracker information, including self-reported symptoms and diagnostic testing results. The app also monitors changes from baseline in resting heart rate, sleep duration, and physical activity, as measured by steps.

Overall, 3,811 participants reported having at least one symptom of some kind (e.g., fatigue, cough, dyspnea, loss of taste or smell). Of these, 54 reported testing positive for COVID-19, and 279 reported testing negative.

Sleep and activity were significantly different for the positive and negative groups, with an AUC of 0.68 (IQR, 0.57-0.79) for the sleep metric and 0.69 (IQR, 0.61-0.77) for the activity metric, suggesting that these parameters were more affected in COVID-19–positive participants.

When the investigators combined resting heart rate, sleep, and activity into a single metric, predictive performance improved to an AUC of 0.72 (IQR, 0.64-0.80).

The next step, Dr. Quer said, is to include an alert to notify users of possible infection.
 

Alerting users to possible COVID-19 infection

In a similar study, an alert feature was already incorporated. The study, led by Michael P. Snyder, PhD, director of the Center for Genomics and Personalized Medicine at Stanford (Calif.) University, will soon be published online in Nature Biomedical Engineering. In that study, presymptomatic detection of COVID-19 was achieved in more than 80% of participants using resting heart rate.

“The median is 4 days prior to symptom formation,” Dr. Snyder said in an interview. “We have an alarm system to notify people when their heart rate is elevated. So a positive signal from a smartwatch can be used to follow up by polymerase chain reaction [testing].”

Dr. Snyder said these approaches offer a roadmap to containing widespread infections. “Public health authorities need to be open to these technologies and begin incorporating them into their tracking,” he said. “Right now, people do temperature checks, which are of limited value. Resting heart rate is much better information.”

Although the DETECT researchers have not yet received feedback on their results, they believe public health authorities could recommend the use of such apps. “These are devices that people routinely wear for tracking their fitness and sleep, so it would be relatively easy to use the data for viral illness tracking,” said co–lead author Jennifer Radin, PhD, an epidemiologist at Scripps. “Testing resources are still limited and don’t allow for routine serial testing of individuals who may be asymptomatic or presymptomatic. Wearables can offer a different way to routinely monitor and screen people for changes in their data that may indicate COVID-19.”

The marshaling of data through consumer digital platforms to fight the coronavirus is gaining ground. New York State and New Jersey are already embracing smartphone apps to alert individuals to possible exposure to the virus.

More than 710,000 New Yorkers have downloaded the COVID NY Alert app, launched in October to help protect individuals and communities from COVID-19 by sending alerts without compromising privacy or personal information. “Upon receiving a notification about a potential exposure, users are then able to self-quarantine, get tested, and reduce the potential exposure risk to family, friends, coworkers, and others,” Jonah Bruno, a spokesperson for the New York State Department of Health, said in an interview.

And recently the Mayo Clinic and Safe Health Systems launched a platform to store COVID-19 testing and vaccination data.

Both the Scripps and Stanford platforms are part of a global technologic response to the COVID-19 pandemic. Prospective studies, led by device manufacturers and academic institutions, allow individuals to voluntarily share sensor and clinical data to address the crisis. Similar approaches have been used to track COVID-19 in large populations in Germany via the Corona Data Donation app.

The study by Dr. Quer and colleagues was funded by a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. One coauthor reported grants from Janssen and personal fees from Otsuka and Livongo outside of the submitted work. The other authors have disclosed no relevant financial relationships. Dr. Snyder has ties to Personalis, Qbio, January, SensOmics, Protos, Mirvie, and Oralome.
 

A version of this article originally appeared on Medscape.com.

The latest recommendations from sports cardiologists on getting athletes with COVID-19 back on the playing field safely emphasize a more judicious approach to screening for cardiac injury.

The new recommendations, made by the American College of Cardiology’s Sports and Exercise Cardiology Section, are for adult athletes in competitive sports and also for two important groups: younger athletes taking part in competitive high school sports and older athletes aged 35 and older, the Masters athletes, who continue to be active throughout their lives. The document was published online in JAMA Cardiology.

Because of the evolving nature of knowledge about COVID-19, updates on recommendations for safe return to play for athletes of all ages will continue to be made, senior author Aaron L. Baggish, MD, director of the cardiovascular performance program at Massachusetts General Hospital, Boston, said.

“The recommendations we released in May were entirely based on our experience taking care of hospitalized patients with COVID-19; we had no athletes in this population. We used a lot of conservative guesswork around how this would apply to otherwise healthy athletes,” Dr. Baggish said in an interview.

“But as sports started to open up, and we started to see large numbers of first professional and then college athletes come back into training, we realized that we needed to stop and ask whether the recommendations we put forward back in May were still appropriate,” Dr. Baggish said.

“Once we started to actually get into the trenches with these athletes, literally hundreds of them, and applying the testing strategies that we had initially recommended in everybody, we realized that we probably had some room for improvement, and that’s why we reconvened, to make these revisions,” he said.

Essentially, the recommendations now urge less cardiac testing. “Cardiac injury is not as common as we may have originally thought,” said Dr. Baggish.

“In the early days of COVID, people who were hospitalized had evidence of heart injury, and so we wondered if that prevalence would also be applicable to otherwise young, healthy people who got COVID. If that had been the case, we would have been in big trouble with respect to getting people back into sports. So this is why we started with a conservative screening approach and a lot of testing in order to not miss a huge burden of disease,” he said.

“But what we’ve learned over the past few months is that young people who get either asymptomatic or mild infection appear to have very, very low risk of having associated heart injury, so the need for testing in that population, when people who have infections recover fully, is almost certainly not going to be high yield,” Dr. Baggish said.
 

First iteration of the recommendations

Published in May in the early weeks of the pandemic, the first recommendations for safe return to play said that all athletes should stop training for at least 2 weeks after their symptoms resolve, then undergo “careful, clinical cardiovascular evaluation in combination with cardiac biomarkers and imaging.”

Additional testing with cardiac MRI, exercise testing, or ambulatory rhythm monitoring was to be done “based on the clinical course and initial testing.”

But experts caution that monitoring on such a scale in everyone is unnecessary and could even be counterproductive.

“Sending young athletes for extensive testing is not warranted and could send them to unnecessary testing, cardiac imaging, and so on,” Dr. Baggish said.

Only those athletes who continue to have symptoms or whose symptoms return when they get back to their athletic activities should go on for more screening.

“There, in essence, is the single main change from May, and that is a move away from screening with testing everyone, [and instead] confining that to the people who had moderate or greater severity disease,” he said.

Both iterations of the recommendations end with the same message.

“We are at the beginning of our knowledge about the cardiotoxic effects of COVID-19 but we are gathering evidence every day,” said Dr. Baggish. “Just as they did earlier, we acknowledge that our approaches are subject to change when we learn more about how COVID affects the heart, and specifically the hearts of athletes. This will be an ongoing process.”
 

Something to lean on

The recommendations are welcome, said James E. Udelson, MD, chief of the division of cardiology at Tufts Medical Center, Boston, coauthor of an accompanying editorial.

“It was a bit of the wild west out there, because each university, each college, all with good intentions, had been all struggling to figure out what to do, and how much to do. Probably the most important message from this new paper is the fact that now there is something out there that all coaches, athletes, families, schools, trainers can get some guidance from,” Dr. Udelson said in an interview.

Refining the cardiac screening criteria was a necessary step, Dr. Udelson said.

“How much cardiac imaging do you do? That is a matter of controversy,” said Dr. Udelson, who coauthored the commentary with Tufts cardiologist Ethan Rowin, MD, and Michael A. Curtis, MEd, a certified strength and conditioning specialist at the University of Virginia, Charlottesville. “The problem is that if you use a very sensitive imaging test on a lot of people, sometimes you find things that you really didn’t need to know about. They’re really not important. And now, the athlete is told he or she cannot play for 3 months because they might have myocarditis.

“Should we be too sensitive, meaning do we want to pick up anything no matter whether it’s important or not?” he added. “There will be a lot of false positives, and we are going to disqualify a lot of people. Or do you tune it a different way?”

Dr. Udelson said he would like to see commercial sports donate money to support research into the potential cardiotoxicity of COVID-19.

“If the organizations that benefit from these athletes, like the National Collegiate Athletic Association and professional sports leagues, can fund some of this research, that would be a huge help,” Dr. Udelson said.

“These are the top sports cardiologists in the country, and they have to start somewhere, and these are all based on what we know right now, as well as their own extensive experience. We all know that we are just at the beginning of our knowledge of this. But we have to have something to guide this huge community out there that is really thirsty for help.”

Dr. Baggish reports receiving research funding for the study of athletes in competitive sports from the National Heart, Lung, and Blood Institute; the National Football League Players Association; and the American Heart Association and receiving compensation for his role as team cardiologist from the US Olympic Committee/US Olympic Training Centers, US Soccer, US Rowing, the New England Patriots, the Boston Bruins, the New England Revolution, and Harvard University. Dr. Udelson has disclosed no relevant financial relationships.
 

A version of this article originally appeared on Medscape.com.

The latest recommendations from sports cardiologists on getting athletes with COVID-19 back on the playing field safely emphasize a more judicious approach to screening for cardiac injury.

The new recommendations, made by the American College of Cardiology’s Sports and Exercise Cardiology Section, are for adult athletes in competitive sports and also for two important groups: younger athletes taking part in competitive high school sports and older athletes aged 35 and older, the Masters athletes, who continue to be active throughout their lives. The document was published online in JAMA Cardiology.

Because of the evolving nature of knowledge about COVID-19, updates on recommendations for safe return to play for athletes of all ages will continue to be made, senior author Aaron L. Baggish, MD, director of the cardiovascular performance program at Massachusetts General Hospital, Boston, said.

“The recommendations we released in May were entirely based on our experience taking care of hospitalized patients with COVID-19; we had no athletes in this population. We used a lot of conservative guesswork around how this would apply to otherwise healthy athletes,” Dr. Baggish said in an interview.

“But as sports started to open up, and we started to see large numbers of first professional and then college athletes come back into training, we realized that we needed to stop and ask whether the recommendations we put forward back in May were still appropriate,” Dr. Baggish said.

“Once we started to actually get into the trenches with these athletes, literally hundreds of them, and applying the testing strategies that we had initially recommended in everybody, we realized that we probably had some room for improvement, and that’s why we reconvened, to make these revisions,” he said.

Essentially, the recommendations now urge less cardiac testing. “Cardiac injury is not as common as we may have originally thought,” said Dr. Baggish.

“In the early days of COVID, people who were hospitalized had evidence of heart injury, and so we wondered if that prevalence would also be applicable to otherwise young, healthy people who got COVID. If that had been the case, we would have been in big trouble with respect to getting people back into sports. So this is why we started with a conservative screening approach and a lot of testing in order to not miss a huge burden of disease,” he said.

“But what we’ve learned over the past few months is that young people who get either asymptomatic or mild infection appear to have very, very low risk of having associated heart injury, so the need for testing in that population, when people who have infections recover fully, is almost certainly not going to be high yield,” Dr. Baggish said.
 

First iteration of the recommendations

Published in May in the early weeks of the pandemic, the first recommendations for safe return to play said that all athletes should stop training for at least 2 weeks after their symptoms resolve, then undergo “careful, clinical cardiovascular evaluation in combination with cardiac biomarkers and imaging.”

Additional testing with cardiac MRI, exercise testing, or ambulatory rhythm monitoring was to be done “based on the clinical course and initial testing.”

But experts caution that monitoring on such a scale in everyone is unnecessary and could even be counterproductive.

“Sending young athletes for extensive testing is not warranted and could send them to unnecessary testing, cardiac imaging, and so on,” Dr. Baggish said.

Only those athletes who continue to have symptoms or whose symptoms return when they get back to their athletic activities should go on for more screening.

“There, in essence, is the single main change from May, and that is a move away from screening with testing everyone, [and instead] confining that to the people who had moderate or greater severity disease,” he said.

Both iterations of the recommendations end with the same message.

“We are at the beginning of our knowledge about the cardiotoxic effects of COVID-19 but we are gathering evidence every day,” said Dr. Baggish. “Just as they did earlier, we acknowledge that our approaches are subject to change when we learn more about how COVID affects the heart, and specifically the hearts of athletes. This will be an ongoing process.”
 

Something to lean on

The recommendations are welcome, said James E. Udelson, MD, chief of the division of cardiology at Tufts Medical Center, Boston, coauthor of an accompanying editorial.

“It was a bit of the wild west out there, because each university, each college, all with good intentions, had been all struggling to figure out what to do, and how much to do. Probably the most important message from this new paper is the fact that now there is something out there that all coaches, athletes, families, schools, trainers can get some guidance from,” Dr. Udelson said in an interview.

Refining the cardiac screening criteria was a necessary step, Dr. Udelson said.

“How much cardiac imaging do you do? That is a matter of controversy,” said Dr. Udelson, who coauthored the commentary with Tufts cardiologist Ethan Rowin, MD, and Michael A. Curtis, MEd, a certified strength and conditioning specialist at the University of Virginia, Charlottesville. “The problem is that if you use a very sensitive imaging test on a lot of people, sometimes you find things that you really didn’t need to know about. They’re really not important. And now, the athlete is told he or she cannot play for 3 months because they might have myocarditis.

“Should we be too sensitive, meaning do we want to pick up anything no matter whether it’s important or not?” he added. “There will be a lot of false positives, and we are going to disqualify a lot of people. Or do you tune it a different way?”

Dr. Udelson said he would like to see commercial sports donate money to support research into the potential cardiotoxicity of COVID-19.

“If the organizations that benefit from these athletes, like the National Collegiate Athletic Association and professional sports leagues, can fund some of this research, that would be a huge help,” Dr. Udelson said.

“These are the top sports cardiologists in the country, and they have to start somewhere, and these are all based on what we know right now, as well as their own extensive experience. We all know that we are just at the beginning of our knowledge of this. But we have to have something to guide this huge community out there that is really thirsty for help.”

Dr. Baggish reports receiving research funding for the study of athletes in competitive sports from the National Heart, Lung, and Blood Institute; the National Football League Players Association; and the American Heart Association and receiving compensation for his role as team cardiologist from the US Olympic Committee/US Olympic Training Centers, US Soccer, US Rowing, the New England Patriots, the Boston Bruins, the New England Revolution, and Harvard University. Dr. Udelson has disclosed no relevant financial relationships.
 

A version of this article originally appeared on Medscape.com.

The latest recommendations from sports cardiologists on getting athletes with COVID-19 back on the playing field safely emphasize a more judicious approach to screening for cardiac injury.

The new recommendations, made by the American College of Cardiology’s Sports and Exercise Cardiology Section, are for adult athletes in competitive sports and also for two important groups: younger athletes taking part in competitive high school sports and older athletes aged 35 and older, the Masters athletes, who continue to be active throughout their lives. The document was published online in JAMA Cardiology.

Because of the evolving nature of knowledge about COVID-19, updates on recommendations for safe return to play for athletes of all ages will continue to be made, senior author Aaron L. Baggish, MD, director of the cardiovascular performance program at Massachusetts General Hospital, Boston, said.

“The recommendations we released in May were entirely based on our experience taking care of hospitalized patients with COVID-19; we had no athletes in this population. We used a lot of conservative guesswork around how this would apply to otherwise healthy athletes,” Dr. Baggish said in an interview.

“But as sports started to open up, and we started to see large numbers of first professional and then college athletes come back into training, we realized that we needed to stop and ask whether the recommendations we put forward back in May were still appropriate,” Dr. Baggish said.

“Once we started to actually get into the trenches with these athletes, literally hundreds of them, and applying the testing strategies that we had initially recommended in everybody, we realized that we probably had some room for improvement, and that’s why we reconvened, to make these revisions,” he said.

Essentially, the recommendations now urge less cardiac testing. “Cardiac injury is not as common as we may have originally thought,” said Dr. Baggish.

“In the early days of COVID, people who were hospitalized had evidence of heart injury, and so we wondered if that prevalence would also be applicable to otherwise young, healthy people who got COVID. If that had been the case, we would have been in big trouble with respect to getting people back into sports. So this is why we started with a conservative screening approach and a lot of testing in order to not miss a huge burden of disease,” he said.

“But what we’ve learned over the past few months is that young people who get either asymptomatic or mild infection appear to have very, very low risk of having associated heart injury, so the need for testing in that population, when people who have infections recover fully, is almost certainly not going to be high yield,” Dr. Baggish said.
 

First iteration of the recommendations

Published in May in the early weeks of the pandemic, the first recommendations for safe return to play said that all athletes should stop training for at least 2 weeks after their symptoms resolve, then undergo “careful, clinical cardiovascular evaluation in combination with cardiac biomarkers and imaging.”

Additional testing with cardiac MRI, exercise testing, or ambulatory rhythm monitoring was to be done “based on the clinical course and initial testing.”

But experts caution that monitoring on such a scale in everyone is unnecessary and could even be counterproductive.

“Sending young athletes for extensive testing is not warranted and could send them to unnecessary testing, cardiac imaging, and so on,” Dr. Baggish said.

Only those athletes who continue to have symptoms or whose symptoms return when they get back to their athletic activities should go on for more screening.

“There, in essence, is the single main change from May, and that is a move away from screening with testing everyone, [and instead] confining that to the people who had moderate or greater severity disease,” he said.

Both iterations of the recommendations end with the same message.

“We are at the beginning of our knowledge about the cardiotoxic effects of COVID-19 but we are gathering evidence every day,” said Dr. Baggish. “Just as they did earlier, we acknowledge that our approaches are subject to change when we learn more about how COVID affects the heart, and specifically the hearts of athletes. This will be an ongoing process.”
 

Something to lean on

The recommendations are welcome, said James E. Udelson, MD, chief of the division of cardiology at Tufts Medical Center, Boston, coauthor of an accompanying editorial.

“It was a bit of the wild west out there, because each university, each college, all with good intentions, had been all struggling to figure out what to do, and how much to do. Probably the most important message from this new paper is the fact that now there is something out there that all coaches, athletes, families, schools, trainers can get some guidance from,” Dr. Udelson said in an interview.

Refining the cardiac screening criteria was a necessary step, Dr. Udelson said.

“How much cardiac imaging do you do? That is a matter of controversy,” said Dr. Udelson, who coauthored the commentary with Tufts cardiologist Ethan Rowin, MD, and Michael A. Curtis, MEd, a certified strength and conditioning specialist at the University of Virginia, Charlottesville. “The problem is that if you use a very sensitive imaging test on a lot of people, sometimes you find things that you really didn’t need to know about. They’re really not important. And now, the athlete is told he or she cannot play for 3 months because they might have myocarditis.

“Should we be too sensitive, meaning do we want to pick up anything no matter whether it’s important or not?” he added. “There will be a lot of false positives, and we are going to disqualify a lot of people. Or do you tune it a different way?”

Dr. Udelson said he would like to see commercial sports donate money to support research into the potential cardiotoxicity of COVID-19.

“If the organizations that benefit from these athletes, like the National Collegiate Athletic Association and professional sports leagues, can fund some of this research, that would be a huge help,” Dr. Udelson said.

“These are the top sports cardiologists in the country, and they have to start somewhere, and these are all based on what we know right now, as well as their own extensive experience. We all know that we are just at the beginning of our knowledge of this. But we have to have something to guide this huge community out there that is really thirsty for help.”

Dr. Baggish reports receiving research funding for the study of athletes in competitive sports from the National Heart, Lung, and Blood Institute; the National Football League Players Association; and the American Heart Association and receiving compensation for his role as team cardiologist from the US Olympic Committee/US Olympic Training Centers, US Soccer, US Rowing, the New England Patriots, the Boston Bruins, the New England Revolution, and Harvard University. Dr. Udelson has disclosed no relevant financial relationships.
 

A version of this article originally appeared on Medscape.com.