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Half of deaths from homozygous FH occur before age 32 years
MANNHEIM, GERMANY –
The researchers looked at almost 40 patients from the HoFH International Clinical Collaborators (HICC) registry who had died before data entry, finding that they had a mean age of diagnosis of 12 years.
Even those who received treatment had high LDL cholesterol levels, and 70% developed atherosclerotic cardiovascular disease (ASCVD) at a median age of 28 years.
Worryingly, the results showed that the median age at death was 32 years. Results were presented at the annual congress of the European Atherosclerosis Society.
Patients with HoFH “have severe atherosclerotic cardiovascular disease risk,” said study presenter Janneke Mulder, a PhD candidate at the department of internal medicine, Erasmus University Medical Center, Rotterdam, the Netherlands.
“Therefore, early diagnosis and initiation of treatments, and also a combination of treatments, is really crucial,” she added.
Call to action
Approached for comment, Maciej Banach, MD, PhD, full professor of cardiology, Polish Mother’s Memorial Hospital Research Institute, Lodz, and Secretary of the EAS, described the results as “terrifying.”
He said in an interview that they are a “call to action,” especially given that so few patients in the study received intensive combination lipid-lowering therapy despite having a baseline LDL cholesterol level that was “very, very high.”
Banach underlined that patients who receive triple lipid-lowering therapy with a high-intensity statin, ezetimibe (Nustendi), and a proprotein convertase subtilisin/kexin type 9 inhibitor, could expect, based on current evidence, to see their LDL cholesterol levels reduced by 85% and be on target.
“Obviously, this is kind of academic,” because in the real-world “this 85% is not observed very often,” but it offers a target for steep reductions in cholesterol levels.
“This is something that we should focus on for these patients from the beginning,” said Dr. Banach, either with a stepwise approach “or for experts in pediatric HoFH, “maybe immediately.”
He emphasized that clinicians have everything at hand to “be both effective in the early diagnosis of HoFH, the earlier the better, and obviously to be effective with its treatment.”
“We should do something to prolong the lives of those people,” because the current results are “terrifying,” Dr. Banach added.
Rare genetic condition
Presenting her findings, Ms. Mulder began by highlighting that HoFH is a “rare genetic condition that occurs due to mutations in cholesterol metabolism.”
This, she continued, leads to “severely increased LDL cholesterol levels, and consequently to very premature cardiovascular disease,” with patients potentially experiencing their first cardiovascular event before age 20 years.
Ms. Mulder pointed out that, although there have been case series in the literature on HoFH, they have had “limited numbers” and patients have typically spent decades being treated at the same lipid management clinic.
To broaden the understanding of the clinical characteristics and management of patients dying with HoFH, the team examined data from the HICC registry, which is “the largest contemporary database of homozygous FH patients,” Ms. Mulder said.
It includes 751 patients with HoFH from 88 centers in 38 countries who were alive in 2010 or later. Data entry was between 2016 and 2020. The current analysis focused on 37 patients who had already died by the time they were included on the registry.
Of those, 49% were women, 38% were of White ethnicity, and 43% were from high-income countries.
The median age at diagnosis was 12 years, Ms. Mulder said, explaining that this is similar to that seen in other studies. The majority (86%) underwent genetic testing, and 92% presented with xanthomas.
Ms. Mulder also noted that, at their final clinical evaluation, which was conducted a median age of 18 years after their initial diagnosis, 43% of patients were recorded as current or former smokers.
In terms of their lipid-lowering therapy, 94% were taking a statin, whereas 68% were on ezetimibe, and 23% were undergoing apheresis.
Ms. Mulder said that the median number of lipid-lowering therapies per patient was two, and that “sadly ... 26% of the deceased patients had only one or no treatment.”
Therefore, perhaps unsurprisingly even those patients who were receiving treatment had LDL cholesterol levels that were “too high,” at 9.4 mmol/L versus 15.6 mmol/L among those who were untreated.
There was a high prevalence of ASCVD, at 70% overall, or 41% for aortic stenosis, 30% for myocardial infarction, 30% for angina pectoris, and 22% each for aortic valve replacement and coronary artery bypass grafting. In addition, 19% underwent percutaneous coronary intervention.
The median age of onset for ASCVD was 28 years. Ms. Mulder pointed out, however, that, as data were not available for all patients, “this might be an underestimation.” About 70% of patients experienced recurrent ASCVD.
There was a wide range in the age at which patients with HoFH died, although the median was, “strikingly,” 32 years, Ms. Mulder said. Death was confirmed as stemming from cardiovascular causes in 76% of cases.
During the postpresentation discussion, session chair Antonio J. Vallejo-Vaz, PhD, from the Research Group of Clinical Epidemiology and Vascular Risk, Institute of Biomedicine of Seville (Spain), highlighted that, if 38% of the patients were of White ethnicity, then the remainder must therefore be from other ethnic groups.
“There could be potential issues with accessibility to lipid centers” for these patients, which could affect the findings, noted Dr. Vallejo-Vaz, who is also chief scientist of the EAS Familial Hypercholesterolaemia Studies Collaboration.
Ms. Mulder agreed, replying that their results, though already striking, may be an underestimation because the patients were all from either high or middle-income countries, “so it would be good to have some data on low-income countries.”
She was also asked about two patients who died at a much older age than did the others, at ages 70 years and 86 years, respectively, and whether they had, for example, a protective genetic mutation.
Ms. Mulder said that they do not yet know, but they are planning an extended case series on these and other long-lived patients so that they can be investigated further.
No funding or relevant financial relationships were declared.
A version of this article first appeared on Medscape.com.
MANNHEIM, GERMANY –
The researchers looked at almost 40 patients from the HoFH International Clinical Collaborators (HICC) registry who had died before data entry, finding that they had a mean age of diagnosis of 12 years.
Even those who received treatment had high LDL cholesterol levels, and 70% developed atherosclerotic cardiovascular disease (ASCVD) at a median age of 28 years.
Worryingly, the results showed that the median age at death was 32 years. Results were presented at the annual congress of the European Atherosclerosis Society.
Patients with HoFH “have severe atherosclerotic cardiovascular disease risk,” said study presenter Janneke Mulder, a PhD candidate at the department of internal medicine, Erasmus University Medical Center, Rotterdam, the Netherlands.
“Therefore, early diagnosis and initiation of treatments, and also a combination of treatments, is really crucial,” she added.
Call to action
Approached for comment, Maciej Banach, MD, PhD, full professor of cardiology, Polish Mother’s Memorial Hospital Research Institute, Lodz, and Secretary of the EAS, described the results as “terrifying.”
He said in an interview that they are a “call to action,” especially given that so few patients in the study received intensive combination lipid-lowering therapy despite having a baseline LDL cholesterol level that was “very, very high.”
Banach underlined that patients who receive triple lipid-lowering therapy with a high-intensity statin, ezetimibe (Nustendi), and a proprotein convertase subtilisin/kexin type 9 inhibitor, could expect, based on current evidence, to see their LDL cholesterol levels reduced by 85% and be on target.
“Obviously, this is kind of academic,” because in the real-world “this 85% is not observed very often,” but it offers a target for steep reductions in cholesterol levels.
“This is something that we should focus on for these patients from the beginning,” said Dr. Banach, either with a stepwise approach “or for experts in pediatric HoFH, “maybe immediately.”
He emphasized that clinicians have everything at hand to “be both effective in the early diagnosis of HoFH, the earlier the better, and obviously to be effective with its treatment.”
“We should do something to prolong the lives of those people,” because the current results are “terrifying,” Dr. Banach added.
Rare genetic condition
Presenting her findings, Ms. Mulder began by highlighting that HoFH is a “rare genetic condition that occurs due to mutations in cholesterol metabolism.”
This, she continued, leads to “severely increased LDL cholesterol levels, and consequently to very premature cardiovascular disease,” with patients potentially experiencing their first cardiovascular event before age 20 years.
Ms. Mulder pointed out that, although there have been case series in the literature on HoFH, they have had “limited numbers” and patients have typically spent decades being treated at the same lipid management clinic.
To broaden the understanding of the clinical characteristics and management of patients dying with HoFH, the team examined data from the HICC registry, which is “the largest contemporary database of homozygous FH patients,” Ms. Mulder said.
It includes 751 patients with HoFH from 88 centers in 38 countries who were alive in 2010 or later. Data entry was between 2016 and 2020. The current analysis focused on 37 patients who had already died by the time they were included on the registry.
Of those, 49% were women, 38% were of White ethnicity, and 43% were from high-income countries.
The median age at diagnosis was 12 years, Ms. Mulder said, explaining that this is similar to that seen in other studies. The majority (86%) underwent genetic testing, and 92% presented with xanthomas.
Ms. Mulder also noted that, at their final clinical evaluation, which was conducted a median age of 18 years after their initial diagnosis, 43% of patients were recorded as current or former smokers.
In terms of their lipid-lowering therapy, 94% were taking a statin, whereas 68% were on ezetimibe, and 23% were undergoing apheresis.
Ms. Mulder said that the median number of lipid-lowering therapies per patient was two, and that “sadly ... 26% of the deceased patients had only one or no treatment.”
Therefore, perhaps unsurprisingly even those patients who were receiving treatment had LDL cholesterol levels that were “too high,” at 9.4 mmol/L versus 15.6 mmol/L among those who were untreated.
There was a high prevalence of ASCVD, at 70% overall, or 41% for aortic stenosis, 30% for myocardial infarction, 30% for angina pectoris, and 22% each for aortic valve replacement and coronary artery bypass grafting. In addition, 19% underwent percutaneous coronary intervention.
The median age of onset for ASCVD was 28 years. Ms. Mulder pointed out, however, that, as data were not available for all patients, “this might be an underestimation.” About 70% of patients experienced recurrent ASCVD.
There was a wide range in the age at which patients with HoFH died, although the median was, “strikingly,” 32 years, Ms. Mulder said. Death was confirmed as stemming from cardiovascular causes in 76% of cases.
During the postpresentation discussion, session chair Antonio J. Vallejo-Vaz, PhD, from the Research Group of Clinical Epidemiology and Vascular Risk, Institute of Biomedicine of Seville (Spain), highlighted that, if 38% of the patients were of White ethnicity, then the remainder must therefore be from other ethnic groups.
“There could be potential issues with accessibility to lipid centers” for these patients, which could affect the findings, noted Dr. Vallejo-Vaz, who is also chief scientist of the EAS Familial Hypercholesterolaemia Studies Collaboration.
Ms. Mulder agreed, replying that their results, though already striking, may be an underestimation because the patients were all from either high or middle-income countries, “so it would be good to have some data on low-income countries.”
She was also asked about two patients who died at a much older age than did the others, at ages 70 years and 86 years, respectively, and whether they had, for example, a protective genetic mutation.
Ms. Mulder said that they do not yet know, but they are planning an extended case series on these and other long-lived patients so that they can be investigated further.
No funding or relevant financial relationships were declared.
A version of this article first appeared on Medscape.com.
MANNHEIM, GERMANY –
The researchers looked at almost 40 patients from the HoFH International Clinical Collaborators (HICC) registry who had died before data entry, finding that they had a mean age of diagnosis of 12 years.
Even those who received treatment had high LDL cholesterol levels, and 70% developed atherosclerotic cardiovascular disease (ASCVD) at a median age of 28 years.
Worryingly, the results showed that the median age at death was 32 years. Results were presented at the annual congress of the European Atherosclerosis Society.
Patients with HoFH “have severe atherosclerotic cardiovascular disease risk,” said study presenter Janneke Mulder, a PhD candidate at the department of internal medicine, Erasmus University Medical Center, Rotterdam, the Netherlands.
“Therefore, early diagnosis and initiation of treatments, and also a combination of treatments, is really crucial,” she added.
Call to action
Approached for comment, Maciej Banach, MD, PhD, full professor of cardiology, Polish Mother’s Memorial Hospital Research Institute, Lodz, and Secretary of the EAS, described the results as “terrifying.”
He said in an interview that they are a “call to action,” especially given that so few patients in the study received intensive combination lipid-lowering therapy despite having a baseline LDL cholesterol level that was “very, very high.”
Banach underlined that patients who receive triple lipid-lowering therapy with a high-intensity statin, ezetimibe (Nustendi), and a proprotein convertase subtilisin/kexin type 9 inhibitor, could expect, based on current evidence, to see their LDL cholesterol levels reduced by 85% and be on target.
“Obviously, this is kind of academic,” because in the real-world “this 85% is not observed very often,” but it offers a target for steep reductions in cholesterol levels.
“This is something that we should focus on for these patients from the beginning,” said Dr. Banach, either with a stepwise approach “or for experts in pediatric HoFH, “maybe immediately.”
He emphasized that clinicians have everything at hand to “be both effective in the early diagnosis of HoFH, the earlier the better, and obviously to be effective with its treatment.”
“We should do something to prolong the lives of those people,” because the current results are “terrifying,” Dr. Banach added.
Rare genetic condition
Presenting her findings, Ms. Mulder began by highlighting that HoFH is a “rare genetic condition that occurs due to mutations in cholesterol metabolism.”
This, she continued, leads to “severely increased LDL cholesterol levels, and consequently to very premature cardiovascular disease,” with patients potentially experiencing their first cardiovascular event before age 20 years.
Ms. Mulder pointed out that, although there have been case series in the literature on HoFH, they have had “limited numbers” and patients have typically spent decades being treated at the same lipid management clinic.
To broaden the understanding of the clinical characteristics and management of patients dying with HoFH, the team examined data from the HICC registry, which is “the largest contemporary database of homozygous FH patients,” Ms. Mulder said.
It includes 751 patients with HoFH from 88 centers in 38 countries who were alive in 2010 or later. Data entry was between 2016 and 2020. The current analysis focused on 37 patients who had already died by the time they were included on the registry.
Of those, 49% were women, 38% were of White ethnicity, and 43% were from high-income countries.
The median age at diagnosis was 12 years, Ms. Mulder said, explaining that this is similar to that seen in other studies. The majority (86%) underwent genetic testing, and 92% presented with xanthomas.
Ms. Mulder also noted that, at their final clinical evaluation, which was conducted a median age of 18 years after their initial diagnosis, 43% of patients were recorded as current or former smokers.
In terms of their lipid-lowering therapy, 94% were taking a statin, whereas 68% were on ezetimibe, and 23% were undergoing apheresis.
Ms. Mulder said that the median number of lipid-lowering therapies per patient was two, and that “sadly ... 26% of the deceased patients had only one or no treatment.”
Therefore, perhaps unsurprisingly even those patients who were receiving treatment had LDL cholesterol levels that were “too high,” at 9.4 mmol/L versus 15.6 mmol/L among those who were untreated.
There was a high prevalence of ASCVD, at 70% overall, or 41% for aortic stenosis, 30% for myocardial infarction, 30% for angina pectoris, and 22% each for aortic valve replacement and coronary artery bypass grafting. In addition, 19% underwent percutaneous coronary intervention.
The median age of onset for ASCVD was 28 years. Ms. Mulder pointed out, however, that, as data were not available for all patients, “this might be an underestimation.” About 70% of patients experienced recurrent ASCVD.
There was a wide range in the age at which patients with HoFH died, although the median was, “strikingly,” 32 years, Ms. Mulder said. Death was confirmed as stemming from cardiovascular causes in 76% of cases.
During the postpresentation discussion, session chair Antonio J. Vallejo-Vaz, PhD, from the Research Group of Clinical Epidemiology and Vascular Risk, Institute of Biomedicine of Seville (Spain), highlighted that, if 38% of the patients were of White ethnicity, then the remainder must therefore be from other ethnic groups.
“There could be potential issues with accessibility to lipid centers” for these patients, which could affect the findings, noted Dr. Vallejo-Vaz, who is also chief scientist of the EAS Familial Hypercholesterolaemia Studies Collaboration.
Ms. Mulder agreed, replying that their results, though already striking, may be an underestimation because the patients were all from either high or middle-income countries, “so it would be good to have some data on low-income countries.”
She was also asked about two patients who died at a much older age than did the others, at ages 70 years and 86 years, respectively, and whether they had, for example, a protective genetic mutation.
Ms. Mulder said that they do not yet know, but they are planning an extended case series on these and other long-lived patients so that they can be investigated further.
No funding or relevant financial relationships were declared.
A version of this article first appeared on Medscape.com.
Coronary artery calcium score bests polygenic risk score in CHD prediction
As a predictor of coronary heart disease (CHD) events, the coronary artery calcium (CAC) score on computed tomography had better risk discrimination than the polygenic risk score, a binational study found. And when added to classic cardiovascular risk factors, the CAC score significantly improved risk classification while the polygenic risk factor score did not.
These findings emerged from two large cohorts of middle-aged and older White adults from the United States and the Netherlands in the first head-to-head comparison of these two approaches. Led by Sadiya S. Kahn, MD, MSc, an assistant professor of medicine (cardiology) and preventive medicine (epidemiology) at Northwestern University, Chicago, the study was published online in JAMA.
There has been much interest in using both genetic factors and CT imaging to better identify individuals at risk for heart disease. “Each approach has advantages and disadvantages, and we wanted to better understand the comparative predictive utility to provide support for what the preferred approach should be,” Dr. Kahn said in an interview. “We focused on middle-aged to older adults for whom current risk prediction equations are relevant in estimating risk with the Pooled Cohort Equation, or PCE.”
The superiority of the CT-imaged coronary artery risk score may be because of its direct visualization of calcification in the arteries and the subclinical disease burden rather than a focus on common genetic variants, Dr. Kahn explained. “In addition, prior studies have demonstrated that genetics, or inherited risk, is not destiny, so this score may not perform as well for risk discrimination as the traditional risk factors themselves along with CT.”
The study
Study participants came from the U.S. Multi-Ethnic Study of Atherosclerosis (MESA, n = 1,991) and the Dutch Rotterdam Study (RS, n = 1,217). Ages ranged from 45 to 79, with the medians in the two cohorts 61 and 68 years, respectively. Slightly more than half of participants in both groups were female.
Traditional risk factors were used to calculate CHD risk with pooled cohort equations, while computed tomography was used to determine the CAC score and genotyped samples for a validated polygenic risk score.
Both scores were significantly associated with 10-year risk of incident CHD.
The median predicted atherosclerotic disease risk based on traditional risk factors was 6.99% in MESA and 5.93% in RS. During the total available follow-up in MESA (median, 16.0 years) and RS (median, 14.2 years), incident CHD occurred in 187 participants (9.4%) and 98 participants (8.1%), respectively.
C (concordance) statistics for the two scores showed the superiority of the CAC. This statistic measures a model’s ability to rank patients from high to low risk, with a value of 1 being perfect risk fit or concordance and 0.70 or more indicating good concordance and risk discrimination. The CAC score had a C statistic of 0.76 (95% confidence interval, 0.71-0.79) vs. 0.69 for the polygenic risk score (95% CI, 0.63-0.71).
When each score was added to PCEs, the C statistics changed as follows: CAC score, 0.09 (95% CI, 0.06-0.13); polygenic risk score, 0.02 (95% CI, 0.00-0.04); and 0.10 (95% CI, 0.07-0.14) for both.
Net reclassification significantly improved with the CAC plus PCEs by the following values: 0.19 (95% CI, 0.06-0.28). The change was not significant, however, with the polygenic risk score plus PCEs: 0.04 (95% CI, –0.05-0.10).
In the clinical setting, Dr. Kahn said, “The use of CT in patients who are at intermediate risk for heart disease can be helpful in refining risk estimation and guiding recommendations for lipid-lowering therapy. Polygenic risk scores are not helpful in middle-aged to older adults above and beyond traditional risk factors for predicting risk of heart disease.”
This study was supported by the National Heart, Lung, and Blood Institute. MESA is supported by the NHLBI. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development; the Research Institute for Diseases in the Elderly; the Netherlands Genomics Initiative; the Ministry of Education, Culture and Science, the Ministry of Health, Welfare and Sports; the European Commission (DG XII); and the Municipality of Rotterdam. Dr. Khan reported grants from the NHLBI and the NIH during the study and outside of the submitted work. Several coauthors reported grant support from, variously, the NIH, the NHLBI, and the American Heart Association.
As a predictor of coronary heart disease (CHD) events, the coronary artery calcium (CAC) score on computed tomography had better risk discrimination than the polygenic risk score, a binational study found. And when added to classic cardiovascular risk factors, the CAC score significantly improved risk classification while the polygenic risk factor score did not.
These findings emerged from two large cohorts of middle-aged and older White adults from the United States and the Netherlands in the first head-to-head comparison of these two approaches. Led by Sadiya S. Kahn, MD, MSc, an assistant professor of medicine (cardiology) and preventive medicine (epidemiology) at Northwestern University, Chicago, the study was published online in JAMA.
There has been much interest in using both genetic factors and CT imaging to better identify individuals at risk for heart disease. “Each approach has advantages and disadvantages, and we wanted to better understand the comparative predictive utility to provide support for what the preferred approach should be,” Dr. Kahn said in an interview. “We focused on middle-aged to older adults for whom current risk prediction equations are relevant in estimating risk with the Pooled Cohort Equation, or PCE.”
The superiority of the CT-imaged coronary artery risk score may be because of its direct visualization of calcification in the arteries and the subclinical disease burden rather than a focus on common genetic variants, Dr. Kahn explained. “In addition, prior studies have demonstrated that genetics, or inherited risk, is not destiny, so this score may not perform as well for risk discrimination as the traditional risk factors themselves along with CT.”
The study
Study participants came from the U.S. Multi-Ethnic Study of Atherosclerosis (MESA, n = 1,991) and the Dutch Rotterdam Study (RS, n = 1,217). Ages ranged from 45 to 79, with the medians in the two cohorts 61 and 68 years, respectively. Slightly more than half of participants in both groups were female.
Traditional risk factors were used to calculate CHD risk with pooled cohort equations, while computed tomography was used to determine the CAC score and genotyped samples for a validated polygenic risk score.
Both scores were significantly associated with 10-year risk of incident CHD.
The median predicted atherosclerotic disease risk based on traditional risk factors was 6.99% in MESA and 5.93% in RS. During the total available follow-up in MESA (median, 16.0 years) and RS (median, 14.2 years), incident CHD occurred in 187 participants (9.4%) and 98 participants (8.1%), respectively.
C (concordance) statistics for the two scores showed the superiority of the CAC. This statistic measures a model’s ability to rank patients from high to low risk, with a value of 1 being perfect risk fit or concordance and 0.70 or more indicating good concordance and risk discrimination. The CAC score had a C statistic of 0.76 (95% confidence interval, 0.71-0.79) vs. 0.69 for the polygenic risk score (95% CI, 0.63-0.71).
When each score was added to PCEs, the C statistics changed as follows: CAC score, 0.09 (95% CI, 0.06-0.13); polygenic risk score, 0.02 (95% CI, 0.00-0.04); and 0.10 (95% CI, 0.07-0.14) for both.
Net reclassification significantly improved with the CAC plus PCEs by the following values: 0.19 (95% CI, 0.06-0.28). The change was not significant, however, with the polygenic risk score plus PCEs: 0.04 (95% CI, –0.05-0.10).
In the clinical setting, Dr. Kahn said, “The use of CT in patients who are at intermediate risk for heart disease can be helpful in refining risk estimation and guiding recommendations for lipid-lowering therapy. Polygenic risk scores are not helpful in middle-aged to older adults above and beyond traditional risk factors for predicting risk of heart disease.”
This study was supported by the National Heart, Lung, and Blood Institute. MESA is supported by the NHLBI. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development; the Research Institute for Diseases in the Elderly; the Netherlands Genomics Initiative; the Ministry of Education, Culture and Science, the Ministry of Health, Welfare and Sports; the European Commission (DG XII); and the Municipality of Rotterdam. Dr. Khan reported grants from the NHLBI and the NIH during the study and outside of the submitted work. Several coauthors reported grant support from, variously, the NIH, the NHLBI, and the American Heart Association.
As a predictor of coronary heart disease (CHD) events, the coronary artery calcium (CAC) score on computed tomography had better risk discrimination than the polygenic risk score, a binational study found. And when added to classic cardiovascular risk factors, the CAC score significantly improved risk classification while the polygenic risk factor score did not.
These findings emerged from two large cohorts of middle-aged and older White adults from the United States and the Netherlands in the first head-to-head comparison of these two approaches. Led by Sadiya S. Kahn, MD, MSc, an assistant professor of medicine (cardiology) and preventive medicine (epidemiology) at Northwestern University, Chicago, the study was published online in JAMA.
There has been much interest in using both genetic factors and CT imaging to better identify individuals at risk for heart disease. “Each approach has advantages and disadvantages, and we wanted to better understand the comparative predictive utility to provide support for what the preferred approach should be,” Dr. Kahn said in an interview. “We focused on middle-aged to older adults for whom current risk prediction equations are relevant in estimating risk with the Pooled Cohort Equation, or PCE.”
The superiority of the CT-imaged coronary artery risk score may be because of its direct visualization of calcification in the arteries and the subclinical disease burden rather than a focus on common genetic variants, Dr. Kahn explained. “In addition, prior studies have demonstrated that genetics, or inherited risk, is not destiny, so this score may not perform as well for risk discrimination as the traditional risk factors themselves along with CT.”
The study
Study participants came from the U.S. Multi-Ethnic Study of Atherosclerosis (MESA, n = 1,991) and the Dutch Rotterdam Study (RS, n = 1,217). Ages ranged from 45 to 79, with the medians in the two cohorts 61 and 68 years, respectively. Slightly more than half of participants in both groups were female.
Traditional risk factors were used to calculate CHD risk with pooled cohort equations, while computed tomography was used to determine the CAC score and genotyped samples for a validated polygenic risk score.
Both scores were significantly associated with 10-year risk of incident CHD.
The median predicted atherosclerotic disease risk based on traditional risk factors was 6.99% in MESA and 5.93% in RS. During the total available follow-up in MESA (median, 16.0 years) and RS (median, 14.2 years), incident CHD occurred in 187 participants (9.4%) and 98 participants (8.1%), respectively.
C (concordance) statistics for the two scores showed the superiority of the CAC. This statistic measures a model’s ability to rank patients from high to low risk, with a value of 1 being perfect risk fit or concordance and 0.70 or more indicating good concordance and risk discrimination. The CAC score had a C statistic of 0.76 (95% confidence interval, 0.71-0.79) vs. 0.69 for the polygenic risk score (95% CI, 0.63-0.71).
When each score was added to PCEs, the C statistics changed as follows: CAC score, 0.09 (95% CI, 0.06-0.13); polygenic risk score, 0.02 (95% CI, 0.00-0.04); and 0.10 (95% CI, 0.07-0.14) for both.
Net reclassification significantly improved with the CAC plus PCEs by the following values: 0.19 (95% CI, 0.06-0.28). The change was not significant, however, with the polygenic risk score plus PCEs: 0.04 (95% CI, –0.05-0.10).
In the clinical setting, Dr. Kahn said, “The use of CT in patients who are at intermediate risk for heart disease can be helpful in refining risk estimation and guiding recommendations for lipid-lowering therapy. Polygenic risk scores are not helpful in middle-aged to older adults above and beyond traditional risk factors for predicting risk of heart disease.”
This study was supported by the National Heart, Lung, and Blood Institute. MESA is supported by the NHLBI. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development; the Research Institute for Diseases in the Elderly; the Netherlands Genomics Initiative; the Ministry of Education, Culture and Science, the Ministry of Health, Welfare and Sports; the European Commission (DG XII); and the Municipality of Rotterdam. Dr. Khan reported grants from the NHLBI and the NIH during the study and outside of the submitted work. Several coauthors reported grant support from, variously, the NIH, the NHLBI, and the American Heart Association.
FROM JAMA
Once-daily nifedipine sufficient for hypertension in pregnancy
BALTIMORE – , according to research presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.*
The findings suggest that starting patients on a once-daily 60-mg dose is therefore reasonable, Isabelle Band, BA, a medical student at the Icahn School of Medicine at Mount Sinai, New York, told attendees. Ms. Band said in an interview that there does not appear to be a consensus on the standard of care for nifedipine dosing regimen in this population but that previous in vitro studies have shown increased metabolism of nifedipine in a physiologic state that mimics pregnancy.
“I’ve spoken to some colleagues here who say that they frequently have this debate of which dosing regimen to go with,” Ms. Band said. “I was pleasantly surprised that there was no significant difference between the two dosing regimens because once-daily dosing is less burdensome for patients and will likely improve compliance and convenience for patients.” An additional benefit of once-daily dosing relates to payers because anecdotal reports suggest insurance companies do not tend to approve twice-daily dosing as readily as once-daily dosing, Ms. Band added.
Ms. Band and her colleagues conducted a retrospective chart review of all patients with hypertensive disorders of pregnancy who were admitted to the Mount Sinai Health System between Jan. 1, 2015, and April 30, 2021, and were prescribed nifedipine in a once-daily (60-mg) or twice-daily (two 30-mg) dose. They excluded patients with renal disease and those already taking hypertensives prior to admission.
Among 237 patients who met the criteria, 59% received 60 mg in a twice-daily 30-mg dose, and 41% received 60 mg in a once-daily dose. Among patients requiring an up titration, two-thirds (67%) needed an increase in the nifedipine dose – the most common adjustment – and 20.7% needed both an increase in nifedipine and an additional medication.
The researchers observed no statistically significant differences in the proportion of patients who required a dose increase or an additional antihypertensive in the group taking the twice-daily dose (33.8%) or those receiving the once-daily dose (35.7%). This finding remained statistically insignificant after controlling for gestational diabetes, delivery mode, administration of Lasix, and receipt of emergency antihypertensive treatment (P = .71). The time that passed before patients needed a dose increase was also statistically similar between the groups: 24.3 hours in the twice-daily group and 24 hours in the once-daily group (P = .49).
There were no statistically significant differences in the need for a dose increase or an additional hypertensive agent based on race, ethnicity, body mass index, or history of preeclampsia as well. However, 24.5% of those taking the once-daily dosage had a history of preeclampsia, compared with 7.2% of those taking the twice-daily dosage (P < .001). Further, the median number of prior pregnancies was two in the twice-daily group versus three in the once-daily group (P = .002).
The authors found no significant difference between the two dosing groups in the need for emergency hypertensive treatment after reaching the study dose or in readmission for blood pressure control. In the twice-daily group, 21.6% of patients needed emergency antihypertensive treatment, compared with 14.3% in the once-daily group (P = .19). Readmission was necessary for 7.2% of the twice-daily group and 6.1% of the once-daily group (P > .99).
A subgroup analysis compared those who started nifedipine antepartum and those who started it post partum, but again, no significant difference in the dosing regimens existed.
Michael Ruma, MD, a maternal-fetal medicine specialist at Perinatal Associates of New Mexico in Albuquerque, was not involved in the study and said he welcomed the results.
“We have too many choices in medicine, so we need to just simplify the plan of attack,” reducing the number of things that clinicians need to think about, Dr. Ruma said in an interview. “A singular dose is always easiest for the patient, always easier for nursing staff, and usually, if you can optimize the dosing, that’s the best approach.”
Annabeth Brewton, MD, a resident at University of Tennessee, Knoxville, agreed, adding that new parents already have a lot going on immediately post partum.
“They’re going to be breastfeeding, they’re not sleeping, they’re going to forget to take that [second] dose,” Dr. Brewton said.
Ms. Band and Dr. Brewton had no disclosures. Dr. Ruma reported consulting and speaking for Hologic and consulting for Philips Ultrasound.
Correction, 5/24/23: An earlier version of this article misstated the daily doses of nifedipine. The study compared a
BALTIMORE – , according to research presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.*
The findings suggest that starting patients on a once-daily 60-mg dose is therefore reasonable, Isabelle Band, BA, a medical student at the Icahn School of Medicine at Mount Sinai, New York, told attendees. Ms. Band said in an interview that there does not appear to be a consensus on the standard of care for nifedipine dosing regimen in this population but that previous in vitro studies have shown increased metabolism of nifedipine in a physiologic state that mimics pregnancy.
“I’ve spoken to some colleagues here who say that they frequently have this debate of which dosing regimen to go with,” Ms. Band said. “I was pleasantly surprised that there was no significant difference between the two dosing regimens because once-daily dosing is less burdensome for patients and will likely improve compliance and convenience for patients.” An additional benefit of once-daily dosing relates to payers because anecdotal reports suggest insurance companies do not tend to approve twice-daily dosing as readily as once-daily dosing, Ms. Band added.
Ms. Band and her colleagues conducted a retrospective chart review of all patients with hypertensive disorders of pregnancy who were admitted to the Mount Sinai Health System between Jan. 1, 2015, and April 30, 2021, and were prescribed nifedipine in a once-daily (60-mg) or twice-daily (two 30-mg) dose. They excluded patients with renal disease and those already taking hypertensives prior to admission.
Among 237 patients who met the criteria, 59% received 60 mg in a twice-daily 30-mg dose, and 41% received 60 mg in a once-daily dose. Among patients requiring an up titration, two-thirds (67%) needed an increase in the nifedipine dose – the most common adjustment – and 20.7% needed both an increase in nifedipine and an additional medication.
The researchers observed no statistically significant differences in the proportion of patients who required a dose increase or an additional antihypertensive in the group taking the twice-daily dose (33.8%) or those receiving the once-daily dose (35.7%). This finding remained statistically insignificant after controlling for gestational diabetes, delivery mode, administration of Lasix, and receipt of emergency antihypertensive treatment (P = .71). The time that passed before patients needed a dose increase was also statistically similar between the groups: 24.3 hours in the twice-daily group and 24 hours in the once-daily group (P = .49).
There were no statistically significant differences in the need for a dose increase or an additional hypertensive agent based on race, ethnicity, body mass index, or history of preeclampsia as well. However, 24.5% of those taking the once-daily dosage had a history of preeclampsia, compared with 7.2% of those taking the twice-daily dosage (P < .001). Further, the median number of prior pregnancies was two in the twice-daily group versus three in the once-daily group (P = .002).
The authors found no significant difference between the two dosing groups in the need for emergency hypertensive treatment after reaching the study dose or in readmission for blood pressure control. In the twice-daily group, 21.6% of patients needed emergency antihypertensive treatment, compared with 14.3% in the once-daily group (P = .19). Readmission was necessary for 7.2% of the twice-daily group and 6.1% of the once-daily group (P > .99).
A subgroup analysis compared those who started nifedipine antepartum and those who started it post partum, but again, no significant difference in the dosing regimens existed.
Michael Ruma, MD, a maternal-fetal medicine specialist at Perinatal Associates of New Mexico in Albuquerque, was not involved in the study and said he welcomed the results.
“We have too many choices in medicine, so we need to just simplify the plan of attack,” reducing the number of things that clinicians need to think about, Dr. Ruma said in an interview. “A singular dose is always easiest for the patient, always easier for nursing staff, and usually, if you can optimize the dosing, that’s the best approach.”
Annabeth Brewton, MD, a resident at University of Tennessee, Knoxville, agreed, adding that new parents already have a lot going on immediately post partum.
“They’re going to be breastfeeding, they’re not sleeping, they’re going to forget to take that [second] dose,” Dr. Brewton said.
Ms. Band and Dr. Brewton had no disclosures. Dr. Ruma reported consulting and speaking for Hologic and consulting for Philips Ultrasound.
Correction, 5/24/23: An earlier version of this article misstated the daily doses of nifedipine. The study compared a
BALTIMORE – , according to research presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.*
The findings suggest that starting patients on a once-daily 60-mg dose is therefore reasonable, Isabelle Band, BA, a medical student at the Icahn School of Medicine at Mount Sinai, New York, told attendees. Ms. Band said in an interview that there does not appear to be a consensus on the standard of care for nifedipine dosing regimen in this population but that previous in vitro studies have shown increased metabolism of nifedipine in a physiologic state that mimics pregnancy.
“I’ve spoken to some colleagues here who say that they frequently have this debate of which dosing regimen to go with,” Ms. Band said. “I was pleasantly surprised that there was no significant difference between the two dosing regimens because once-daily dosing is less burdensome for patients and will likely improve compliance and convenience for patients.” An additional benefit of once-daily dosing relates to payers because anecdotal reports suggest insurance companies do not tend to approve twice-daily dosing as readily as once-daily dosing, Ms. Band added.
Ms. Band and her colleagues conducted a retrospective chart review of all patients with hypertensive disorders of pregnancy who were admitted to the Mount Sinai Health System between Jan. 1, 2015, and April 30, 2021, and were prescribed nifedipine in a once-daily (60-mg) or twice-daily (two 30-mg) dose. They excluded patients with renal disease and those already taking hypertensives prior to admission.
Among 237 patients who met the criteria, 59% received 60 mg in a twice-daily 30-mg dose, and 41% received 60 mg in a once-daily dose. Among patients requiring an up titration, two-thirds (67%) needed an increase in the nifedipine dose – the most common adjustment – and 20.7% needed both an increase in nifedipine and an additional medication.
The researchers observed no statistically significant differences in the proportion of patients who required a dose increase or an additional antihypertensive in the group taking the twice-daily dose (33.8%) or those receiving the once-daily dose (35.7%). This finding remained statistically insignificant after controlling for gestational diabetes, delivery mode, administration of Lasix, and receipt of emergency antihypertensive treatment (P = .71). The time that passed before patients needed a dose increase was also statistically similar between the groups: 24.3 hours in the twice-daily group and 24 hours in the once-daily group (P = .49).
There were no statistically significant differences in the need for a dose increase or an additional hypertensive agent based on race, ethnicity, body mass index, or history of preeclampsia as well. However, 24.5% of those taking the once-daily dosage had a history of preeclampsia, compared with 7.2% of those taking the twice-daily dosage (P < .001). Further, the median number of prior pregnancies was two in the twice-daily group versus three in the once-daily group (P = .002).
The authors found no significant difference between the two dosing groups in the need for emergency hypertensive treatment after reaching the study dose or in readmission for blood pressure control. In the twice-daily group, 21.6% of patients needed emergency antihypertensive treatment, compared with 14.3% in the once-daily group (P = .19). Readmission was necessary for 7.2% of the twice-daily group and 6.1% of the once-daily group (P > .99).
A subgroup analysis compared those who started nifedipine antepartum and those who started it post partum, but again, no significant difference in the dosing regimens existed.
Michael Ruma, MD, a maternal-fetal medicine specialist at Perinatal Associates of New Mexico in Albuquerque, was not involved in the study and said he welcomed the results.
“We have too many choices in medicine, so we need to just simplify the plan of attack,” reducing the number of things that clinicians need to think about, Dr. Ruma said in an interview. “A singular dose is always easiest for the patient, always easier for nursing staff, and usually, if you can optimize the dosing, that’s the best approach.”
Annabeth Brewton, MD, a resident at University of Tennessee, Knoxville, agreed, adding that new parents already have a lot going on immediately post partum.
“They’re going to be breastfeeding, they’re not sleeping, they’re going to forget to take that [second] dose,” Dr. Brewton said.
Ms. Band and Dr. Brewton had no disclosures. Dr. Ruma reported consulting and speaking for Hologic and consulting for Philips Ultrasound.
Correction, 5/24/23: An earlier version of this article misstated the daily doses of nifedipine. The study compared a
AT ACOG 2023
Marijuana linked to higher PAD risk
But death, intervention rates same
PHOENIX – although there was no greater risk of death from myocardial infarction or other cardiac causes or need for revascularization.
The researchers noted, however, that the study population was young, with an average age of 37.4 years, and that the study period, from 2016 to 2019, predates the legalization of recreational marijuana in a number of states.
Nonetheless, even in this young study population, marijuana users’ risk of developing peripheral artery disease (PAD) was 3.68 times greater (P < .001) than that of nonusers. PAD at a young age could precede worse outcomes later in life, the study authors said.
“Basically, marijuana users were at increased risk of being diagnosed with peripheral artery disease, but there was no increased risk for them requiring any intervention, such as a peripheral vascular intervention, nor were they at increased risk of death from what we found,” said Hirva Vyas, DO, an internal medicine resident at Hackensack University Medical Center in New Jersey, who presented the results at the Society for Cardiovascular Angiography & Interventions annual scientific sessions.
The study used data on 623,768 marijuana users from the National Inpatient Sample, a nationwide database of inpatient visits covered by all public and commercial payers, then extracted a diagnosis for PAD from all 30 million–plus patient encounters to compare PAD rates between marijuana users and nonusers. Marijuana users were more likely to be White and to have elective rather than emergency admissions (P < .001). The researchers used diagnostic codes to identify marijuana users and PAD patients.
Recreational marijuana is legal in 22 states and the District of Columbia, according to ProCon.org. Since 2019, the last year of the study, 11 states have legalized marijuana for recreational use. “It’s a data point that we studied at one point in time, only from 2016 to 2019,” Dr. Vyas said in an interview.
“As we’ve seen over the past 4-5 years, legalization has skyrocketed and recreational use has become more and more favorable not only among younger folks but older folks,” study coauthor Harsh Jain, MD, a second-year internal medicine resident at Montefiore Medical Center in New York, said in the interview. “It would be really refreshing to see how these data change as we look at endpoints from 2019 to 2023.”
Because of the young age of the study population, Dr. Jain said, these findings may not accurately represent the true cardiovascular risks of marijuana use, especially later in life.
“One of the biggest secondary endpoints that we wanted to study was the development of chronic conditions that lead to multiple rehospitalizations, the most significant one of which would be the development of heart failure,” Dr. Jain said. “However, it was difficult to stratify because, again, many of these patients were very young and so they did not carry the diagnosis for heart failure, so we couldn’t complete that subset analysis.”
The goal is to extend the study period out to 2023, Dr. Jain said. “We know that these are very crude and rudimentary data findings that we presented so far, but we’re hoping that the final paper gives us a chance to flesh out all the details of our study and also gives us a chance to expand going forward,” he said.
The findings are in line with other research into the effects of marijuana and cardiovascular disease, said Carl “Chip” Lavie, MD, medical director for cardiac rehabilitation and prevention at the John Ochsner Heart and Vascular Institute in New Orleans who’s published a number of studies on PAD and substance use, including marijuana.
“It is known that cannabis is associated with more vasoconstriction, has sympathomimetic effects, causes endothelial dysfunction and increased platelet aggregation, and is known to increase the risk of acute myocardial infarction, especially in the hour or so after use,” he said in written comments sent to this news organization.
“It is also well known to be a cause of thromboangiitis obliterans, which is in the PAD family,” he added. “Based on these mechanisms, one would expect an increased PAD and, especially, PAD events. The 3.7-fold increased risk is supportive of this increased PAD.”
One study strength, Dr. Lavie pointed out, is that it’s one of the few studies that found an association between marijuana and PAD, which hasn’t been studied as well as other cardiovascular endpoints. “However,” he said, “the limitation is this is just an inpatient sample, and it is all based on coding – e.g., a patient could have PAD and it may not have been coded.”
But death, intervention rates same
But death, intervention rates same
PHOENIX – although there was no greater risk of death from myocardial infarction or other cardiac causes or need for revascularization.
The researchers noted, however, that the study population was young, with an average age of 37.4 years, and that the study period, from 2016 to 2019, predates the legalization of recreational marijuana in a number of states.
Nonetheless, even in this young study population, marijuana users’ risk of developing peripheral artery disease (PAD) was 3.68 times greater (P < .001) than that of nonusers. PAD at a young age could precede worse outcomes later in life, the study authors said.
“Basically, marijuana users were at increased risk of being diagnosed with peripheral artery disease, but there was no increased risk for them requiring any intervention, such as a peripheral vascular intervention, nor were they at increased risk of death from what we found,” said Hirva Vyas, DO, an internal medicine resident at Hackensack University Medical Center in New Jersey, who presented the results at the Society for Cardiovascular Angiography & Interventions annual scientific sessions.
The study used data on 623,768 marijuana users from the National Inpatient Sample, a nationwide database of inpatient visits covered by all public and commercial payers, then extracted a diagnosis for PAD from all 30 million–plus patient encounters to compare PAD rates between marijuana users and nonusers. Marijuana users were more likely to be White and to have elective rather than emergency admissions (P < .001). The researchers used diagnostic codes to identify marijuana users and PAD patients.
Recreational marijuana is legal in 22 states and the District of Columbia, according to ProCon.org. Since 2019, the last year of the study, 11 states have legalized marijuana for recreational use. “It’s a data point that we studied at one point in time, only from 2016 to 2019,” Dr. Vyas said in an interview.
“As we’ve seen over the past 4-5 years, legalization has skyrocketed and recreational use has become more and more favorable not only among younger folks but older folks,” study coauthor Harsh Jain, MD, a second-year internal medicine resident at Montefiore Medical Center in New York, said in the interview. “It would be really refreshing to see how these data change as we look at endpoints from 2019 to 2023.”
Because of the young age of the study population, Dr. Jain said, these findings may not accurately represent the true cardiovascular risks of marijuana use, especially later in life.
“One of the biggest secondary endpoints that we wanted to study was the development of chronic conditions that lead to multiple rehospitalizations, the most significant one of which would be the development of heart failure,” Dr. Jain said. “However, it was difficult to stratify because, again, many of these patients were very young and so they did not carry the diagnosis for heart failure, so we couldn’t complete that subset analysis.”
The goal is to extend the study period out to 2023, Dr. Jain said. “We know that these are very crude and rudimentary data findings that we presented so far, but we’re hoping that the final paper gives us a chance to flesh out all the details of our study and also gives us a chance to expand going forward,” he said.
The findings are in line with other research into the effects of marijuana and cardiovascular disease, said Carl “Chip” Lavie, MD, medical director for cardiac rehabilitation and prevention at the John Ochsner Heart and Vascular Institute in New Orleans who’s published a number of studies on PAD and substance use, including marijuana.
“It is known that cannabis is associated with more vasoconstriction, has sympathomimetic effects, causes endothelial dysfunction and increased platelet aggregation, and is known to increase the risk of acute myocardial infarction, especially in the hour or so after use,” he said in written comments sent to this news organization.
“It is also well known to be a cause of thromboangiitis obliterans, which is in the PAD family,” he added. “Based on these mechanisms, one would expect an increased PAD and, especially, PAD events. The 3.7-fold increased risk is supportive of this increased PAD.”
One study strength, Dr. Lavie pointed out, is that it’s one of the few studies that found an association between marijuana and PAD, which hasn’t been studied as well as other cardiovascular endpoints. “However,” he said, “the limitation is this is just an inpatient sample, and it is all based on coding – e.g., a patient could have PAD and it may not have been coded.”
PHOENIX – although there was no greater risk of death from myocardial infarction or other cardiac causes or need for revascularization.
The researchers noted, however, that the study population was young, with an average age of 37.4 years, and that the study period, from 2016 to 2019, predates the legalization of recreational marijuana in a number of states.
Nonetheless, even in this young study population, marijuana users’ risk of developing peripheral artery disease (PAD) was 3.68 times greater (P < .001) than that of nonusers. PAD at a young age could precede worse outcomes later in life, the study authors said.
“Basically, marijuana users were at increased risk of being diagnosed with peripheral artery disease, but there was no increased risk for them requiring any intervention, such as a peripheral vascular intervention, nor were they at increased risk of death from what we found,” said Hirva Vyas, DO, an internal medicine resident at Hackensack University Medical Center in New Jersey, who presented the results at the Society for Cardiovascular Angiography & Interventions annual scientific sessions.
The study used data on 623,768 marijuana users from the National Inpatient Sample, a nationwide database of inpatient visits covered by all public and commercial payers, then extracted a diagnosis for PAD from all 30 million–plus patient encounters to compare PAD rates between marijuana users and nonusers. Marijuana users were more likely to be White and to have elective rather than emergency admissions (P < .001). The researchers used diagnostic codes to identify marijuana users and PAD patients.
Recreational marijuana is legal in 22 states and the District of Columbia, according to ProCon.org. Since 2019, the last year of the study, 11 states have legalized marijuana for recreational use. “It’s a data point that we studied at one point in time, only from 2016 to 2019,” Dr. Vyas said in an interview.
“As we’ve seen over the past 4-5 years, legalization has skyrocketed and recreational use has become more and more favorable not only among younger folks but older folks,” study coauthor Harsh Jain, MD, a second-year internal medicine resident at Montefiore Medical Center in New York, said in the interview. “It would be really refreshing to see how these data change as we look at endpoints from 2019 to 2023.”
Because of the young age of the study population, Dr. Jain said, these findings may not accurately represent the true cardiovascular risks of marijuana use, especially later in life.
“One of the biggest secondary endpoints that we wanted to study was the development of chronic conditions that lead to multiple rehospitalizations, the most significant one of which would be the development of heart failure,” Dr. Jain said. “However, it was difficult to stratify because, again, many of these patients were very young and so they did not carry the diagnosis for heart failure, so we couldn’t complete that subset analysis.”
The goal is to extend the study period out to 2023, Dr. Jain said. “We know that these are very crude and rudimentary data findings that we presented so far, but we’re hoping that the final paper gives us a chance to flesh out all the details of our study and also gives us a chance to expand going forward,” he said.
The findings are in line with other research into the effects of marijuana and cardiovascular disease, said Carl “Chip” Lavie, MD, medical director for cardiac rehabilitation and prevention at the John Ochsner Heart and Vascular Institute in New Orleans who’s published a number of studies on PAD and substance use, including marijuana.
“It is known that cannabis is associated with more vasoconstriction, has sympathomimetic effects, causes endothelial dysfunction and increased platelet aggregation, and is known to increase the risk of acute myocardial infarction, especially in the hour or so after use,” he said in written comments sent to this news organization.
“It is also well known to be a cause of thromboangiitis obliterans, which is in the PAD family,” he added. “Based on these mechanisms, one would expect an increased PAD and, especially, PAD events. The 3.7-fold increased risk is supportive of this increased PAD.”
One study strength, Dr. Lavie pointed out, is that it’s one of the few studies that found an association between marijuana and PAD, which hasn’t been studied as well as other cardiovascular endpoints. “However,” he said, “the limitation is this is just an inpatient sample, and it is all based on coding – e.g., a patient could have PAD and it may not have been coded.”
AT SCAI 2023
Differences in 30-Day Readmission Rates in Older Adults With Dementia
Study 1 Overview (Park et al)
Objective: To compare rates of adverse events and 30-day readmission among patients with dementia who undergo percutaneous coronary intervention (PCI) with those without dementia.
Design: This cohort study used a national database of hospital readmissions developed by the Agency for Healthcare Research and Quality.
Setting and participants: Data from State Inpatient Databases were used to derive this national readmissions database representing 80% of hospitals from 28 states that contribute data. The study included all individuals aged 18 years and older who were identified to have had a PCI procedure in the years 2017 and 2018. International Classification of Diseases, Tenth Revision (ICD-10) codes were used to identify PCI procedures, including drug-eluting stent placement, bare-metal stent placement, and balloon angioplasty, performed in patients who presented with myocardial infarction and unstable angina and those with stable ischemic heart disease. Patients were stratified into those with or without dementia, also defined using ICD-10 codes. A total of 755,406 index hospitalizations were included; 2.3% of the patients had dementia.
Main outcome measures: The primary study outcome was 30-day all-cause readmission, with the cause classified as cardiovascular or noncardiovascular. Secondary outcome measures examined were delirium, in-hospital mortality, cardiac arrest, blood transfusion, acute kidney injury, fall in hospital, length of hospital stay, and other adverse outcomes. Location at discharge was also examined. Other covariates included in the analysis were age, sex, comorbidities, hospital characteristics, primary payer, and median income. For analysis, a propensity score matching algorithm was applied to match patients with and without dementia. Kaplan-Meier curves were used to examine 30-day readmission rates, and a Cox proportional hazards model was used to calculate hazard ratios (HR) for those with and without dementia. For secondary outcomes, logistic regression models were used to calculate odds ratios (OR) of outcomes between those with and without dementia.
Main results: The average age of those with dementia was 78.8 years vs 64.9 years in those without dementia. Women made up 42.8% of those with dementia and 31.3% of those without dementia. Those with dementia also had higher rates of comorbidities, such as heart failure, renal failure, and depression. After propensity score matching, 17,309 and 17,187 patients with and without dementia, respectively, were included. Covariates were balanced between the 2 groups after matching. For the primary outcome, patients with dementia were more likely to be readmitted at 30 days (HR, 1.11; 95% CI, 1.05-1.18; P < .01) when compared to those without dementia. For other adverse outcomes, delirium was significantly more likely to occur for those with dementia (OR, 4.37; 95% CI, 3.69-5.16; P < .01). Patients with dementia were also more likely to die in hospital (OR, 1.15; 95% CI, 1.01-1.30; P = .03), have cardiac arrest (OR, 1.19; 95% CI, 1.01-1.39; P = .04), receive a blood transfusion (OR, 1.17; 95% CI, 1.00-1.36; P = .05), experience acute kidney injury (OR, 1.30; 95% CI, 1.21-1.39; P < .01), and fall in hospital (OR, 2.51; 95% CI, 2.06-3.07; P < .01). Hospital length of stay was higher for those with dementia, with a mean difference of 1.43 days. For discharge location, patients with dementia were more likely to be sent to a skilled nursing facility (30.1% vs 12.2%) and less likely to be discharged home.
Conclusion: Patients with dementia are more likely to experience adverse events, including delirium, mortality, kidney injury, and falls after PCI, and are more likely to be readmitted to the hospital in 30 days compared to those without dementia.
Study 2 Overview (Gilmore-Bykovskyi et al)
Objective: To examine the association between race and 30-day readmissions in Black and non-Hispanic White Medicare beneficiaries with dementia.
Design: This was a retrospective cohort study that used 100% Medicare fee-for service claims data from all hospitalizations between January 1, 2014, and November 30, 2014, for all enrollees with a dementia diagnosis. The claims data were linked to the patient, hospital stay, and hospital factors. Patients with dementia were identified using a validated algorithm that requires an inpatient, skilled nursing facility, home health, or Part B institutional or noninstitutional claim with a qualifying diagnostic code during a 3-year period. Persons enrolled in a health maintenance organization plan were excluded.
Main outcome measures: The primary outcome examined in this study was 30-day all-cause readmission. Self-reported race and ethnic identity was a baseline covariate. Persons who self-reported Black or non-Hispanic White race were included in the study; other categories of race and ethnicity were excluded because of prior evidence suggesting low accuracy of these categories in Medicare claims data. Other covariates included neighborhood disadvantage, measured using the Area Deprivation Index (ADI), and rurality; hospital-level and hospital stay–level characteristics such as for-profit status and number of annual discharges; and individual demographic characteristics and comorbidities. The ADI is constructed using variables of poverty, education, housing, and employment and is represented as a percentile ranking of level of disadvantage. Unadjusted and adjusted analyses of 30-day hospital readmission were conducted. Models using various levels of adjustment were constructed to examine the contributions of the identified covariates to the estimated association between 30-day readmission and race.
Main results: A total of 1,523,142 index hospital stays among 945,481 beneficiaries were included; 215,815 episodes were among Black beneficiaries and 1,307,327 episodes were among non-Hispanic White beneficiaries. Mean age was 81.5 years, and approximately 61% of beneficiaries were female. Black beneficiaries were younger but had higher rates of dual Medicare/Medicaid eligibility and disability; they were also more likely to reside in disadvantaged neighborhoods. Black beneficiaries had a 30-day readmission rate of 24.1% compared with 18.5% in non-Hispanic White beneficiaries (unadjusted OR, 1.37; 95% CI, 1.35-1.39). The differences in outcomes persisted after adjusting for geographic factors, social factors, hospital characteristics, hospital stay factors, demographics, and comorbidities, suggesting that unmeasured underlying racial disparities not included in this model accounted for the differences. The effects of certain variables, such as neighborhood, differed by race; for example, the protective effect of living in a less disadvantaged neighborhood was observed among White beneficiaries but not Black beneficiaries.
Conclusion: Racial and geographic disparities in 30-day readmission rates were observed among Medicare beneficiaries with dementia. Protective effects associated with neighborhood advantage may confer different levels of benefit for people of different race.
Commentary
Adults living with dementia are at higher risk of adverse outcomes across settings. In the first study, by Park et al, among adults who underwent a cardiac procedure (PCI), those with dementia were more likely to experience adverse events compared to those without dementia. These outcomes include increased rates of 30-day readmissions, delirium, cardiac arrest, and falls. These findings are consistent with other studies that found a similar association among patients who underwent other cardiac procedures, such as transcatheter aortic valve replacement.1 Because dementia is a strong predisposing factor for delirium, it is not surprising that delirium is observed across patients who underwent different procedures or hospitalization episodes.2 Because of the potential hazards for inpatients with dementia, hospitals have developed risk-reduction programs, such as those that promote recognition of dementia, and management strategies that reduce the risk of delirium.3 Delirium prevention may also impact other adverse outcomes, such as falls, discharge to institutional care, and readmissions.
Racial disparities in care outcomes have been documented across settings, including hospital4 and hospice care settings.5 In study 2, by Gilmore-Bykovskyi et al, the findings of higher rates of hospital readmission among Black patients when compared to non-Hispanic White patients were not surprising. The central finding of this study is that even when accounting for various levels of factors, including hospital-level, hospital stay–level, individual (demographics, comorbidities), and neighborhood characteristics (disadvantage), the observed disparity diminished but persisted, suggesting that while these various levels of factors contributed to the observed disparity, other unmeasured factors also contributed. Another key finding is that the effect of the various factors examined in this study may affect different subgroups in different ways, suggesting underlying factors, and thus potential solutions to reduce disparities in care outcomes, could differ among subgroups.
Applications for Clinical Practice and System Implementation
These 2 studies add to the literature on factors that can affect 30-day hospital readmission rates in patients with dementia. These data could allow for more robust discussions of what to anticipate when adults with dementia undergo specific procedures, and also further build the case that improvements in care, such as delirium prevention programs, could offer benefits. The observation about racial and ethnic disparities in care outcomes among patients with dementia highlights the continued need to better understand the drivers of these disparities so that hospital systems and policy makers can consider and test possible solutions. Future studies should further disentangle the relationships among the various levels of factors and observed disparities in outcomes, especially for this vulnerable population of adults living with dementia.
Practice Points
- Clinicians should be aware of the additional risks for poor outcomes that dementia confers.
- Awareness of this increased risk will inform discussions of risks and benefits for older adults considered for procedures.
–William W. Hung, MD, MPH
1. Park DY, Sana MK, Shoura S, et al. Readmission and in-hospital outcomes after transcatheter aortic valve replacement in patients with dementia. Cardiovasc Revasc Med. 2023;46:70-77. doi:10.1016/j.carrev.2022.08.016
2. McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc. 2003;51(5):591-598. doi:10.1034/j.1600-0579.2003.00201.x
3. Weldingh NM, Mellingsæter MR, Hegna BW, et al. Impact of a dementia-friendly program on detection and management of patients with cognitive impairment and delirium in acute-care hospital units: a controlled clinical trial design. BMC Geriatr. 2022;22(1):266. doi:10.1186/s12877-022-02949-0
4. Hermosura AH, Noonan CJ, Fyfe-Johnson AL, et al. Hospital disparities between native Hawaiian and other pacific islanders and non-Hispanic whites with Alzheimer’s disease and related dementias. J Aging Health. 2020;32(10):1579-1590. doi:10.1177/0898264320945177
5. Zhang Y, Shao H, Zhang M, Li J. Healthcare utilization and mortality after hospice live discharge among Medicare patients with and without Alzheimer’s disease and related dementias. J Gen Intern Med. 2023 Jan 17. doi:10.1007/s11606-023-08031-8
Study 1 Overview (Park et al)
Objective: To compare rates of adverse events and 30-day readmission among patients with dementia who undergo percutaneous coronary intervention (PCI) with those without dementia.
Design: This cohort study used a national database of hospital readmissions developed by the Agency for Healthcare Research and Quality.
Setting and participants: Data from State Inpatient Databases were used to derive this national readmissions database representing 80% of hospitals from 28 states that contribute data. The study included all individuals aged 18 years and older who were identified to have had a PCI procedure in the years 2017 and 2018. International Classification of Diseases, Tenth Revision (ICD-10) codes were used to identify PCI procedures, including drug-eluting stent placement, bare-metal stent placement, and balloon angioplasty, performed in patients who presented with myocardial infarction and unstable angina and those with stable ischemic heart disease. Patients were stratified into those with or without dementia, also defined using ICD-10 codes. A total of 755,406 index hospitalizations were included; 2.3% of the patients had dementia.
Main outcome measures: The primary study outcome was 30-day all-cause readmission, with the cause classified as cardiovascular or noncardiovascular. Secondary outcome measures examined were delirium, in-hospital mortality, cardiac arrest, blood transfusion, acute kidney injury, fall in hospital, length of hospital stay, and other adverse outcomes. Location at discharge was also examined. Other covariates included in the analysis were age, sex, comorbidities, hospital characteristics, primary payer, and median income. For analysis, a propensity score matching algorithm was applied to match patients with and without dementia. Kaplan-Meier curves were used to examine 30-day readmission rates, and a Cox proportional hazards model was used to calculate hazard ratios (HR) for those with and without dementia. For secondary outcomes, logistic regression models were used to calculate odds ratios (OR) of outcomes between those with and without dementia.
Main results: The average age of those with dementia was 78.8 years vs 64.9 years in those without dementia. Women made up 42.8% of those with dementia and 31.3% of those without dementia. Those with dementia also had higher rates of comorbidities, such as heart failure, renal failure, and depression. After propensity score matching, 17,309 and 17,187 patients with and without dementia, respectively, were included. Covariates were balanced between the 2 groups after matching. For the primary outcome, patients with dementia were more likely to be readmitted at 30 days (HR, 1.11; 95% CI, 1.05-1.18; P < .01) when compared to those without dementia. For other adverse outcomes, delirium was significantly more likely to occur for those with dementia (OR, 4.37; 95% CI, 3.69-5.16; P < .01). Patients with dementia were also more likely to die in hospital (OR, 1.15; 95% CI, 1.01-1.30; P = .03), have cardiac arrest (OR, 1.19; 95% CI, 1.01-1.39; P = .04), receive a blood transfusion (OR, 1.17; 95% CI, 1.00-1.36; P = .05), experience acute kidney injury (OR, 1.30; 95% CI, 1.21-1.39; P < .01), and fall in hospital (OR, 2.51; 95% CI, 2.06-3.07; P < .01). Hospital length of stay was higher for those with dementia, with a mean difference of 1.43 days. For discharge location, patients with dementia were more likely to be sent to a skilled nursing facility (30.1% vs 12.2%) and less likely to be discharged home.
Conclusion: Patients with dementia are more likely to experience adverse events, including delirium, mortality, kidney injury, and falls after PCI, and are more likely to be readmitted to the hospital in 30 days compared to those without dementia.
Study 2 Overview (Gilmore-Bykovskyi et al)
Objective: To examine the association between race and 30-day readmissions in Black and non-Hispanic White Medicare beneficiaries with dementia.
Design: This was a retrospective cohort study that used 100% Medicare fee-for service claims data from all hospitalizations between January 1, 2014, and November 30, 2014, for all enrollees with a dementia diagnosis. The claims data were linked to the patient, hospital stay, and hospital factors. Patients with dementia were identified using a validated algorithm that requires an inpatient, skilled nursing facility, home health, or Part B institutional or noninstitutional claim with a qualifying diagnostic code during a 3-year period. Persons enrolled in a health maintenance organization plan were excluded.
Main outcome measures: The primary outcome examined in this study was 30-day all-cause readmission. Self-reported race and ethnic identity was a baseline covariate. Persons who self-reported Black or non-Hispanic White race were included in the study; other categories of race and ethnicity were excluded because of prior evidence suggesting low accuracy of these categories in Medicare claims data. Other covariates included neighborhood disadvantage, measured using the Area Deprivation Index (ADI), and rurality; hospital-level and hospital stay–level characteristics such as for-profit status and number of annual discharges; and individual demographic characteristics and comorbidities. The ADI is constructed using variables of poverty, education, housing, and employment and is represented as a percentile ranking of level of disadvantage. Unadjusted and adjusted analyses of 30-day hospital readmission were conducted. Models using various levels of adjustment were constructed to examine the contributions of the identified covariates to the estimated association between 30-day readmission and race.
Main results: A total of 1,523,142 index hospital stays among 945,481 beneficiaries were included; 215,815 episodes were among Black beneficiaries and 1,307,327 episodes were among non-Hispanic White beneficiaries. Mean age was 81.5 years, and approximately 61% of beneficiaries were female. Black beneficiaries were younger but had higher rates of dual Medicare/Medicaid eligibility and disability; they were also more likely to reside in disadvantaged neighborhoods. Black beneficiaries had a 30-day readmission rate of 24.1% compared with 18.5% in non-Hispanic White beneficiaries (unadjusted OR, 1.37; 95% CI, 1.35-1.39). The differences in outcomes persisted after adjusting for geographic factors, social factors, hospital characteristics, hospital stay factors, demographics, and comorbidities, suggesting that unmeasured underlying racial disparities not included in this model accounted for the differences. The effects of certain variables, such as neighborhood, differed by race; for example, the protective effect of living in a less disadvantaged neighborhood was observed among White beneficiaries but not Black beneficiaries.
Conclusion: Racial and geographic disparities in 30-day readmission rates were observed among Medicare beneficiaries with dementia. Protective effects associated with neighborhood advantage may confer different levels of benefit for people of different race.
Commentary
Adults living with dementia are at higher risk of adverse outcomes across settings. In the first study, by Park et al, among adults who underwent a cardiac procedure (PCI), those with dementia were more likely to experience adverse events compared to those without dementia. These outcomes include increased rates of 30-day readmissions, delirium, cardiac arrest, and falls. These findings are consistent with other studies that found a similar association among patients who underwent other cardiac procedures, such as transcatheter aortic valve replacement.1 Because dementia is a strong predisposing factor for delirium, it is not surprising that delirium is observed across patients who underwent different procedures or hospitalization episodes.2 Because of the potential hazards for inpatients with dementia, hospitals have developed risk-reduction programs, such as those that promote recognition of dementia, and management strategies that reduce the risk of delirium.3 Delirium prevention may also impact other adverse outcomes, such as falls, discharge to institutional care, and readmissions.
Racial disparities in care outcomes have been documented across settings, including hospital4 and hospice care settings.5 In study 2, by Gilmore-Bykovskyi et al, the findings of higher rates of hospital readmission among Black patients when compared to non-Hispanic White patients were not surprising. The central finding of this study is that even when accounting for various levels of factors, including hospital-level, hospital stay–level, individual (demographics, comorbidities), and neighborhood characteristics (disadvantage), the observed disparity diminished but persisted, suggesting that while these various levels of factors contributed to the observed disparity, other unmeasured factors also contributed. Another key finding is that the effect of the various factors examined in this study may affect different subgroups in different ways, suggesting underlying factors, and thus potential solutions to reduce disparities in care outcomes, could differ among subgroups.
Applications for Clinical Practice and System Implementation
These 2 studies add to the literature on factors that can affect 30-day hospital readmission rates in patients with dementia. These data could allow for more robust discussions of what to anticipate when adults with dementia undergo specific procedures, and also further build the case that improvements in care, such as delirium prevention programs, could offer benefits. The observation about racial and ethnic disparities in care outcomes among patients with dementia highlights the continued need to better understand the drivers of these disparities so that hospital systems and policy makers can consider and test possible solutions. Future studies should further disentangle the relationships among the various levels of factors and observed disparities in outcomes, especially for this vulnerable population of adults living with dementia.
Practice Points
- Clinicians should be aware of the additional risks for poor outcomes that dementia confers.
- Awareness of this increased risk will inform discussions of risks and benefits for older adults considered for procedures.
–William W. Hung, MD, MPH
Study 1 Overview (Park et al)
Objective: To compare rates of adverse events and 30-day readmission among patients with dementia who undergo percutaneous coronary intervention (PCI) with those without dementia.
Design: This cohort study used a national database of hospital readmissions developed by the Agency for Healthcare Research and Quality.
Setting and participants: Data from State Inpatient Databases were used to derive this national readmissions database representing 80% of hospitals from 28 states that contribute data. The study included all individuals aged 18 years and older who were identified to have had a PCI procedure in the years 2017 and 2018. International Classification of Diseases, Tenth Revision (ICD-10) codes were used to identify PCI procedures, including drug-eluting stent placement, bare-metal stent placement, and balloon angioplasty, performed in patients who presented with myocardial infarction and unstable angina and those with stable ischemic heart disease. Patients were stratified into those with or without dementia, also defined using ICD-10 codes. A total of 755,406 index hospitalizations were included; 2.3% of the patients had dementia.
Main outcome measures: The primary study outcome was 30-day all-cause readmission, with the cause classified as cardiovascular or noncardiovascular. Secondary outcome measures examined were delirium, in-hospital mortality, cardiac arrest, blood transfusion, acute kidney injury, fall in hospital, length of hospital stay, and other adverse outcomes. Location at discharge was also examined. Other covariates included in the analysis were age, sex, comorbidities, hospital characteristics, primary payer, and median income. For analysis, a propensity score matching algorithm was applied to match patients with and without dementia. Kaplan-Meier curves were used to examine 30-day readmission rates, and a Cox proportional hazards model was used to calculate hazard ratios (HR) for those with and without dementia. For secondary outcomes, logistic regression models were used to calculate odds ratios (OR) of outcomes between those with and without dementia.
Main results: The average age of those with dementia was 78.8 years vs 64.9 years in those without dementia. Women made up 42.8% of those with dementia and 31.3% of those without dementia. Those with dementia also had higher rates of comorbidities, such as heart failure, renal failure, and depression. After propensity score matching, 17,309 and 17,187 patients with and without dementia, respectively, were included. Covariates were balanced between the 2 groups after matching. For the primary outcome, patients with dementia were more likely to be readmitted at 30 days (HR, 1.11; 95% CI, 1.05-1.18; P < .01) when compared to those without dementia. For other adverse outcomes, delirium was significantly more likely to occur for those with dementia (OR, 4.37; 95% CI, 3.69-5.16; P < .01). Patients with dementia were also more likely to die in hospital (OR, 1.15; 95% CI, 1.01-1.30; P = .03), have cardiac arrest (OR, 1.19; 95% CI, 1.01-1.39; P = .04), receive a blood transfusion (OR, 1.17; 95% CI, 1.00-1.36; P = .05), experience acute kidney injury (OR, 1.30; 95% CI, 1.21-1.39; P < .01), and fall in hospital (OR, 2.51; 95% CI, 2.06-3.07; P < .01). Hospital length of stay was higher for those with dementia, with a mean difference of 1.43 days. For discharge location, patients with dementia were more likely to be sent to a skilled nursing facility (30.1% vs 12.2%) and less likely to be discharged home.
Conclusion: Patients with dementia are more likely to experience adverse events, including delirium, mortality, kidney injury, and falls after PCI, and are more likely to be readmitted to the hospital in 30 days compared to those without dementia.
Study 2 Overview (Gilmore-Bykovskyi et al)
Objective: To examine the association between race and 30-day readmissions in Black and non-Hispanic White Medicare beneficiaries with dementia.
Design: This was a retrospective cohort study that used 100% Medicare fee-for service claims data from all hospitalizations between January 1, 2014, and November 30, 2014, for all enrollees with a dementia diagnosis. The claims data were linked to the patient, hospital stay, and hospital factors. Patients with dementia were identified using a validated algorithm that requires an inpatient, skilled nursing facility, home health, or Part B institutional or noninstitutional claim with a qualifying diagnostic code during a 3-year period. Persons enrolled in a health maintenance organization plan were excluded.
Main outcome measures: The primary outcome examined in this study was 30-day all-cause readmission. Self-reported race and ethnic identity was a baseline covariate. Persons who self-reported Black or non-Hispanic White race were included in the study; other categories of race and ethnicity were excluded because of prior evidence suggesting low accuracy of these categories in Medicare claims data. Other covariates included neighborhood disadvantage, measured using the Area Deprivation Index (ADI), and rurality; hospital-level and hospital stay–level characteristics such as for-profit status and number of annual discharges; and individual demographic characteristics and comorbidities. The ADI is constructed using variables of poverty, education, housing, and employment and is represented as a percentile ranking of level of disadvantage. Unadjusted and adjusted analyses of 30-day hospital readmission were conducted. Models using various levels of adjustment were constructed to examine the contributions of the identified covariates to the estimated association between 30-day readmission and race.
Main results: A total of 1,523,142 index hospital stays among 945,481 beneficiaries were included; 215,815 episodes were among Black beneficiaries and 1,307,327 episodes were among non-Hispanic White beneficiaries. Mean age was 81.5 years, and approximately 61% of beneficiaries were female. Black beneficiaries were younger but had higher rates of dual Medicare/Medicaid eligibility and disability; they were also more likely to reside in disadvantaged neighborhoods. Black beneficiaries had a 30-day readmission rate of 24.1% compared with 18.5% in non-Hispanic White beneficiaries (unadjusted OR, 1.37; 95% CI, 1.35-1.39). The differences in outcomes persisted after adjusting for geographic factors, social factors, hospital characteristics, hospital stay factors, demographics, and comorbidities, suggesting that unmeasured underlying racial disparities not included in this model accounted for the differences. The effects of certain variables, such as neighborhood, differed by race; for example, the protective effect of living in a less disadvantaged neighborhood was observed among White beneficiaries but not Black beneficiaries.
Conclusion: Racial and geographic disparities in 30-day readmission rates were observed among Medicare beneficiaries with dementia. Protective effects associated with neighborhood advantage may confer different levels of benefit for people of different race.
Commentary
Adults living with dementia are at higher risk of adverse outcomes across settings. In the first study, by Park et al, among adults who underwent a cardiac procedure (PCI), those with dementia were more likely to experience adverse events compared to those without dementia. These outcomes include increased rates of 30-day readmissions, delirium, cardiac arrest, and falls. These findings are consistent with other studies that found a similar association among patients who underwent other cardiac procedures, such as transcatheter aortic valve replacement.1 Because dementia is a strong predisposing factor for delirium, it is not surprising that delirium is observed across patients who underwent different procedures or hospitalization episodes.2 Because of the potential hazards for inpatients with dementia, hospitals have developed risk-reduction programs, such as those that promote recognition of dementia, and management strategies that reduce the risk of delirium.3 Delirium prevention may also impact other adverse outcomes, such as falls, discharge to institutional care, and readmissions.
Racial disparities in care outcomes have been documented across settings, including hospital4 and hospice care settings.5 In study 2, by Gilmore-Bykovskyi et al, the findings of higher rates of hospital readmission among Black patients when compared to non-Hispanic White patients were not surprising. The central finding of this study is that even when accounting for various levels of factors, including hospital-level, hospital stay–level, individual (demographics, comorbidities), and neighborhood characteristics (disadvantage), the observed disparity diminished but persisted, suggesting that while these various levels of factors contributed to the observed disparity, other unmeasured factors also contributed. Another key finding is that the effect of the various factors examined in this study may affect different subgroups in different ways, suggesting underlying factors, and thus potential solutions to reduce disparities in care outcomes, could differ among subgroups.
Applications for Clinical Practice and System Implementation
These 2 studies add to the literature on factors that can affect 30-day hospital readmission rates in patients with dementia. These data could allow for more robust discussions of what to anticipate when adults with dementia undergo specific procedures, and also further build the case that improvements in care, such as delirium prevention programs, could offer benefits. The observation about racial and ethnic disparities in care outcomes among patients with dementia highlights the continued need to better understand the drivers of these disparities so that hospital systems and policy makers can consider and test possible solutions. Future studies should further disentangle the relationships among the various levels of factors and observed disparities in outcomes, especially for this vulnerable population of adults living with dementia.
Practice Points
- Clinicians should be aware of the additional risks for poor outcomes that dementia confers.
- Awareness of this increased risk will inform discussions of risks and benefits for older adults considered for procedures.
–William W. Hung, MD, MPH
1. Park DY, Sana MK, Shoura S, et al. Readmission and in-hospital outcomes after transcatheter aortic valve replacement in patients with dementia. Cardiovasc Revasc Med. 2023;46:70-77. doi:10.1016/j.carrev.2022.08.016
2. McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc. 2003;51(5):591-598. doi:10.1034/j.1600-0579.2003.00201.x
3. Weldingh NM, Mellingsæter MR, Hegna BW, et al. Impact of a dementia-friendly program on detection and management of patients with cognitive impairment and delirium in acute-care hospital units: a controlled clinical trial design. BMC Geriatr. 2022;22(1):266. doi:10.1186/s12877-022-02949-0
4. Hermosura AH, Noonan CJ, Fyfe-Johnson AL, et al. Hospital disparities between native Hawaiian and other pacific islanders and non-Hispanic whites with Alzheimer’s disease and related dementias. J Aging Health. 2020;32(10):1579-1590. doi:10.1177/0898264320945177
5. Zhang Y, Shao H, Zhang M, Li J. Healthcare utilization and mortality after hospice live discharge among Medicare patients with and without Alzheimer’s disease and related dementias. J Gen Intern Med. 2023 Jan 17. doi:10.1007/s11606-023-08031-8
1. Park DY, Sana MK, Shoura S, et al. Readmission and in-hospital outcomes after transcatheter aortic valve replacement in patients with dementia. Cardiovasc Revasc Med. 2023;46:70-77. doi:10.1016/j.carrev.2022.08.016
2. McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc. 2003;51(5):591-598. doi:10.1034/j.1600-0579.2003.00201.x
3. Weldingh NM, Mellingsæter MR, Hegna BW, et al. Impact of a dementia-friendly program on detection and management of patients with cognitive impairment and delirium in acute-care hospital units: a controlled clinical trial design. BMC Geriatr. 2022;22(1):266. doi:10.1186/s12877-022-02949-0
4. Hermosura AH, Noonan CJ, Fyfe-Johnson AL, et al. Hospital disparities between native Hawaiian and other pacific islanders and non-Hispanic whites with Alzheimer’s disease and related dementias. J Aging Health. 2020;32(10):1579-1590. doi:10.1177/0898264320945177
5. Zhang Y, Shao H, Zhang M, Li J. Healthcare utilization and mortality after hospice live discharge among Medicare patients with and without Alzheimer’s disease and related dementias. J Gen Intern Med. 2023 Jan 17. doi:10.1007/s11606-023-08031-8
HFpEF: New guidelines are pertinent for primary care
This transcript has been edited for clarity.
I’m Dr. Neil Skolnik. The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.
We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.
I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.
When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).
Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.
For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.
Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.
Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.
To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.
Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.
After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.
Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.
In summary:
- Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
- Initially evaluate with an NT-proBNP level and an echocardiogram.
- First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.
This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
I’m Dr. Neil Skolnik. The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.
We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.
I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.
When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).
Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.
For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.
Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.
Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.
To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.
Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.
After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.
Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.
In summary:
- Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
- Initially evaluate with an NT-proBNP level and an echocardiogram.
- First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.
This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
I’m Dr. Neil Skolnik. The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.
We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.
I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.
When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).
Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.
For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.
Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.
Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.
To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.
Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.
After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.
Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.
In summary:
- Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
- Initially evaluate with an NT-proBNP level and an echocardiogram.
- First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.
This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.
A version of this article first appeared on Medscape.com.
AHA urges action against racial inequities in stroke care
Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.
including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.
“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.
The scientific statement was published online in the journal Stroke.
It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.
Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.
They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.
For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.
However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.
In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.
“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.
Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.
“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.
“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.
Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”
The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.
The research had no commercial funding.
A version of this article first appeared on Medscape.com.
Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.
including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.
“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.
The scientific statement was published online in the journal Stroke.
It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.
Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.
They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.
For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.
However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.
In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.
“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.
Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.
“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.
“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.
Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”
The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.
The research had no commercial funding.
A version of this article first appeared on Medscape.com.
Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.
including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.
“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.
The scientific statement was published online in the journal Stroke.
It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.
Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.
They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.
For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.
However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.
In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.
“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.
Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.
“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.
“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.
Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”
The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.
The research had no commercial funding.
A version of this article first appeared on Medscape.com.
FROM STROKE
Gestational HTN, preeclampsia worsen long-term risk for ischemic, nonischemic heart failure
, an observational study suggests.
The risks were most pronounced, jumping more than sixfold in the case of ischemic HF, during the first 6 years after the pregnancy. They then receded to plateau at a lower, still significantly elevated level of risk that persisted even years later, in the analysis of women in a Swedish medical birth registry.
The case-matching study compared women with no history of cardiovascular (CV) disease and a first successful pregnancy during which they either developed or did not experience gestational hypertension or preeclampsia.
It’s among the first studies to explore the impact of pregnancy-induced hypertensive disease on subsequent HF risk separately for both ischemic and nonischemic HF and to find that the severity of such risk differs for the two HF etiologies, according to a report published in JACC: Heart Failure.
The adjusted risk for any HF during a median of 13 years after the pregnancy rose 70% for those who had developed gestational hypertension or preeclampsia. Their risk of nonischemic HF went up 60%, and their risk of ischemic HF more than doubled.
Hypertensive disorders of pregnancy “are so much more than short-term disorders confined to the pregnancy period. They have long-term implications throughout a lifetime,” lead author Ängla Mantel, MD, PhD, said in an interview.
Obstetric history doesn’t figure into any formal HF risk scoring systems, observed Dr. Mantel of Karolinska Institutet, Stockholm. Still, women who develop gestational hypertension, preeclampsia, or other pregnancy complications “should be considered a high-risk population even after the pregnancy and monitored for cardiovascular risk factors regularly throughout life.”
In many studies, she said, “knowledge of women-specific risk factors for cardiovascular disease is poor among both clinicians and patients.” The current findings should help raise awareness about such obstetric risk factors for HF, “especially” in patients with HF with preserved ejection fraction (HFpEF), which isn’t closely related to a number of traditional CV risk factors.
Even though pregnancy complications such as gestational hypertension and preeclampsia don’t feature in risk calculators, “they are actually risk enhancers per the 2019 primary prevention guidelines,” Natalie A. Bello, MD, MPH, who was not involved in the current study, said in an interview.
“We’re working to educate physicians and cardiovascular team members to take a pregnancy history” for risk stratification of women in primary prevention,” said Dr. Bello, director of hypertension research at the Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.
The current study, she said, “is an important step” for its finding that hypertensive disorders of pregnancy are associated separately with both ischemic and nonischemic HF.
She pointed out, however, that because the study excluded women with peripartum cardiomyopathy, a form of nonischemic HF, it may “underestimate the impact of hypertensive disorders on the short-term risk of nonischemic heart failure.” Women who had peripartum cardiomyopathy were excluded to avoid misclassification of other HF outcomes, the authors stated.
Also, Dr. Bello said, the study’s inclusion of patients with either gestational hypertension or preeclampsia may complicate its interpretation. Compared with the former condition, she said, preeclampsia “involves more inflammation and more endothelial dysfunction. It may cause a different impact on the heart and the vasculature.”
In the analysis, about 79,000 women with gestational hypertension or preeclampsia were identified among more than 1.4 million primiparous women who entered the Swedish Medical Birth Register over a period of about 30 years. They were matched with about 396,000 women in the registry who had normotensive pregnancies.
Excluded, besides women with peripartum cardiomyopathy, were women with a prepregnancy history of HF, hypertension, ischemic heart disease, atrial fibrillation, or valvular heart disease.
Hazard ratios (HRs) for HF, ischemic HF, and nonischemic HF were significantly elevated over among the women with gestational hypertension or preeclampsia compared to those with normotensive pregnancies:
- Any HF: HR, 1.70 (95% confidence interval [CI], 1.51-1.91)
- Nonischemic HF: HR, 1.60 (95% CI, 1.40-1.83)
- Ischemic HF: HR, 2.28 (95% CI, 1.74-2.98)
The analyses were adjusted for maternal age at delivery, year of delivery, prepregnancy comorbidities, maternal education level, smoking status, and body mass index.
Sharper risk increases were seen among women with gestational hypertension or preeclampsia who delivered prior to gestational week 34:
- Any HF: HR, 2.46 (95% CI, 1.82-3.32)
- Nonischemic HF: HR, 2.33 (95% CI, 1.65-3.31)
- Ischemic HF: HR, 3.64 (95% CI, 1.97-6.74)
Risks for HF developing within 6 years of pregnancy characterized by gestational hypertension or preeclampsia were far more pronounced for ischemic HF than for nonischemic HF:
- Any HF: HR, 2.09 (95% CI, 1.52-2.89)
- Nonischemic HF: HR, 1.86 (95% CI, 1.32-2.61)
- Ischemic HF: HR, 6.52 (95% CI, 2.00-12.34).
The study couldn’t directly explore potential mechanisms for the associations between pregnancy-induced hypertensive disorders and different forms of HF, but it may have provided clues, Dr. Mantel said.
The hypertensive disorders and ischemic HF appear to share risk factors that could lead to both conditions, she noted. Also, hypertension itself is a risk factor for ischemic heart disease.
In contrast, “the risk of nonischemic heart failure might be driven by other factors, such as the inflammatory profile, endothelial dysfunction, and cardiac remodeling induced by preeclampsia or gestational hypertension.”
Those disorders, moreover, are associated with cardiac structural changes that are also seen in HFpEF, Dr. Mantel said. And both HFpEF and preeclampsia are characterized by systemic inflammation and endothelial dysfunction.
“These pathophysiological similarities,” she proposed, “might explain the link between pregnancy-induced hypertensive disorder and HFpEF.”
The authors have disclosed no relevant financial relationships. Dr. Bello has received grants from the National Institutes of Health.
A version of this article first appeared on Medscape.com.
, an observational study suggests.
The risks were most pronounced, jumping more than sixfold in the case of ischemic HF, during the first 6 years after the pregnancy. They then receded to plateau at a lower, still significantly elevated level of risk that persisted even years later, in the analysis of women in a Swedish medical birth registry.
The case-matching study compared women with no history of cardiovascular (CV) disease and a first successful pregnancy during which they either developed or did not experience gestational hypertension or preeclampsia.
It’s among the first studies to explore the impact of pregnancy-induced hypertensive disease on subsequent HF risk separately for both ischemic and nonischemic HF and to find that the severity of such risk differs for the two HF etiologies, according to a report published in JACC: Heart Failure.
The adjusted risk for any HF during a median of 13 years after the pregnancy rose 70% for those who had developed gestational hypertension or preeclampsia. Their risk of nonischemic HF went up 60%, and their risk of ischemic HF more than doubled.
Hypertensive disorders of pregnancy “are so much more than short-term disorders confined to the pregnancy period. They have long-term implications throughout a lifetime,” lead author Ängla Mantel, MD, PhD, said in an interview.
Obstetric history doesn’t figure into any formal HF risk scoring systems, observed Dr. Mantel of Karolinska Institutet, Stockholm. Still, women who develop gestational hypertension, preeclampsia, or other pregnancy complications “should be considered a high-risk population even after the pregnancy and monitored for cardiovascular risk factors regularly throughout life.”
In many studies, she said, “knowledge of women-specific risk factors for cardiovascular disease is poor among both clinicians and patients.” The current findings should help raise awareness about such obstetric risk factors for HF, “especially” in patients with HF with preserved ejection fraction (HFpEF), which isn’t closely related to a number of traditional CV risk factors.
Even though pregnancy complications such as gestational hypertension and preeclampsia don’t feature in risk calculators, “they are actually risk enhancers per the 2019 primary prevention guidelines,” Natalie A. Bello, MD, MPH, who was not involved in the current study, said in an interview.
“We’re working to educate physicians and cardiovascular team members to take a pregnancy history” for risk stratification of women in primary prevention,” said Dr. Bello, director of hypertension research at the Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.
The current study, she said, “is an important step” for its finding that hypertensive disorders of pregnancy are associated separately with both ischemic and nonischemic HF.
She pointed out, however, that because the study excluded women with peripartum cardiomyopathy, a form of nonischemic HF, it may “underestimate the impact of hypertensive disorders on the short-term risk of nonischemic heart failure.” Women who had peripartum cardiomyopathy were excluded to avoid misclassification of other HF outcomes, the authors stated.
Also, Dr. Bello said, the study’s inclusion of patients with either gestational hypertension or preeclampsia may complicate its interpretation. Compared with the former condition, she said, preeclampsia “involves more inflammation and more endothelial dysfunction. It may cause a different impact on the heart and the vasculature.”
In the analysis, about 79,000 women with gestational hypertension or preeclampsia were identified among more than 1.4 million primiparous women who entered the Swedish Medical Birth Register over a period of about 30 years. They were matched with about 396,000 women in the registry who had normotensive pregnancies.
Excluded, besides women with peripartum cardiomyopathy, were women with a prepregnancy history of HF, hypertension, ischemic heart disease, atrial fibrillation, or valvular heart disease.
Hazard ratios (HRs) for HF, ischemic HF, and nonischemic HF were significantly elevated over among the women with gestational hypertension or preeclampsia compared to those with normotensive pregnancies:
- Any HF: HR, 1.70 (95% confidence interval [CI], 1.51-1.91)
- Nonischemic HF: HR, 1.60 (95% CI, 1.40-1.83)
- Ischemic HF: HR, 2.28 (95% CI, 1.74-2.98)
The analyses were adjusted for maternal age at delivery, year of delivery, prepregnancy comorbidities, maternal education level, smoking status, and body mass index.
Sharper risk increases were seen among women with gestational hypertension or preeclampsia who delivered prior to gestational week 34:
- Any HF: HR, 2.46 (95% CI, 1.82-3.32)
- Nonischemic HF: HR, 2.33 (95% CI, 1.65-3.31)
- Ischemic HF: HR, 3.64 (95% CI, 1.97-6.74)
Risks for HF developing within 6 years of pregnancy characterized by gestational hypertension or preeclampsia were far more pronounced for ischemic HF than for nonischemic HF:
- Any HF: HR, 2.09 (95% CI, 1.52-2.89)
- Nonischemic HF: HR, 1.86 (95% CI, 1.32-2.61)
- Ischemic HF: HR, 6.52 (95% CI, 2.00-12.34).
The study couldn’t directly explore potential mechanisms for the associations between pregnancy-induced hypertensive disorders and different forms of HF, but it may have provided clues, Dr. Mantel said.
The hypertensive disorders and ischemic HF appear to share risk factors that could lead to both conditions, she noted. Also, hypertension itself is a risk factor for ischemic heart disease.
In contrast, “the risk of nonischemic heart failure might be driven by other factors, such as the inflammatory profile, endothelial dysfunction, and cardiac remodeling induced by preeclampsia or gestational hypertension.”
Those disorders, moreover, are associated with cardiac structural changes that are also seen in HFpEF, Dr. Mantel said. And both HFpEF and preeclampsia are characterized by systemic inflammation and endothelial dysfunction.
“These pathophysiological similarities,” she proposed, “might explain the link between pregnancy-induced hypertensive disorder and HFpEF.”
The authors have disclosed no relevant financial relationships. Dr. Bello has received grants from the National Institutes of Health.
A version of this article first appeared on Medscape.com.
, an observational study suggests.
The risks were most pronounced, jumping more than sixfold in the case of ischemic HF, during the first 6 years after the pregnancy. They then receded to plateau at a lower, still significantly elevated level of risk that persisted even years later, in the analysis of women in a Swedish medical birth registry.
The case-matching study compared women with no history of cardiovascular (CV) disease and a first successful pregnancy during which they either developed or did not experience gestational hypertension or preeclampsia.
It’s among the first studies to explore the impact of pregnancy-induced hypertensive disease on subsequent HF risk separately for both ischemic and nonischemic HF and to find that the severity of such risk differs for the two HF etiologies, according to a report published in JACC: Heart Failure.
The adjusted risk for any HF during a median of 13 years after the pregnancy rose 70% for those who had developed gestational hypertension or preeclampsia. Their risk of nonischemic HF went up 60%, and their risk of ischemic HF more than doubled.
Hypertensive disorders of pregnancy “are so much more than short-term disorders confined to the pregnancy period. They have long-term implications throughout a lifetime,” lead author Ängla Mantel, MD, PhD, said in an interview.
Obstetric history doesn’t figure into any formal HF risk scoring systems, observed Dr. Mantel of Karolinska Institutet, Stockholm. Still, women who develop gestational hypertension, preeclampsia, or other pregnancy complications “should be considered a high-risk population even after the pregnancy and monitored for cardiovascular risk factors regularly throughout life.”
In many studies, she said, “knowledge of women-specific risk factors for cardiovascular disease is poor among both clinicians and patients.” The current findings should help raise awareness about such obstetric risk factors for HF, “especially” in patients with HF with preserved ejection fraction (HFpEF), which isn’t closely related to a number of traditional CV risk factors.
Even though pregnancy complications such as gestational hypertension and preeclampsia don’t feature in risk calculators, “they are actually risk enhancers per the 2019 primary prevention guidelines,” Natalie A. Bello, MD, MPH, who was not involved in the current study, said in an interview.
“We’re working to educate physicians and cardiovascular team members to take a pregnancy history” for risk stratification of women in primary prevention,” said Dr. Bello, director of hypertension research at the Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.
The current study, she said, “is an important step” for its finding that hypertensive disorders of pregnancy are associated separately with both ischemic and nonischemic HF.
She pointed out, however, that because the study excluded women with peripartum cardiomyopathy, a form of nonischemic HF, it may “underestimate the impact of hypertensive disorders on the short-term risk of nonischemic heart failure.” Women who had peripartum cardiomyopathy were excluded to avoid misclassification of other HF outcomes, the authors stated.
Also, Dr. Bello said, the study’s inclusion of patients with either gestational hypertension or preeclampsia may complicate its interpretation. Compared with the former condition, she said, preeclampsia “involves more inflammation and more endothelial dysfunction. It may cause a different impact on the heart and the vasculature.”
In the analysis, about 79,000 women with gestational hypertension or preeclampsia were identified among more than 1.4 million primiparous women who entered the Swedish Medical Birth Register over a period of about 30 years. They were matched with about 396,000 women in the registry who had normotensive pregnancies.
Excluded, besides women with peripartum cardiomyopathy, were women with a prepregnancy history of HF, hypertension, ischemic heart disease, atrial fibrillation, or valvular heart disease.
Hazard ratios (HRs) for HF, ischemic HF, and nonischemic HF were significantly elevated over among the women with gestational hypertension or preeclampsia compared to those with normotensive pregnancies:
- Any HF: HR, 1.70 (95% confidence interval [CI], 1.51-1.91)
- Nonischemic HF: HR, 1.60 (95% CI, 1.40-1.83)
- Ischemic HF: HR, 2.28 (95% CI, 1.74-2.98)
The analyses were adjusted for maternal age at delivery, year of delivery, prepregnancy comorbidities, maternal education level, smoking status, and body mass index.
Sharper risk increases were seen among women with gestational hypertension or preeclampsia who delivered prior to gestational week 34:
- Any HF: HR, 2.46 (95% CI, 1.82-3.32)
- Nonischemic HF: HR, 2.33 (95% CI, 1.65-3.31)
- Ischemic HF: HR, 3.64 (95% CI, 1.97-6.74)
Risks for HF developing within 6 years of pregnancy characterized by gestational hypertension or preeclampsia were far more pronounced for ischemic HF than for nonischemic HF:
- Any HF: HR, 2.09 (95% CI, 1.52-2.89)
- Nonischemic HF: HR, 1.86 (95% CI, 1.32-2.61)
- Ischemic HF: HR, 6.52 (95% CI, 2.00-12.34).
The study couldn’t directly explore potential mechanisms for the associations between pregnancy-induced hypertensive disorders and different forms of HF, but it may have provided clues, Dr. Mantel said.
The hypertensive disorders and ischemic HF appear to share risk factors that could lead to both conditions, she noted. Also, hypertension itself is a risk factor for ischemic heart disease.
In contrast, “the risk of nonischemic heart failure might be driven by other factors, such as the inflammatory profile, endothelial dysfunction, and cardiac remodeling induced by preeclampsia or gestational hypertension.”
Those disorders, moreover, are associated with cardiac structural changes that are also seen in HFpEF, Dr. Mantel said. And both HFpEF and preeclampsia are characterized by systemic inflammation and endothelial dysfunction.
“These pathophysiological similarities,” she proposed, “might explain the link between pregnancy-induced hypertensive disorder and HFpEF.”
The authors have disclosed no relevant financial relationships. Dr. Bello has received grants from the National Institutes of Health.
A version of this article first appeared on Medscape.com.
FROM JACC: HEART FAILURE
Statins appear to guard against liver disease progression
The Swedish population-based study found that adults with noncirrhotic CLD who were on statin therapy had a statistically significant 40% lower risk of developing severe liver disease, compared with matched patients who were not on statin therapy.
The statin users were also less apt to progress to cirrhosis or hepatocellular carcinoma (HCC) and to die of liver disease, Rajani Sharma, MD, MSc, division of digestive and liver diseases, Columbia University Irving Medical Center, New York, and colleagues reported.
Their study was published online in Clinical Gastroenterology and Hepatology.
More than just cholesterol lowering
The study “continues the theme that cholesterol-lowering statins are good for a lot more things than just lowering cholesterol,” William Carey, MD, who wasn’t involved with the study, said in an interview.
The results are “very consistent with other trials that show that people with liver disease on statins do better in many respects than those who are not on statins,” said Dr. Carey, acting head of the hepatology section, department of gastroenterology, hepatology, and nutrition, Cleveland Clinic.
“The effects are not trivial,” Dr. Carey added. “It’s a very significant advantage in terms of fibrosis progression and survival.”
Statins have been shown to inhibit inflammatory pathways, promote endothelial cell function, and reduce hepatic stellate cell activity, suggesting that statins could lessen the progression of liver fibrosis, Dr. Sharma and coauthors wrote.
A few prior studies have looked at the effects of statins in noncirrhotic CLD specifically, but most only included patients with viral hepatitis, and the identification of precirrhotic liver disease was largely based on fibrosis scores or ICD coding, leading to a risk for misclassification and heterogeneity in results, they wrote.
Using histopathology data in a nationwide Swedish cohort, Dr. Sharma and colleagues identified 3862 adults with noncirrhotic CLD who were statin users and a like number of propensity score–matched nonstatin users with noncirrhotic CLD. The adults with CLD included in the study were required to have a liver biopsy showing fibrosis or inflammation between the years 1969 and 2017 and at least one ICD code for CLD.
In both groups, 45% of patients had nonalcoholic fatty liver disease (NAFLD), 22% had alcohol-related liver disease (ALD), 18% had viral hepatitis, and 15% had autoimmune hepatitis (AIH).
The analysis found 234 (6.1%) statin users developed severe liver disease versus 276 (7.1%) nonusers, with incidence rates of 10.5 versus 18.1 per 1,000 person-years, respectively.
Statin use was associated with a statistically significant 40% lower rate of severe liver disease (hazard ratio, 0.60; 95% confidence interval, 0.48-0.74).
This was the case in ALD (HR, 0.30; 95% CI, 0.19-0.49) and NAFLD (HR, 0.68; 95% CI 0.45-1.00), but the results were not statistically significant for individuals with viral hepatitis (HR, 0.76; 95% CI, 0.51-1.14) or AIH (HR, 0.88; 0.48-1.58).
Statin use had a protective association in both prefibrosis and fibrosis stages at diagnosis, the researchers reported.
Statin use was also associated with lower rates of progression to cirrhosis (HR, 0.62; 95% CI, 0.49-0.78), HCC (HR, 0.44; 95% CI, 0.27-0.71) and liver-related death or liver transplant (HR, 0.55; 95% CI, 0.36-0.82).
The authors noted that their “study provides the most robust estimates available thus far.” However, they cautioned that “prospective randomized controlled trials are necessary in order to recommend statin use in clinical practice.”
‘Reassuring and pleasantly surprising’
The study is “very interesting, reassuring, and pleasantly surprising,” Scott L. Friedman, MD, chief of the division of liver diseases and dean for therapeutic discovery at the Icahn School of Medicine at Mount Sinai. New York, said in an interview.
“Statins have been around for a long time, and in earlier days, there was fear of using them because they might induce liver injury. But ample and consistent data exclude the possibility that they are more toxic in patients with liver disease,” said Dr. Friedman, who was not associated with this research.
“What’s interesting and new about this paper is that those studies that have looked at the effects of statins on liver disease have primarily focused on patients who have cirrhosis because there’s some scientific evidence [that] statins can lead to vasodilation and reduce the elevated liver blood flow that occurs in cirrhosis,” he explained.
“Instead, this study, which is quite sizable, includes patients who do not have evidence of cirrhosis based on biopsies. The results suggest that statins have a significant protective effect in these patients,” Dr. Friedman said.
The study was supported by the Karolinska Institute in Stockholm, the Columbia University Irving Medical Center, the Swedish Research Council, the Swedish Cancer Society, and the U.S. National Institutes of Health. Dr. Sharma is a consultant for Takeda and Volv. Other coauthors reported current or past relationships with Bristol-Myers Squibb, Gilead, Salix, and GlaxoSmithKline. Dr. Carey and Dr. Friedman reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The Swedish population-based study found that adults with noncirrhotic CLD who were on statin therapy had a statistically significant 40% lower risk of developing severe liver disease, compared with matched patients who were not on statin therapy.
The statin users were also less apt to progress to cirrhosis or hepatocellular carcinoma (HCC) and to die of liver disease, Rajani Sharma, MD, MSc, division of digestive and liver diseases, Columbia University Irving Medical Center, New York, and colleagues reported.
Their study was published online in Clinical Gastroenterology and Hepatology.
More than just cholesterol lowering
The study “continues the theme that cholesterol-lowering statins are good for a lot more things than just lowering cholesterol,” William Carey, MD, who wasn’t involved with the study, said in an interview.
The results are “very consistent with other trials that show that people with liver disease on statins do better in many respects than those who are not on statins,” said Dr. Carey, acting head of the hepatology section, department of gastroenterology, hepatology, and nutrition, Cleveland Clinic.
“The effects are not trivial,” Dr. Carey added. “It’s a very significant advantage in terms of fibrosis progression and survival.”
Statins have been shown to inhibit inflammatory pathways, promote endothelial cell function, and reduce hepatic stellate cell activity, suggesting that statins could lessen the progression of liver fibrosis, Dr. Sharma and coauthors wrote.
A few prior studies have looked at the effects of statins in noncirrhotic CLD specifically, but most only included patients with viral hepatitis, and the identification of precirrhotic liver disease was largely based on fibrosis scores or ICD coding, leading to a risk for misclassification and heterogeneity in results, they wrote.
Using histopathology data in a nationwide Swedish cohort, Dr. Sharma and colleagues identified 3862 adults with noncirrhotic CLD who were statin users and a like number of propensity score–matched nonstatin users with noncirrhotic CLD. The adults with CLD included in the study were required to have a liver biopsy showing fibrosis or inflammation between the years 1969 and 2017 and at least one ICD code for CLD.
In both groups, 45% of patients had nonalcoholic fatty liver disease (NAFLD), 22% had alcohol-related liver disease (ALD), 18% had viral hepatitis, and 15% had autoimmune hepatitis (AIH).
The analysis found 234 (6.1%) statin users developed severe liver disease versus 276 (7.1%) nonusers, with incidence rates of 10.5 versus 18.1 per 1,000 person-years, respectively.
Statin use was associated with a statistically significant 40% lower rate of severe liver disease (hazard ratio, 0.60; 95% confidence interval, 0.48-0.74).
This was the case in ALD (HR, 0.30; 95% CI, 0.19-0.49) and NAFLD (HR, 0.68; 95% CI 0.45-1.00), but the results were not statistically significant for individuals with viral hepatitis (HR, 0.76; 95% CI, 0.51-1.14) or AIH (HR, 0.88; 0.48-1.58).
Statin use had a protective association in both prefibrosis and fibrosis stages at diagnosis, the researchers reported.
Statin use was also associated with lower rates of progression to cirrhosis (HR, 0.62; 95% CI, 0.49-0.78), HCC (HR, 0.44; 95% CI, 0.27-0.71) and liver-related death or liver transplant (HR, 0.55; 95% CI, 0.36-0.82).
The authors noted that their “study provides the most robust estimates available thus far.” However, they cautioned that “prospective randomized controlled trials are necessary in order to recommend statin use in clinical practice.”
‘Reassuring and pleasantly surprising’
The study is “very interesting, reassuring, and pleasantly surprising,” Scott L. Friedman, MD, chief of the division of liver diseases and dean for therapeutic discovery at the Icahn School of Medicine at Mount Sinai. New York, said in an interview.
“Statins have been around for a long time, and in earlier days, there was fear of using them because they might induce liver injury. But ample and consistent data exclude the possibility that they are more toxic in patients with liver disease,” said Dr. Friedman, who was not associated with this research.
“What’s interesting and new about this paper is that those studies that have looked at the effects of statins on liver disease have primarily focused on patients who have cirrhosis because there’s some scientific evidence [that] statins can lead to vasodilation and reduce the elevated liver blood flow that occurs in cirrhosis,” he explained.
“Instead, this study, which is quite sizable, includes patients who do not have evidence of cirrhosis based on biopsies. The results suggest that statins have a significant protective effect in these patients,” Dr. Friedman said.
The study was supported by the Karolinska Institute in Stockholm, the Columbia University Irving Medical Center, the Swedish Research Council, the Swedish Cancer Society, and the U.S. National Institutes of Health. Dr. Sharma is a consultant for Takeda and Volv. Other coauthors reported current or past relationships with Bristol-Myers Squibb, Gilead, Salix, and GlaxoSmithKline. Dr. Carey and Dr. Friedman reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The Swedish population-based study found that adults with noncirrhotic CLD who were on statin therapy had a statistically significant 40% lower risk of developing severe liver disease, compared with matched patients who were not on statin therapy.
The statin users were also less apt to progress to cirrhosis or hepatocellular carcinoma (HCC) and to die of liver disease, Rajani Sharma, MD, MSc, division of digestive and liver diseases, Columbia University Irving Medical Center, New York, and colleagues reported.
Their study was published online in Clinical Gastroenterology and Hepatology.
More than just cholesterol lowering
The study “continues the theme that cholesterol-lowering statins are good for a lot more things than just lowering cholesterol,” William Carey, MD, who wasn’t involved with the study, said in an interview.
The results are “very consistent with other trials that show that people with liver disease on statins do better in many respects than those who are not on statins,” said Dr. Carey, acting head of the hepatology section, department of gastroenterology, hepatology, and nutrition, Cleveland Clinic.
“The effects are not trivial,” Dr. Carey added. “It’s a very significant advantage in terms of fibrosis progression and survival.”
Statins have been shown to inhibit inflammatory pathways, promote endothelial cell function, and reduce hepatic stellate cell activity, suggesting that statins could lessen the progression of liver fibrosis, Dr. Sharma and coauthors wrote.
A few prior studies have looked at the effects of statins in noncirrhotic CLD specifically, but most only included patients with viral hepatitis, and the identification of precirrhotic liver disease was largely based on fibrosis scores or ICD coding, leading to a risk for misclassification and heterogeneity in results, they wrote.
Using histopathology data in a nationwide Swedish cohort, Dr. Sharma and colleagues identified 3862 adults with noncirrhotic CLD who were statin users and a like number of propensity score–matched nonstatin users with noncirrhotic CLD. The adults with CLD included in the study were required to have a liver biopsy showing fibrosis or inflammation between the years 1969 and 2017 and at least one ICD code for CLD.
In both groups, 45% of patients had nonalcoholic fatty liver disease (NAFLD), 22% had alcohol-related liver disease (ALD), 18% had viral hepatitis, and 15% had autoimmune hepatitis (AIH).
The analysis found 234 (6.1%) statin users developed severe liver disease versus 276 (7.1%) nonusers, with incidence rates of 10.5 versus 18.1 per 1,000 person-years, respectively.
Statin use was associated with a statistically significant 40% lower rate of severe liver disease (hazard ratio, 0.60; 95% confidence interval, 0.48-0.74).
This was the case in ALD (HR, 0.30; 95% CI, 0.19-0.49) and NAFLD (HR, 0.68; 95% CI 0.45-1.00), but the results were not statistically significant for individuals with viral hepatitis (HR, 0.76; 95% CI, 0.51-1.14) or AIH (HR, 0.88; 0.48-1.58).
Statin use had a protective association in both prefibrosis and fibrosis stages at diagnosis, the researchers reported.
Statin use was also associated with lower rates of progression to cirrhosis (HR, 0.62; 95% CI, 0.49-0.78), HCC (HR, 0.44; 95% CI, 0.27-0.71) and liver-related death or liver transplant (HR, 0.55; 95% CI, 0.36-0.82).
The authors noted that their “study provides the most robust estimates available thus far.” However, they cautioned that “prospective randomized controlled trials are necessary in order to recommend statin use in clinical practice.”
‘Reassuring and pleasantly surprising’
The study is “very interesting, reassuring, and pleasantly surprising,” Scott L. Friedman, MD, chief of the division of liver diseases and dean for therapeutic discovery at the Icahn School of Medicine at Mount Sinai. New York, said in an interview.
“Statins have been around for a long time, and in earlier days, there was fear of using them because they might induce liver injury. But ample and consistent data exclude the possibility that they are more toxic in patients with liver disease,” said Dr. Friedman, who was not associated with this research.
“What’s interesting and new about this paper is that those studies that have looked at the effects of statins on liver disease have primarily focused on patients who have cirrhosis because there’s some scientific evidence [that] statins can lead to vasodilation and reduce the elevated liver blood flow that occurs in cirrhosis,” he explained.
“Instead, this study, which is quite sizable, includes patients who do not have evidence of cirrhosis based on biopsies. The results suggest that statins have a significant protective effect in these patients,” Dr. Friedman said.
The study was supported by the Karolinska Institute in Stockholm, the Columbia University Irving Medical Center, the Swedish Research Council, the Swedish Cancer Society, and the U.S. National Institutes of Health. Dr. Sharma is a consultant for Takeda and Volv. Other coauthors reported current or past relationships with Bristol-Myers Squibb, Gilead, Salix, and GlaxoSmithKline. Dr. Carey and Dr. Friedman reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
High cholesterol in seniors: Use statins for primary prevention?
LONG BEACH, CALIF. – For years, clinicians have debated whether prescribing statins to patients older than 75 for the prevention of cardiovascular events is appropriate.
In 2022, the U.S. Preventive Services Task Force concluded that scientific evidence was insufficient to assess the balance between the benefits and harms of the therapy for this older population.
At a session of the annual meeting of the American Geriatrics Society, experts laid out new preliminary recommendations of the AGS and the National Lipid Association on assessing risk and deciding on treatment.
The group concluded that LDL cholesterol levels are associated with incident arteriosclerotic cardiovascular disease (ASCVD), that the coronary artery calcium (CAC) score can be a valuable measure, and that statins may be reasonable to prescribe, even given the risks that have been linked to statins, such as that for muscle pain. Final recommendations are expected by fall 2023.
“This is still a work in progress,” said Daniel E. Forman, MD, professor of medicine and chair of geriatric cardiology at the University of Pittsburgh.
The AGS-NLA panel concluded that, for those aged 75 or older without established ASCVD, LDL cholesterol is associated with incident ASCVD, the only recommendation to be given a class I (strong) rating; others were classed as moderate or weak.
Dr. Forman reviewed the evidence for lowering LDL cholesterol to decrease ASCVD, citing a 2018 study that concluded, “Reverse causation may contribute to the association of lower TC with higher mortality in nonrandomized studies.”
However, research overall shows that, as LDL cholesterol levels increase, patients are more likely to experience a heart event.
Dr. Forman noted that the utility of equations for assessing 5- or 10-year risk of ASCVD is uncertain. However, he said, traditional risk factors, such as family history and ethnicity, still have value.
Assessing risk “has been enriched in the past few years by the introduction of the coronary artery calcium [CAC] score,” he said.
Lower scores predict lower rates of CVD events, Forman said. The AGS-NLA recommends measuring CAC if clinical uncertainty exists about the value of statins.
“It’s reasonable to measure CAC and to withhold statins when the CAC is zero,” Dr. Forman said. “When the CAC score is zero ... the risk of having a cardiovascular event is really next to nil. Patients are happy to know they have a CAC of zero.”
Likewise, patients appreciate knowing whether their score is high, which would indicate increased risk. He said the CAC score is underused by geriatric physicians.
The group also determined, after reviewing the research, that starting treatment is reasonable for patients with an LDL cholesterol level of 70-189 if they have no life-limiting illness and their life expectancy is over 5 years.
Other preliminary recommendations include the use of statins for those aged 75 and older, irrespective of risk for statin-associated muscle symptoms, type 2 diabetes, or impaired cognition. These associations are often weak, Dr. Forman added.
Focusing on person-centered decisions
Ariel Green, MD, MPH, PhD, associate professor of medicine at Johns Hopkins University, Baltimore, said statin therapy “should be individualized” to weigh benefits, noncardiac risks, and other considerations.
Clinicians can incorporate life expectancy into prevention decisions using tools such as ePrognosis, from the University of California, San Francisco, Dr. Green said.
If life expectancy is greater than the time to benefit, statin therapy may help. Dr. Green cited research that showed that 2.5 years of statin therapy was needed to prevent one major adverse cardiovascular event (MACE) per 100 patients in a population aged 50-75. Other data show reductions in MACE for those older than 75, but overall, the data are limited in this population.
The proposed recommendation is to use tools such as life tables that include comorbid conditions and functional status to guide clinical decisions.
“Another aspect of assessing net benefits of statin therapy is to consider competing health risks,” Dr. Green said.
The group recommends considering using competing risk-adjusted CVD models, though these are not widely used.
The group also recommends integrating screenings for frailty (Clinical Frailty Scale), dementia (Mini-Cog), and functional status (Vulnerable Elders Scale–13) into assessments.
“The presence of these syndromes should prompt elicitation of patient values and preferences related to prevention and medication use,” Dr. Green said.
Clinicians can use decision aids, but these are not always practical, owing to obstacles such as patients’ cognitive problems, Dr. Green said.
“Another approach is asking people to prioritize a set of universal health outcomes that apply across health conditions, such as maintaining independence, staying alive, reducing, or eliminating symptoms and focusing on comfort,” Dr. Green said.
She addressed the evidence about deprescribing statins, with a focus on those with a life expectancy of less than a year. Researchers have found an increase in quality of life and no increases in cardiovascular events or death when statins were deprescribed.
A welcome framework
Cory Krueger, MD, an internal medicine and geriatric physician in Cornville, Ariz., who attended the talk, said he welcomed the presentation, in which preliminary recommendations were explained.
“This has been a controversial area in geriatrics,” Dr. Krueger said. “At least this gave me a framework for discussing this with my patients in a reasonable way.”
Dr. Forman and Dr. Krueger disclosed no relevant financial relationships. Dr. Green receives funding from the National Institute of Aging and Impact Collaboratory.
A version of this article first appeared on Medscape.com.
LONG BEACH, CALIF. – For years, clinicians have debated whether prescribing statins to patients older than 75 for the prevention of cardiovascular events is appropriate.
In 2022, the U.S. Preventive Services Task Force concluded that scientific evidence was insufficient to assess the balance between the benefits and harms of the therapy for this older population.
At a session of the annual meeting of the American Geriatrics Society, experts laid out new preliminary recommendations of the AGS and the National Lipid Association on assessing risk and deciding on treatment.
The group concluded that LDL cholesterol levels are associated with incident arteriosclerotic cardiovascular disease (ASCVD), that the coronary artery calcium (CAC) score can be a valuable measure, and that statins may be reasonable to prescribe, even given the risks that have been linked to statins, such as that for muscle pain. Final recommendations are expected by fall 2023.
“This is still a work in progress,” said Daniel E. Forman, MD, professor of medicine and chair of geriatric cardiology at the University of Pittsburgh.
The AGS-NLA panel concluded that, for those aged 75 or older without established ASCVD, LDL cholesterol is associated with incident ASCVD, the only recommendation to be given a class I (strong) rating; others were classed as moderate or weak.
Dr. Forman reviewed the evidence for lowering LDL cholesterol to decrease ASCVD, citing a 2018 study that concluded, “Reverse causation may contribute to the association of lower TC with higher mortality in nonrandomized studies.”
However, research overall shows that, as LDL cholesterol levels increase, patients are more likely to experience a heart event.
Dr. Forman noted that the utility of equations for assessing 5- or 10-year risk of ASCVD is uncertain. However, he said, traditional risk factors, such as family history and ethnicity, still have value.
Assessing risk “has been enriched in the past few years by the introduction of the coronary artery calcium [CAC] score,” he said.
Lower scores predict lower rates of CVD events, Forman said. The AGS-NLA recommends measuring CAC if clinical uncertainty exists about the value of statins.
“It’s reasonable to measure CAC and to withhold statins when the CAC is zero,” Dr. Forman said. “When the CAC score is zero ... the risk of having a cardiovascular event is really next to nil. Patients are happy to know they have a CAC of zero.”
Likewise, patients appreciate knowing whether their score is high, which would indicate increased risk. He said the CAC score is underused by geriatric physicians.
The group also determined, after reviewing the research, that starting treatment is reasonable for patients with an LDL cholesterol level of 70-189 if they have no life-limiting illness and their life expectancy is over 5 years.
Other preliminary recommendations include the use of statins for those aged 75 and older, irrespective of risk for statin-associated muscle symptoms, type 2 diabetes, or impaired cognition. These associations are often weak, Dr. Forman added.
Focusing on person-centered decisions
Ariel Green, MD, MPH, PhD, associate professor of medicine at Johns Hopkins University, Baltimore, said statin therapy “should be individualized” to weigh benefits, noncardiac risks, and other considerations.
Clinicians can incorporate life expectancy into prevention decisions using tools such as ePrognosis, from the University of California, San Francisco, Dr. Green said.
If life expectancy is greater than the time to benefit, statin therapy may help. Dr. Green cited research that showed that 2.5 years of statin therapy was needed to prevent one major adverse cardiovascular event (MACE) per 100 patients in a population aged 50-75. Other data show reductions in MACE for those older than 75, but overall, the data are limited in this population.
The proposed recommendation is to use tools such as life tables that include comorbid conditions and functional status to guide clinical decisions.
“Another aspect of assessing net benefits of statin therapy is to consider competing health risks,” Dr. Green said.
The group recommends considering using competing risk-adjusted CVD models, though these are not widely used.
The group also recommends integrating screenings for frailty (Clinical Frailty Scale), dementia (Mini-Cog), and functional status (Vulnerable Elders Scale–13) into assessments.
“The presence of these syndromes should prompt elicitation of patient values and preferences related to prevention and medication use,” Dr. Green said.
Clinicians can use decision aids, but these are not always practical, owing to obstacles such as patients’ cognitive problems, Dr. Green said.
“Another approach is asking people to prioritize a set of universal health outcomes that apply across health conditions, such as maintaining independence, staying alive, reducing, or eliminating symptoms and focusing on comfort,” Dr. Green said.
She addressed the evidence about deprescribing statins, with a focus on those with a life expectancy of less than a year. Researchers have found an increase in quality of life and no increases in cardiovascular events or death when statins were deprescribed.
A welcome framework
Cory Krueger, MD, an internal medicine and geriatric physician in Cornville, Ariz., who attended the talk, said he welcomed the presentation, in which preliminary recommendations were explained.
“This has been a controversial area in geriatrics,” Dr. Krueger said. “At least this gave me a framework for discussing this with my patients in a reasonable way.”
Dr. Forman and Dr. Krueger disclosed no relevant financial relationships. Dr. Green receives funding from the National Institute of Aging and Impact Collaboratory.
A version of this article first appeared on Medscape.com.
LONG BEACH, CALIF. – For years, clinicians have debated whether prescribing statins to patients older than 75 for the prevention of cardiovascular events is appropriate.
In 2022, the U.S. Preventive Services Task Force concluded that scientific evidence was insufficient to assess the balance between the benefits and harms of the therapy for this older population.
At a session of the annual meeting of the American Geriatrics Society, experts laid out new preliminary recommendations of the AGS and the National Lipid Association on assessing risk and deciding on treatment.
The group concluded that LDL cholesterol levels are associated with incident arteriosclerotic cardiovascular disease (ASCVD), that the coronary artery calcium (CAC) score can be a valuable measure, and that statins may be reasonable to prescribe, even given the risks that have been linked to statins, such as that for muscle pain. Final recommendations are expected by fall 2023.
“This is still a work in progress,” said Daniel E. Forman, MD, professor of medicine and chair of geriatric cardiology at the University of Pittsburgh.
The AGS-NLA panel concluded that, for those aged 75 or older without established ASCVD, LDL cholesterol is associated with incident ASCVD, the only recommendation to be given a class I (strong) rating; others were classed as moderate or weak.
Dr. Forman reviewed the evidence for lowering LDL cholesterol to decrease ASCVD, citing a 2018 study that concluded, “Reverse causation may contribute to the association of lower TC with higher mortality in nonrandomized studies.”
However, research overall shows that, as LDL cholesterol levels increase, patients are more likely to experience a heart event.
Dr. Forman noted that the utility of equations for assessing 5- or 10-year risk of ASCVD is uncertain. However, he said, traditional risk factors, such as family history and ethnicity, still have value.
Assessing risk “has been enriched in the past few years by the introduction of the coronary artery calcium [CAC] score,” he said.
Lower scores predict lower rates of CVD events, Forman said. The AGS-NLA recommends measuring CAC if clinical uncertainty exists about the value of statins.
“It’s reasonable to measure CAC and to withhold statins when the CAC is zero,” Dr. Forman said. “When the CAC score is zero ... the risk of having a cardiovascular event is really next to nil. Patients are happy to know they have a CAC of zero.”
Likewise, patients appreciate knowing whether their score is high, which would indicate increased risk. He said the CAC score is underused by geriatric physicians.
The group also determined, after reviewing the research, that starting treatment is reasonable for patients with an LDL cholesterol level of 70-189 if they have no life-limiting illness and their life expectancy is over 5 years.
Other preliminary recommendations include the use of statins for those aged 75 and older, irrespective of risk for statin-associated muscle symptoms, type 2 diabetes, or impaired cognition. These associations are often weak, Dr. Forman added.
Focusing on person-centered decisions
Ariel Green, MD, MPH, PhD, associate professor of medicine at Johns Hopkins University, Baltimore, said statin therapy “should be individualized” to weigh benefits, noncardiac risks, and other considerations.
Clinicians can incorporate life expectancy into prevention decisions using tools such as ePrognosis, from the University of California, San Francisco, Dr. Green said.
If life expectancy is greater than the time to benefit, statin therapy may help. Dr. Green cited research that showed that 2.5 years of statin therapy was needed to prevent one major adverse cardiovascular event (MACE) per 100 patients in a population aged 50-75. Other data show reductions in MACE for those older than 75, but overall, the data are limited in this population.
The proposed recommendation is to use tools such as life tables that include comorbid conditions and functional status to guide clinical decisions.
“Another aspect of assessing net benefits of statin therapy is to consider competing health risks,” Dr. Green said.
The group recommends considering using competing risk-adjusted CVD models, though these are not widely used.
The group also recommends integrating screenings for frailty (Clinical Frailty Scale), dementia (Mini-Cog), and functional status (Vulnerable Elders Scale–13) into assessments.
“The presence of these syndromes should prompt elicitation of patient values and preferences related to prevention and medication use,” Dr. Green said.
Clinicians can use decision aids, but these are not always practical, owing to obstacles such as patients’ cognitive problems, Dr. Green said.
“Another approach is asking people to prioritize a set of universal health outcomes that apply across health conditions, such as maintaining independence, staying alive, reducing, or eliminating symptoms and focusing on comfort,” Dr. Green said.
She addressed the evidence about deprescribing statins, with a focus on those with a life expectancy of less than a year. Researchers have found an increase in quality of life and no increases in cardiovascular events or death when statins were deprescribed.
A welcome framework
Cory Krueger, MD, an internal medicine and geriatric physician in Cornville, Ariz., who attended the talk, said he welcomed the presentation, in which preliminary recommendations were explained.
“This has been a controversial area in geriatrics,” Dr. Krueger said. “At least this gave me a framework for discussing this with my patients in a reasonable way.”
Dr. Forman and Dr. Krueger disclosed no relevant financial relationships. Dr. Green receives funding from the National Institute of Aging and Impact Collaboratory.
A version of this article first appeared on Medscape.com.
AT AGS 2023