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Older patients who stop statins may be increasing their cardiovascular risk
Discontinuing statins was associated with an increased risk of hospital admission for a cardiovascular event, according to a study of elderly French patients with no history of heart disease.
“The results of this study suggest potential cardiovascular risk reduction associated with continuing statin therapy after the age of 75 years in persons already taking these drugs for primary prevention,” wrote Philippe Giral, MD, of Hôpital La Pitié Salpêtrière (France) and coauthors. The study was published in the European Heart Journal.
To determine if statins are a cardiovascular benefit or detriment to older people, the researchers reviewed data from 120,173 patients in French health care databases who turned 75 during 2012-2014. Patients with a diagnosis of cardiovascular disease in the previous 2 years were excluded, and all eligible patients were required to have a statin medication possession ratio of at least 80% in each of the previous 2 years.
Over a follow-up period that averaged 2.4 years, 17,204 patients (14.3%) discontinued statins and 5,396 (4.5%) were admitted for a cardiovascular event. The adjusted hazard ratios for admissions after statin discontinuation were 1.33 (95% confidence interval, 1.18-1.50) for a cardiovascular event, 1.46 (95% CI, 1.21-1.75) for a coronary event, 1.26 (95% CI, 1.05-1.51) for a cerebrovascular event, and 1.02 (95% CI, 0.74-1.40) for other vascular events, respectively.
The coauthors acknowledged their study’s limitations, including being unable to account for certain cardiovascular risk factors such as baseline LDL cholesterol level, tobacco use, obesity, and frailty markers. In addition, no information was available as to why patients discontinued statins. However, the presence of other major cardiovascular risk factors was investigated and accounted for, as was discontinuation of other cardiovascular drug therapies.
The study was not funded, and the authors declared no conflicts of interest.
SOURCE: Giral P at al. Eur Heart J. 2019 July 31. doi: 10.1093/eurheartj/ehz458.
Discontinuing statins was associated with an increased risk of hospital admission for a cardiovascular event, according to a study of elderly French patients with no history of heart disease.
“The results of this study suggest potential cardiovascular risk reduction associated with continuing statin therapy after the age of 75 years in persons already taking these drugs for primary prevention,” wrote Philippe Giral, MD, of Hôpital La Pitié Salpêtrière (France) and coauthors. The study was published in the European Heart Journal.
To determine if statins are a cardiovascular benefit or detriment to older people, the researchers reviewed data from 120,173 patients in French health care databases who turned 75 during 2012-2014. Patients with a diagnosis of cardiovascular disease in the previous 2 years were excluded, and all eligible patients were required to have a statin medication possession ratio of at least 80% in each of the previous 2 years.
Over a follow-up period that averaged 2.4 years, 17,204 patients (14.3%) discontinued statins and 5,396 (4.5%) were admitted for a cardiovascular event. The adjusted hazard ratios for admissions after statin discontinuation were 1.33 (95% confidence interval, 1.18-1.50) for a cardiovascular event, 1.46 (95% CI, 1.21-1.75) for a coronary event, 1.26 (95% CI, 1.05-1.51) for a cerebrovascular event, and 1.02 (95% CI, 0.74-1.40) for other vascular events, respectively.
The coauthors acknowledged their study’s limitations, including being unable to account for certain cardiovascular risk factors such as baseline LDL cholesterol level, tobacco use, obesity, and frailty markers. In addition, no information was available as to why patients discontinued statins. However, the presence of other major cardiovascular risk factors was investigated and accounted for, as was discontinuation of other cardiovascular drug therapies.
The study was not funded, and the authors declared no conflicts of interest.
SOURCE: Giral P at al. Eur Heart J. 2019 July 31. doi: 10.1093/eurheartj/ehz458.
Discontinuing statins was associated with an increased risk of hospital admission for a cardiovascular event, according to a study of elderly French patients with no history of heart disease.
“The results of this study suggest potential cardiovascular risk reduction associated with continuing statin therapy after the age of 75 years in persons already taking these drugs for primary prevention,” wrote Philippe Giral, MD, of Hôpital La Pitié Salpêtrière (France) and coauthors. The study was published in the European Heart Journal.
To determine if statins are a cardiovascular benefit or detriment to older people, the researchers reviewed data from 120,173 patients in French health care databases who turned 75 during 2012-2014. Patients with a diagnosis of cardiovascular disease in the previous 2 years were excluded, and all eligible patients were required to have a statin medication possession ratio of at least 80% in each of the previous 2 years.
Over a follow-up period that averaged 2.4 years, 17,204 patients (14.3%) discontinued statins and 5,396 (4.5%) were admitted for a cardiovascular event. The adjusted hazard ratios for admissions after statin discontinuation were 1.33 (95% confidence interval, 1.18-1.50) for a cardiovascular event, 1.46 (95% CI, 1.21-1.75) for a coronary event, 1.26 (95% CI, 1.05-1.51) for a cerebrovascular event, and 1.02 (95% CI, 0.74-1.40) for other vascular events, respectively.
The coauthors acknowledged their study’s limitations, including being unable to account for certain cardiovascular risk factors such as baseline LDL cholesterol level, tobacco use, obesity, and frailty markers. In addition, no information was available as to why patients discontinued statins. However, the presence of other major cardiovascular risk factors was investigated and accounted for, as was discontinuation of other cardiovascular drug therapies.
The study was not funded, and the authors declared no conflicts of interest.
SOURCE: Giral P at al. Eur Heart J. 2019 July 31. doi: 10.1093/eurheartj/ehz458.
FROM THE EUROPEAN HEART JOURNAL
Atherosclerotic disease risk persists decades after smoking cessation
Adults who quit smoking reduced their risk for peripheral artery disease in the short term, but remained at increased risk for up to 30 years, compared with never-smokers, based on data from more than 13,000 adults in a community-based study.
Most reports on the impact of smoking cessation on cardiovascular disease have focused on coronary heart disease (CHD), and stroke, while data on the effects of smoking cessation on peripheral artery disease (PAD) are limited, wrote Ning Ding, MBBS, SCM, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, Md., and colleagues.
To compare the impact of smoking on PAD, CHD, and stroke, the researchers used data from the Atherosclerosis Risk in Communities (ARIC) study, which included 15,792 adults aged 45-64 years in four communities. The findings were published in the Journal of the American College of Cardiology.
The study population of 13,355 individuals had no baseline history of PAD, CHD, or stroke. Over a median 26 years of follow-up, the researchers identified 492 cases of PAD, 1,798 cases of CHD, and 1,106 cases of stroke.
The risk of all three conditions began to decline within 5 years of smoking cessation, which could be encouraging to smokers who wish to quit, the researchers noted. In addition, the longer the duration of smoking cessation, the lower the risk for all three conditions (See central illustration).
However, a significantly elevated risk remained for PAD for up to 30 years after smoking cessation and for CHD for up to 20 years after smoking cessation, compared with never-smokers.
The researchers also found a roughly fourfold increased risk for PAD for smokers who smoked for 40 or more pack-years, compared with never-smokers, which was greater than the 2.1 hazard ratio for CHD and 1.8 HR for stroke. In addition, current smokers of at least one pack per day had a significantly greater risk of PAD, compared with never-smokers (HR, 5.36) that was higher than the risk for CHD or stroke (HR, 2.38 and HR, 1.88, respectively).
The study findings were limited by several factors including the reliance on self-reports, potential misclassification of data, and the potential exclusion of mild PAD cases that did not require hospitalization, the researchers noted. However, the results support the value of encouraging smokers to quit and support the need to include PAD risk in public health information, they said. “Although public statements about smoking and [cardiovascular disease] have been focusing on CHD and stroke, our results indicate the need to take account of PAD as well for comprehensively acknowledging the effect of smoking on overall cardiovascular health,” they added.
The ARIC study was funded by the National Heart, Lung, and Blood Institute, National Institutes of Health. Lead author Dr. Ding had no financial conflicts to disclose; coauthors disclosed relationships with Bristol-Myers Squibb and Fukuda Denshi.
SOURCE: Ding N et al. J Am Coll Cardiol. 2019 Jul 22;74:498-507. doi: 10.1016/j.jacc.2019.06.003.
Although the pathophysiology of smoking and cardiovascular disease has yet to be teased out, the current study findings support the public health message that any and all smokers can improve their health by quitting any time: “It is never too early or too late to benefit from quitting,” wrote Nancy A. Rigotti, MD, and Mary M. McDermott, MD, in an accompanying editorial. The editorialists questioned whether the findings were generalizable to patients with mild PAD or those who are not hospitalized. However, they found the data consistent with previous studies suggesting that atherosclerosis is not homogeneous. “Differences in shear stress and hemodynamic forces among the femoral, coronary, and carotid arterial beds may also explain variability in associations of smoking and smoking cessation with the incidence of PAD versus myocardial infarction or stroke,” they said.
The findings also support the need to emphasize PAD in public health messages and provide an opportunity to educate patients about the risks of limb loss and impaired mobility associated with PAD, they said.
Many clinicians put a low priority on smoking cessation, the editorialists wrote, but “long-term tobacco abstinence is achievable using a chronic disease management approach resembling the strategies used to manage other risk factors,” they said. They cited the American College of Cardiology’s recently released “Expert Consensus Decision Pathway on Tobacco Cessation Treatment.” The pathway outlines advice for clinicians, including how to provide a brief intervention and resources along with advice to quit smoking.
Dr. Rigotti is affiliated with Harvard Medical School, Boston. Dr. McDermott is affiliated with Northwestern University, Chicago. Dr. Rigotti disclosed royalties from UpToDate, serving as a consultant for Achieve Life Sciences, and travel expenses from Pfizer for unpaid consulting. Dr. McDermott disclosed research funding from Regeneron, the National Heart, Lung, and Blood Institute, the National Institute on Aging, and the American Heart Association, plus research support from Chromadex, ReserveAge, Hershey, and ViroMed.
Although the pathophysiology of smoking and cardiovascular disease has yet to be teased out, the current study findings support the public health message that any and all smokers can improve their health by quitting any time: “It is never too early or too late to benefit from quitting,” wrote Nancy A. Rigotti, MD, and Mary M. McDermott, MD, in an accompanying editorial. The editorialists questioned whether the findings were generalizable to patients with mild PAD or those who are not hospitalized. However, they found the data consistent with previous studies suggesting that atherosclerosis is not homogeneous. “Differences in shear stress and hemodynamic forces among the femoral, coronary, and carotid arterial beds may also explain variability in associations of smoking and smoking cessation with the incidence of PAD versus myocardial infarction or stroke,” they said.
The findings also support the need to emphasize PAD in public health messages and provide an opportunity to educate patients about the risks of limb loss and impaired mobility associated with PAD, they said.
Many clinicians put a low priority on smoking cessation, the editorialists wrote, but “long-term tobacco abstinence is achievable using a chronic disease management approach resembling the strategies used to manage other risk factors,” they said. They cited the American College of Cardiology’s recently released “Expert Consensus Decision Pathway on Tobacco Cessation Treatment.” The pathway outlines advice for clinicians, including how to provide a brief intervention and resources along with advice to quit smoking.
Dr. Rigotti is affiliated with Harvard Medical School, Boston. Dr. McDermott is affiliated with Northwestern University, Chicago. Dr. Rigotti disclosed royalties from UpToDate, serving as a consultant for Achieve Life Sciences, and travel expenses from Pfizer for unpaid consulting. Dr. McDermott disclosed research funding from Regeneron, the National Heart, Lung, and Blood Institute, the National Institute on Aging, and the American Heart Association, plus research support from Chromadex, ReserveAge, Hershey, and ViroMed.
Although the pathophysiology of smoking and cardiovascular disease has yet to be teased out, the current study findings support the public health message that any and all smokers can improve their health by quitting any time: “It is never too early or too late to benefit from quitting,” wrote Nancy A. Rigotti, MD, and Mary M. McDermott, MD, in an accompanying editorial. The editorialists questioned whether the findings were generalizable to patients with mild PAD or those who are not hospitalized. However, they found the data consistent with previous studies suggesting that atherosclerosis is not homogeneous. “Differences in shear stress and hemodynamic forces among the femoral, coronary, and carotid arterial beds may also explain variability in associations of smoking and smoking cessation with the incidence of PAD versus myocardial infarction or stroke,” they said.
The findings also support the need to emphasize PAD in public health messages and provide an opportunity to educate patients about the risks of limb loss and impaired mobility associated with PAD, they said.
Many clinicians put a low priority on smoking cessation, the editorialists wrote, but “long-term tobacco abstinence is achievable using a chronic disease management approach resembling the strategies used to manage other risk factors,” they said. They cited the American College of Cardiology’s recently released “Expert Consensus Decision Pathway on Tobacco Cessation Treatment.” The pathway outlines advice for clinicians, including how to provide a brief intervention and resources along with advice to quit smoking.
Dr. Rigotti is affiliated with Harvard Medical School, Boston. Dr. McDermott is affiliated with Northwestern University, Chicago. Dr. Rigotti disclosed royalties from UpToDate, serving as a consultant for Achieve Life Sciences, and travel expenses from Pfizer for unpaid consulting. Dr. McDermott disclosed research funding from Regeneron, the National Heart, Lung, and Blood Institute, the National Institute on Aging, and the American Heart Association, plus research support from Chromadex, ReserveAge, Hershey, and ViroMed.
Adults who quit smoking reduced their risk for peripheral artery disease in the short term, but remained at increased risk for up to 30 years, compared with never-smokers, based on data from more than 13,000 adults in a community-based study.
Most reports on the impact of smoking cessation on cardiovascular disease have focused on coronary heart disease (CHD), and stroke, while data on the effects of smoking cessation on peripheral artery disease (PAD) are limited, wrote Ning Ding, MBBS, SCM, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, Md., and colleagues.
To compare the impact of smoking on PAD, CHD, and stroke, the researchers used data from the Atherosclerosis Risk in Communities (ARIC) study, which included 15,792 adults aged 45-64 years in four communities. The findings were published in the Journal of the American College of Cardiology.
The study population of 13,355 individuals had no baseline history of PAD, CHD, or stroke. Over a median 26 years of follow-up, the researchers identified 492 cases of PAD, 1,798 cases of CHD, and 1,106 cases of stroke.
The risk of all three conditions began to decline within 5 years of smoking cessation, which could be encouraging to smokers who wish to quit, the researchers noted. In addition, the longer the duration of smoking cessation, the lower the risk for all three conditions (See central illustration).
However, a significantly elevated risk remained for PAD for up to 30 years after smoking cessation and for CHD for up to 20 years after smoking cessation, compared with never-smokers.
The researchers also found a roughly fourfold increased risk for PAD for smokers who smoked for 40 or more pack-years, compared with never-smokers, which was greater than the 2.1 hazard ratio for CHD and 1.8 HR for stroke. In addition, current smokers of at least one pack per day had a significantly greater risk of PAD, compared with never-smokers (HR, 5.36) that was higher than the risk for CHD or stroke (HR, 2.38 and HR, 1.88, respectively).
The study findings were limited by several factors including the reliance on self-reports, potential misclassification of data, and the potential exclusion of mild PAD cases that did not require hospitalization, the researchers noted. However, the results support the value of encouraging smokers to quit and support the need to include PAD risk in public health information, they said. “Although public statements about smoking and [cardiovascular disease] have been focusing on CHD and stroke, our results indicate the need to take account of PAD as well for comprehensively acknowledging the effect of smoking on overall cardiovascular health,” they added.
The ARIC study was funded by the National Heart, Lung, and Blood Institute, National Institutes of Health. Lead author Dr. Ding had no financial conflicts to disclose; coauthors disclosed relationships with Bristol-Myers Squibb and Fukuda Denshi.
SOURCE: Ding N et al. J Am Coll Cardiol. 2019 Jul 22;74:498-507. doi: 10.1016/j.jacc.2019.06.003.
Adults who quit smoking reduced their risk for peripheral artery disease in the short term, but remained at increased risk for up to 30 years, compared with never-smokers, based on data from more than 13,000 adults in a community-based study.
Most reports on the impact of smoking cessation on cardiovascular disease have focused on coronary heart disease (CHD), and stroke, while data on the effects of smoking cessation on peripheral artery disease (PAD) are limited, wrote Ning Ding, MBBS, SCM, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, Md., and colleagues.
To compare the impact of smoking on PAD, CHD, and stroke, the researchers used data from the Atherosclerosis Risk in Communities (ARIC) study, which included 15,792 adults aged 45-64 years in four communities. The findings were published in the Journal of the American College of Cardiology.
The study population of 13,355 individuals had no baseline history of PAD, CHD, or stroke. Over a median 26 years of follow-up, the researchers identified 492 cases of PAD, 1,798 cases of CHD, and 1,106 cases of stroke.
The risk of all three conditions began to decline within 5 years of smoking cessation, which could be encouraging to smokers who wish to quit, the researchers noted. In addition, the longer the duration of smoking cessation, the lower the risk for all three conditions (See central illustration).
However, a significantly elevated risk remained for PAD for up to 30 years after smoking cessation and for CHD for up to 20 years after smoking cessation, compared with never-smokers.
The researchers also found a roughly fourfold increased risk for PAD for smokers who smoked for 40 or more pack-years, compared with never-smokers, which was greater than the 2.1 hazard ratio for CHD and 1.8 HR for stroke. In addition, current smokers of at least one pack per day had a significantly greater risk of PAD, compared with never-smokers (HR, 5.36) that was higher than the risk for CHD or stroke (HR, 2.38 and HR, 1.88, respectively).
The study findings were limited by several factors including the reliance on self-reports, potential misclassification of data, and the potential exclusion of mild PAD cases that did not require hospitalization, the researchers noted. However, the results support the value of encouraging smokers to quit and support the need to include PAD risk in public health information, they said. “Although public statements about smoking and [cardiovascular disease] have been focusing on CHD and stroke, our results indicate the need to take account of PAD as well for comprehensively acknowledging the effect of smoking on overall cardiovascular health,” they added.
The ARIC study was funded by the National Heart, Lung, and Blood Institute, National Institutes of Health. Lead author Dr. Ding had no financial conflicts to disclose; coauthors disclosed relationships with Bristol-Myers Squibb and Fukuda Denshi.
SOURCE: Ding N et al. J Am Coll Cardiol. 2019 Jul 22;74:498-507. doi: 10.1016/j.jacc.2019.06.003.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Plant-based foods could keep type 2 diabetes at bay
according to a new systematic review and meta-analysis of nine observational studies.
The findings aren’t conclusive, but the study authors wrote in JAMA Internal Medicine that they suggest that “plant-based dietary patterns were associated with lower risk of type 2 diabetes, even after adjustment for [body mass index].”
According to 2015 figures provided by the American Diabetes Association, about 29 million people in the United States have type 2 diabetes. Overall, diabetes contributes to hundreds of thousands of deaths each year, which makes it the seventh-leading cause of death in the nation.
For the new analysis, researchers led by Frank Qian, MPH, of Harvard T.H. Chan School of Public Health included nine studies that examined diet and type 2 diabetes. In all, the studies included 307,099 participants, and there were 23,544 cases of incident type 2 diabetes. They were conducted in five countries, including the United States, and tracked participants for 2-28 years; the studies were all published within the last 11 years. The mean ages of participants ranged from 36-65 years.
The meta-analysis linked higher consumption of plant-based foods to a 23% reduced risk of type 2 diabetes, compared with lower consumption (relative risk, 0.77; 95% confidence interval, 0.71-0.84; P = .07 for heterogeneity). The risk dipped even further (down to 30%) when the researchers analyzed four studies that focused on healthy plant-based foods, such as fruits and vegetables, instead of foods such as refined grains, starches, and sugars (RR, 0.70; 95% CI, 0.62-0.79).
The researchers suggested that plant-based diets may lower the risk of diabetes type 2 by limiting weight gain. They also noted various limitations to their analysis, such as the reliance on self-reports and the observational nature of the studies.
Still, “in general populations that do not practice strict vegetarian or vegan diets, replacing animal products with healthful plant-based foods is likely to exert a significant reduction in the risk of diabetes,” the authors wrote.
The study was funded by the National Institutes of Health, and one author received support from the National Institute of Diabetes and Digestive and Kidney Diseases. The remaining authors reported no conflicts of interest withing the scope of this study.
SOURCE: Qian F et al. JAMA Internal Medicine. 2019 Jul 22. doi: 10.1001/jamainternmed.2019.2195.
according to a new systematic review and meta-analysis of nine observational studies.
The findings aren’t conclusive, but the study authors wrote in JAMA Internal Medicine that they suggest that “plant-based dietary patterns were associated with lower risk of type 2 diabetes, even after adjustment for [body mass index].”
According to 2015 figures provided by the American Diabetes Association, about 29 million people in the United States have type 2 diabetes. Overall, diabetes contributes to hundreds of thousands of deaths each year, which makes it the seventh-leading cause of death in the nation.
For the new analysis, researchers led by Frank Qian, MPH, of Harvard T.H. Chan School of Public Health included nine studies that examined diet and type 2 diabetes. In all, the studies included 307,099 participants, and there were 23,544 cases of incident type 2 diabetes. They were conducted in five countries, including the United States, and tracked participants for 2-28 years; the studies were all published within the last 11 years. The mean ages of participants ranged from 36-65 years.
The meta-analysis linked higher consumption of plant-based foods to a 23% reduced risk of type 2 diabetes, compared with lower consumption (relative risk, 0.77; 95% confidence interval, 0.71-0.84; P = .07 for heterogeneity). The risk dipped even further (down to 30%) when the researchers analyzed four studies that focused on healthy plant-based foods, such as fruits and vegetables, instead of foods such as refined grains, starches, and sugars (RR, 0.70; 95% CI, 0.62-0.79).
The researchers suggested that plant-based diets may lower the risk of diabetes type 2 by limiting weight gain. They also noted various limitations to their analysis, such as the reliance on self-reports and the observational nature of the studies.
Still, “in general populations that do not practice strict vegetarian or vegan diets, replacing animal products with healthful plant-based foods is likely to exert a significant reduction in the risk of diabetes,” the authors wrote.
The study was funded by the National Institutes of Health, and one author received support from the National Institute of Diabetes and Digestive and Kidney Diseases. The remaining authors reported no conflicts of interest withing the scope of this study.
SOURCE: Qian F et al. JAMA Internal Medicine. 2019 Jul 22. doi: 10.1001/jamainternmed.2019.2195.
according to a new systematic review and meta-analysis of nine observational studies.
The findings aren’t conclusive, but the study authors wrote in JAMA Internal Medicine that they suggest that “plant-based dietary patterns were associated with lower risk of type 2 diabetes, even after adjustment for [body mass index].”
According to 2015 figures provided by the American Diabetes Association, about 29 million people in the United States have type 2 diabetes. Overall, diabetes contributes to hundreds of thousands of deaths each year, which makes it the seventh-leading cause of death in the nation.
For the new analysis, researchers led by Frank Qian, MPH, of Harvard T.H. Chan School of Public Health included nine studies that examined diet and type 2 diabetes. In all, the studies included 307,099 participants, and there were 23,544 cases of incident type 2 diabetes. They were conducted in five countries, including the United States, and tracked participants for 2-28 years; the studies were all published within the last 11 years. The mean ages of participants ranged from 36-65 years.
The meta-analysis linked higher consumption of plant-based foods to a 23% reduced risk of type 2 diabetes, compared with lower consumption (relative risk, 0.77; 95% confidence interval, 0.71-0.84; P = .07 for heterogeneity). The risk dipped even further (down to 30%) when the researchers analyzed four studies that focused on healthy plant-based foods, such as fruits and vegetables, instead of foods such as refined grains, starches, and sugars (RR, 0.70; 95% CI, 0.62-0.79).
The researchers suggested that plant-based diets may lower the risk of diabetes type 2 by limiting weight gain. They also noted various limitations to their analysis, such as the reliance on self-reports and the observational nature of the studies.
Still, “in general populations that do not practice strict vegetarian or vegan diets, replacing animal products with healthful plant-based foods is likely to exert a significant reduction in the risk of diabetes,” the authors wrote.
The study was funded by the National Institutes of Health, and one author received support from the National Institute of Diabetes and Digestive and Kidney Diseases. The remaining authors reported no conflicts of interest withing the scope of this study.
SOURCE: Qian F et al. JAMA Internal Medicine. 2019 Jul 22. doi: 10.1001/jamainternmed.2019.2195.
FROM JAMA INTERNAL MEDICINE
Statins crush early seizure risk poststroke
BANGKOK – Statin therapy, even when initiated only upon hospitalization for acute ischemic stroke, was associated with a striking reduction in the risk of early poststroke symptomatic seizure in a large observational study.
Using propensity-score matching to control for potential confounders, use of a statin during acute stroke management was associated with a “robust” 77% reduction in the risk of developing a symptomatic seizure within 7 days after hospital admission, Soichiro Matsubara, MD, reported at the International Epilepsy Congress.
This is an important finding because early symptomatic seizure (ESS) occurs in 2%-7% of patients following an acute ischemic stroke. Moreover, an Italian meta-analysis concluded that ESS was associated with a 4.4-fold increased risk of developing poststroke epilepsy (Epilepsia. 2016 Aug;57[8]:1205-14), noted Dr. Matsubara, a neurologist at the National Cerebral and Cardiovascular Center in Suita, Japan, as well as at Kumamoto (Japan) University.
He presented a study of 2,969 consecutive acute ischemic stroke patients with no history of epilepsy who were admitted to the Japanese comprehensive stroke center, of whom 2.2% experienced ESS. At physician discretion, 19% of the ESS cohort were on a statin during their acute stroke management, as were 55% of the no-ESS group. Four-fifths of patients on a statin initiated the drug only upon hospital admission.
Strokes tended to be more severe in the ESS group, with a median initial National Institutes of Health Stroke Scale score of 12.5, compared with 4 in the seizure-free patients. A cortical stroke lesion was evident upon imaging in 89% of the ESS group and 55% of no-ESS patients. Among ESS patients, 46% had a cardiometabolic stroke, compared with 34% of the no-ESS cohort. Mean C-reactive protein levels and white blood cell counts were significantly higher in the ESS cohort as well. Their median hospital length of stay was 25.5 days, versus 18 days in the no-ESS group, Dr. Matsubara said at the congress sponsored by the International League Against Epilepsy.
Of the 76 ESSs that occurred in 66 patients, 37% were focal awareness seizures, 35% were focal to bilateral tonic-clonic seizures, and 28% were focal impaired awareness seizures.
In a multivariate analysis adjusted for age, sex, body mass index, stroke subtype, and other potential confounders, statin therapy during acute management of stroke was independently associated with a 56% reduction in the relative risk of ESS. In contrast, a cortical stroke lesion was associated with a 2.83-fold increased risk.
Since this wasn’t a randomized trial of statin therapy, Dr. Matsubara and his coinvestigators felt the need to go further in analyzing the data. After extensive propensity score matching for atrial fibrillation, current smoking, systolic blood pressure, the presence or absence of a cortical stroke lesion, large vessel stenosis, and other possible confounders, they were left with two closely comparable groups: 886 statin-treated stroke patients and an equal number who were not on statin therapy during their acute stroke management. The key finding: The risk of ESS was reduced by a whopping 77% in the patients on statin therapy.
The neurologist observed that these new findings in acute ischemic stroke patients are consistent with an earlier study in a U.S. Veterans Affairs population, which demonstrated that statin therapy was associated with a significantly lower risk of new-onset geriatric epilepsy (J Am Geriatr Soc. 2009 Feb;57[2]:237-42).
As to the possible mechanism by which statins may protect against ESS, Dr. Matsubara noted that acute ischemic stroke causes toxic neuronal excitation because of blood-brain barrier disruption, ion channel dysfunction, altered gene expression, and increased release of neurotransmitters. In animal models, statins provide a neuroprotective effect by reducing glutamate levels, activating endothelial nitric oxide synthase, and inhibiting production of interleukin-6, tumor necrosis factor-alpha, and other inflammatory cytokines.
Asked about the intensity of the statin therapy, Dr. Matsubara replied that the target was typically an LDL cholesterol below 100 mg/dL.
He reported having no financial conflicts regarding the study, conducted free of commercial support.
SOURCE: Matsubara S et al. IEC 219, Abstract P002.
BANGKOK – Statin therapy, even when initiated only upon hospitalization for acute ischemic stroke, was associated with a striking reduction in the risk of early poststroke symptomatic seizure in a large observational study.
Using propensity-score matching to control for potential confounders, use of a statin during acute stroke management was associated with a “robust” 77% reduction in the risk of developing a symptomatic seizure within 7 days after hospital admission, Soichiro Matsubara, MD, reported at the International Epilepsy Congress.
This is an important finding because early symptomatic seizure (ESS) occurs in 2%-7% of patients following an acute ischemic stroke. Moreover, an Italian meta-analysis concluded that ESS was associated with a 4.4-fold increased risk of developing poststroke epilepsy (Epilepsia. 2016 Aug;57[8]:1205-14), noted Dr. Matsubara, a neurologist at the National Cerebral and Cardiovascular Center in Suita, Japan, as well as at Kumamoto (Japan) University.
He presented a study of 2,969 consecutive acute ischemic stroke patients with no history of epilepsy who were admitted to the Japanese comprehensive stroke center, of whom 2.2% experienced ESS. At physician discretion, 19% of the ESS cohort were on a statin during their acute stroke management, as were 55% of the no-ESS group. Four-fifths of patients on a statin initiated the drug only upon hospital admission.
Strokes tended to be more severe in the ESS group, with a median initial National Institutes of Health Stroke Scale score of 12.5, compared with 4 in the seizure-free patients. A cortical stroke lesion was evident upon imaging in 89% of the ESS group and 55% of no-ESS patients. Among ESS patients, 46% had a cardiometabolic stroke, compared with 34% of the no-ESS cohort. Mean C-reactive protein levels and white blood cell counts were significantly higher in the ESS cohort as well. Their median hospital length of stay was 25.5 days, versus 18 days in the no-ESS group, Dr. Matsubara said at the congress sponsored by the International League Against Epilepsy.
Of the 76 ESSs that occurred in 66 patients, 37% were focal awareness seizures, 35% were focal to bilateral tonic-clonic seizures, and 28% were focal impaired awareness seizures.
In a multivariate analysis adjusted for age, sex, body mass index, stroke subtype, and other potential confounders, statin therapy during acute management of stroke was independently associated with a 56% reduction in the relative risk of ESS. In contrast, a cortical stroke lesion was associated with a 2.83-fold increased risk.
Since this wasn’t a randomized trial of statin therapy, Dr. Matsubara and his coinvestigators felt the need to go further in analyzing the data. After extensive propensity score matching for atrial fibrillation, current smoking, systolic blood pressure, the presence or absence of a cortical stroke lesion, large vessel stenosis, and other possible confounders, they were left with two closely comparable groups: 886 statin-treated stroke patients and an equal number who were not on statin therapy during their acute stroke management. The key finding: The risk of ESS was reduced by a whopping 77% in the patients on statin therapy.
The neurologist observed that these new findings in acute ischemic stroke patients are consistent with an earlier study in a U.S. Veterans Affairs population, which demonstrated that statin therapy was associated with a significantly lower risk of new-onset geriatric epilepsy (J Am Geriatr Soc. 2009 Feb;57[2]:237-42).
As to the possible mechanism by which statins may protect against ESS, Dr. Matsubara noted that acute ischemic stroke causes toxic neuronal excitation because of blood-brain barrier disruption, ion channel dysfunction, altered gene expression, and increased release of neurotransmitters. In animal models, statins provide a neuroprotective effect by reducing glutamate levels, activating endothelial nitric oxide synthase, and inhibiting production of interleukin-6, tumor necrosis factor-alpha, and other inflammatory cytokines.
Asked about the intensity of the statin therapy, Dr. Matsubara replied that the target was typically an LDL cholesterol below 100 mg/dL.
He reported having no financial conflicts regarding the study, conducted free of commercial support.
SOURCE: Matsubara S et al. IEC 219, Abstract P002.
BANGKOK – Statin therapy, even when initiated only upon hospitalization for acute ischemic stroke, was associated with a striking reduction in the risk of early poststroke symptomatic seizure in a large observational study.
Using propensity-score matching to control for potential confounders, use of a statin during acute stroke management was associated with a “robust” 77% reduction in the risk of developing a symptomatic seizure within 7 days after hospital admission, Soichiro Matsubara, MD, reported at the International Epilepsy Congress.
This is an important finding because early symptomatic seizure (ESS) occurs in 2%-7% of patients following an acute ischemic stroke. Moreover, an Italian meta-analysis concluded that ESS was associated with a 4.4-fold increased risk of developing poststroke epilepsy (Epilepsia. 2016 Aug;57[8]:1205-14), noted Dr. Matsubara, a neurologist at the National Cerebral and Cardiovascular Center in Suita, Japan, as well as at Kumamoto (Japan) University.
He presented a study of 2,969 consecutive acute ischemic stroke patients with no history of epilepsy who were admitted to the Japanese comprehensive stroke center, of whom 2.2% experienced ESS. At physician discretion, 19% of the ESS cohort were on a statin during their acute stroke management, as were 55% of the no-ESS group. Four-fifths of patients on a statin initiated the drug only upon hospital admission.
Strokes tended to be more severe in the ESS group, with a median initial National Institutes of Health Stroke Scale score of 12.5, compared with 4 in the seizure-free patients. A cortical stroke lesion was evident upon imaging in 89% of the ESS group and 55% of no-ESS patients. Among ESS patients, 46% had a cardiometabolic stroke, compared with 34% of the no-ESS cohort. Mean C-reactive protein levels and white blood cell counts were significantly higher in the ESS cohort as well. Their median hospital length of stay was 25.5 days, versus 18 days in the no-ESS group, Dr. Matsubara said at the congress sponsored by the International League Against Epilepsy.
Of the 76 ESSs that occurred in 66 patients, 37% were focal awareness seizures, 35% were focal to bilateral tonic-clonic seizures, and 28% were focal impaired awareness seizures.
In a multivariate analysis adjusted for age, sex, body mass index, stroke subtype, and other potential confounders, statin therapy during acute management of stroke was independently associated with a 56% reduction in the relative risk of ESS. In contrast, a cortical stroke lesion was associated with a 2.83-fold increased risk.
Since this wasn’t a randomized trial of statin therapy, Dr. Matsubara and his coinvestigators felt the need to go further in analyzing the data. After extensive propensity score matching for atrial fibrillation, current smoking, systolic blood pressure, the presence or absence of a cortical stroke lesion, large vessel stenosis, and other possible confounders, they were left with two closely comparable groups: 886 statin-treated stroke patients and an equal number who were not on statin therapy during their acute stroke management. The key finding: The risk of ESS was reduced by a whopping 77% in the patients on statin therapy.
The neurologist observed that these new findings in acute ischemic stroke patients are consistent with an earlier study in a U.S. Veterans Affairs population, which demonstrated that statin therapy was associated with a significantly lower risk of new-onset geriatric epilepsy (J Am Geriatr Soc. 2009 Feb;57[2]:237-42).
As to the possible mechanism by which statins may protect against ESS, Dr. Matsubara noted that acute ischemic stroke causes toxic neuronal excitation because of blood-brain barrier disruption, ion channel dysfunction, altered gene expression, and increased release of neurotransmitters. In animal models, statins provide a neuroprotective effect by reducing glutamate levels, activating endothelial nitric oxide synthase, and inhibiting production of interleukin-6, tumor necrosis factor-alpha, and other inflammatory cytokines.
Asked about the intensity of the statin therapy, Dr. Matsubara replied that the target was typically an LDL cholesterol below 100 mg/dL.
He reported having no financial conflicts regarding the study, conducted free of commercial support.
SOURCE: Matsubara S et al. IEC 219, Abstract P002.
REPORTING FROM IEC 2019
BMI screening trigger for type 2 diabetes is unreliable for at-risk black, Hispanic adults
SAN FRANCISCO – according to findings presented at the annual scientific sessions of the American Diabetes Association.
The conclusions come from a review of 5,656 participants aged 45-84 years in the Multi-Ethnic Study of Atherosclerosis (MESA), an ongoing prospective cohort study. The participants had no signs of cardiovascular disease at enrollment.
The goal of the study reported at the meeting was to see if current ADA screening guidelines are appropriate across racial groups in an increasingly diverse United States. The guidelines recommend body mass index (BMI) as a trigger for screening for type 2 diabetes. The current advice is to screen any adult who has a BMI at or above 25 kg/m2 (23 kg/m2 for Asian Americans) and at least one risk factor for type 2 diabetes, such as hypertension, dyslipidemia, or physical inactivity.
Being black, Asian American, Hispanic, Pacific Islander, or American Indian is itself a risk factor, so “someone from a minority group just needs to meet the BMI criteria,” said lead investigator Luis Rodriguez, a PhD candidate in epidemiology at the University of California, San Francisco.
He and his colleagues focused on 2,383 white, 653 Chinese American, 1,459 black, and 1,161 Hispanic participants in MESA who did not have type 2 diabetes at baseline. Participants were in their early 60s at baseline, on average, and just more than half of them were women. They had five medical exams between 2000 and 2012. The investigators calculated the BMI at which each group hit a 10% risk of developing diabetes within the next 10 years.
In general, the lines crossed at a BMI of about 23 kg/m2 for Chinese Americans; 25 kg/m2 for black and Hispanic participants; and 27 kg/m2 for white participants, which is consistent with ADA advice. The guideline cut points are “appropriate for population-based screening where you may not know if the person in front of you has any diabetes risk factors,” Mr. Rodriguez said.
With known risk factors, however, BMI didn’t hold up. Black participants with one or more risk factor hit the 10% mark at a BMI of 24.7 kg/m2, Hispanics at 23.8 kg/m2, and Chinese Americans at 21.7 kg/m2, all of which are below the recommended cut-points.
“Almost 80%-90% of participants” in minority groups “who had one or more risk factors were above the 10% threshold, so if they have at least one factor, they should pretty much be screened for diabetes, regardless of BMI,” he said.
The 25-kg/m2 threshold worked for white participants; the investigators found that with one or more risk factors, white participants crossed the 10% line at a BMI of 26.2 kg/m2. In addition, white participants with no diabetes risk factors crossed the 10% mark at around a BMI of 30 kg/m2, which the investigators suggested as an appropriate screening trigger.
Participants were in their early 60s at baseline, on average, and just more than half of them were women. In all, 696 cases of type 2 diabetes were diagnosed over a median follow-up of about 9 years, which translated to an incidence rate of 11 cases per 1,000 person-years in white participants, 16 cases for Chinese Americans, 21 for black participants, and 22 for Hispanic participants. Well over half of the participants were overweight or obese at baseline, including about 80% of black and Hispanic participants.
The sample size reported in the abstract was smaller than that in the final presentation because the investigators did not adjust for diet in the final presentation, Mr. Rodriguez explained. Because some study participants did not report diet, by excluding diet from the model adjustment, the number of participants increased, as reflected in this text. Adjusting for diet did not alter the findings.
The National Heart, Lung, and Blood Institute sponsors MESA. Mr. Rodriguez was supported by a grant from the National Institutes of Health/National Institute of Diabetes and Kidney Disease. The other investigators reported having no disclosures.
SOURCE: Rodriguez L et al. ADA 2019, Abstract 115-OR.
SAN FRANCISCO – according to findings presented at the annual scientific sessions of the American Diabetes Association.
The conclusions come from a review of 5,656 participants aged 45-84 years in the Multi-Ethnic Study of Atherosclerosis (MESA), an ongoing prospective cohort study. The participants had no signs of cardiovascular disease at enrollment.
The goal of the study reported at the meeting was to see if current ADA screening guidelines are appropriate across racial groups in an increasingly diverse United States. The guidelines recommend body mass index (BMI) as a trigger for screening for type 2 diabetes. The current advice is to screen any adult who has a BMI at or above 25 kg/m2 (23 kg/m2 for Asian Americans) and at least one risk factor for type 2 diabetes, such as hypertension, dyslipidemia, or physical inactivity.
Being black, Asian American, Hispanic, Pacific Islander, or American Indian is itself a risk factor, so “someone from a minority group just needs to meet the BMI criteria,” said lead investigator Luis Rodriguez, a PhD candidate in epidemiology at the University of California, San Francisco.
He and his colleagues focused on 2,383 white, 653 Chinese American, 1,459 black, and 1,161 Hispanic participants in MESA who did not have type 2 diabetes at baseline. Participants were in their early 60s at baseline, on average, and just more than half of them were women. They had five medical exams between 2000 and 2012. The investigators calculated the BMI at which each group hit a 10% risk of developing diabetes within the next 10 years.
In general, the lines crossed at a BMI of about 23 kg/m2 for Chinese Americans; 25 kg/m2 for black and Hispanic participants; and 27 kg/m2 for white participants, which is consistent with ADA advice. The guideline cut points are “appropriate for population-based screening where you may not know if the person in front of you has any diabetes risk factors,” Mr. Rodriguez said.
With known risk factors, however, BMI didn’t hold up. Black participants with one or more risk factor hit the 10% mark at a BMI of 24.7 kg/m2, Hispanics at 23.8 kg/m2, and Chinese Americans at 21.7 kg/m2, all of which are below the recommended cut-points.
“Almost 80%-90% of participants” in minority groups “who had one or more risk factors were above the 10% threshold, so if they have at least one factor, they should pretty much be screened for diabetes, regardless of BMI,” he said.
The 25-kg/m2 threshold worked for white participants; the investigators found that with one or more risk factors, white participants crossed the 10% line at a BMI of 26.2 kg/m2. In addition, white participants with no diabetes risk factors crossed the 10% mark at around a BMI of 30 kg/m2, which the investigators suggested as an appropriate screening trigger.
Participants were in their early 60s at baseline, on average, and just more than half of them were women. In all, 696 cases of type 2 diabetes were diagnosed over a median follow-up of about 9 years, which translated to an incidence rate of 11 cases per 1,000 person-years in white participants, 16 cases for Chinese Americans, 21 for black participants, and 22 for Hispanic participants. Well over half of the participants were overweight or obese at baseline, including about 80% of black and Hispanic participants.
The sample size reported in the abstract was smaller than that in the final presentation because the investigators did not adjust for diet in the final presentation, Mr. Rodriguez explained. Because some study participants did not report diet, by excluding diet from the model adjustment, the number of participants increased, as reflected in this text. Adjusting for diet did not alter the findings.
The National Heart, Lung, and Blood Institute sponsors MESA. Mr. Rodriguez was supported by a grant from the National Institutes of Health/National Institute of Diabetes and Kidney Disease. The other investigators reported having no disclosures.
SOURCE: Rodriguez L et al. ADA 2019, Abstract 115-OR.
SAN FRANCISCO – according to findings presented at the annual scientific sessions of the American Diabetes Association.
The conclusions come from a review of 5,656 participants aged 45-84 years in the Multi-Ethnic Study of Atherosclerosis (MESA), an ongoing prospective cohort study. The participants had no signs of cardiovascular disease at enrollment.
The goal of the study reported at the meeting was to see if current ADA screening guidelines are appropriate across racial groups in an increasingly diverse United States. The guidelines recommend body mass index (BMI) as a trigger for screening for type 2 diabetes. The current advice is to screen any adult who has a BMI at or above 25 kg/m2 (23 kg/m2 for Asian Americans) and at least one risk factor for type 2 diabetes, such as hypertension, dyslipidemia, or physical inactivity.
Being black, Asian American, Hispanic, Pacific Islander, or American Indian is itself a risk factor, so “someone from a minority group just needs to meet the BMI criteria,” said lead investigator Luis Rodriguez, a PhD candidate in epidemiology at the University of California, San Francisco.
He and his colleagues focused on 2,383 white, 653 Chinese American, 1,459 black, and 1,161 Hispanic participants in MESA who did not have type 2 diabetes at baseline. Participants were in their early 60s at baseline, on average, and just more than half of them were women. They had five medical exams between 2000 and 2012. The investigators calculated the BMI at which each group hit a 10% risk of developing diabetes within the next 10 years.
In general, the lines crossed at a BMI of about 23 kg/m2 for Chinese Americans; 25 kg/m2 for black and Hispanic participants; and 27 kg/m2 for white participants, which is consistent with ADA advice. The guideline cut points are “appropriate for population-based screening where you may not know if the person in front of you has any diabetes risk factors,” Mr. Rodriguez said.
With known risk factors, however, BMI didn’t hold up. Black participants with one or more risk factor hit the 10% mark at a BMI of 24.7 kg/m2, Hispanics at 23.8 kg/m2, and Chinese Americans at 21.7 kg/m2, all of which are below the recommended cut-points.
“Almost 80%-90% of participants” in minority groups “who had one or more risk factors were above the 10% threshold, so if they have at least one factor, they should pretty much be screened for diabetes, regardless of BMI,” he said.
The 25-kg/m2 threshold worked for white participants; the investigators found that with one or more risk factors, white participants crossed the 10% line at a BMI of 26.2 kg/m2. In addition, white participants with no diabetes risk factors crossed the 10% mark at around a BMI of 30 kg/m2, which the investigators suggested as an appropriate screening trigger.
Participants were in their early 60s at baseline, on average, and just more than half of them were women. In all, 696 cases of type 2 diabetes were diagnosed over a median follow-up of about 9 years, which translated to an incidence rate of 11 cases per 1,000 person-years in white participants, 16 cases for Chinese Americans, 21 for black participants, and 22 for Hispanic participants. Well over half of the participants were overweight or obese at baseline, including about 80% of black and Hispanic participants.
The sample size reported in the abstract was smaller than that in the final presentation because the investigators did not adjust for diet in the final presentation, Mr. Rodriguez explained. Because some study participants did not report diet, by excluding diet from the model adjustment, the number of participants increased, as reflected in this text. Adjusting for diet did not alter the findings.
The National Heart, Lung, and Blood Institute sponsors MESA. Mr. Rodriguez was supported by a grant from the National Institutes of Health/National Institute of Diabetes and Kidney Disease. The other investigators reported having no disclosures.
SOURCE: Rodriguez L et al. ADA 2019, Abstract 115-OR.
REPORTING FROM ADA 2019
Key clinical point:
Major finding: Black participants with one or more risk factors had a 10% or greater risk of type 2 diabetes at a BMI of 24.7 kg/m2; Hispanic participants had the same risk at 23.8 kg/m2; and Chinese Americans at 21.7 kg/mg2, all of which are below the BMI cut points recommended by the ADA.
Study details: Review of 5,656 participants in the Multi-Ethnic Study of Atherosclerosis .
Disclosures: The National Heart, Lung, and Blood Institute sponsors MESA. Mr. Rodriguez was supported by grant from the National Institutes of Health/National Institute of Diabetes and Kidney Disease. The other investigators reported having no disclosures.
Source: Rodriguez L et al. ADA 2019, Abstract 115-OR.
Higher omega-3 fatty acid levels cut heart failure risk
Higher levels of eicosapentaenoic acid, a type of omega-3 polyunsaturated fatty acid, were associated with a significantly reduced risk of heart failure in a large, multi-ethnic cohort of adults in the United States.
Despite the potential benefits of omega-3s eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for heart health, their use has been controversial, although data in a mouse model showed that dietary EPA was protective against heart failure, wrote Robert C. Block, MD, of the University of Rochester (N.Y.), and colleagues. Their report is in the Journal of the American College of Cardiology.
To examine the impact of EPA on heart failure in humans, the researchers used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a longitudinal cohort study of U.S. adults, including those who are African American, Hispanic, Asian, and white.
The researchers included 6,562 MESA participants aged 45-84 years from six communities. Participants underwent a baseline exam between July 2000 and July 2002 that included phospholipid measurements used to identify plasma EPA percentage, and they completed study visits approximately every other year for a median follow-up of 13 years.
A total of 292 heart failure events occurred during the follow-up period: 128 with reduced ejection fraction (EF less than 45%), 110 with preserved ejection fraction (EF at least 45%), and 54 with unknown EF status.
The percent EPA for individuals without heart failure was significantly higher compared with those with heart failure (0.76% vs. 0.69%, P =.005). The association remained significant after the researchers controlled for age, sex, race, body mass index, smoking, diabetes, blood pressure, lipids and lipid-lowering drugs, albuminuria, and the lead fatty acid (defined as the fatty acid with the largest in-cluster correlation).
An EPA level greater than 2.5% was considered sufficient to prevent heart failure based on prior definitions. A total of 73% of the participants had insufficient EPA (less than 1.0%), 2.4% had marginal levels (1.0%-2.5%), and 4.5% had sufficient levels. However, given that EPA levels can be easily and safely increased with the consumption of seafood or fish oil capsules, increasing EPA is a feasible heart failure prevention strategy, the researchers said.
The study included 2,532 white, 1,794 black, 1,442 Hispanic, and 794 Chinese participants. Overall, the fewest Hispanic participants met the criteria for sufficient EPA (1.4%), followed by black (4.4%), white (4.9%), and Chinese participants (9.8%).
The study findings were limited by several factors, including relatively few participants with preserved ejection fractions and sufficient EPA levels, as well as the inability to account for changes in omega-3 levels and other risk factors over time, the researchers noted.
“We consider this study to strongly determine a benefit of EPA exists, but insufficient to determine whether a threshold for %EPA exists near 3%,” they said. They proposed a follow-up study including individuals with higher levels of EPA to better detect a protective effect.
Lead author Dr. Block had no financial conflicts to disclose. Several coauthors received honoraria from Amarin Pharmaceuticals. The study was funded in part by the National Heart, Lung, and Blood Institute.
The study findings suggest that revisiting omega-3 fatty acids to improve outcomes in patients with or at risk of cardiovascular disease may be worthwhile. Not only did the study predict heart failure in a range of ethnicities, but the same authors showed previously in animal models that these dietary supplements can preserve left ventricular function and reduce interstitial fibrosis.
The question is: Is it sufficient to give dietary recommendations of an increased fish consumption, or do we need to take purified pharmaceutical supplements such as those tested in trials? In other words, shall we have to go to the fish market or to the pharmacy to elevate our circulating levels of omega-3 fatty acids and, in this way, to try to prevent (or treat) HF?
The answer, at least in part, lies in additional large, randomized clinical trials that test high doses of omega-3 fatty acids along and combined with pharmacological and nonpharmacological treatments. Considering the very favorable tolerability and safety profile of this therapeutic approach, any positive results of these trials could provide us with an additional strategy to improve the outcomes of patients with HF or at high risk to develop it.
Aldo P. Maggioni, MD, of the ANMCO Research Center Heart Care Foundation, in Florence, Italy, made these remarks in an editorial. He disclosed honoraria for participation in committees of studies sponsored by Bayer, Novartis, and Fresenius.
The study findings suggest that revisiting omega-3 fatty acids to improve outcomes in patients with or at risk of cardiovascular disease may be worthwhile. Not only did the study predict heart failure in a range of ethnicities, but the same authors showed previously in animal models that these dietary supplements can preserve left ventricular function and reduce interstitial fibrosis.
The question is: Is it sufficient to give dietary recommendations of an increased fish consumption, or do we need to take purified pharmaceutical supplements such as those tested in trials? In other words, shall we have to go to the fish market or to the pharmacy to elevate our circulating levels of omega-3 fatty acids and, in this way, to try to prevent (or treat) HF?
The answer, at least in part, lies in additional large, randomized clinical trials that test high doses of omega-3 fatty acids along and combined with pharmacological and nonpharmacological treatments. Considering the very favorable tolerability and safety profile of this therapeutic approach, any positive results of these trials could provide us with an additional strategy to improve the outcomes of patients with HF or at high risk to develop it.
Aldo P. Maggioni, MD, of the ANMCO Research Center Heart Care Foundation, in Florence, Italy, made these remarks in an editorial. He disclosed honoraria for participation in committees of studies sponsored by Bayer, Novartis, and Fresenius.
The study findings suggest that revisiting omega-3 fatty acids to improve outcomes in patients with or at risk of cardiovascular disease may be worthwhile. Not only did the study predict heart failure in a range of ethnicities, but the same authors showed previously in animal models that these dietary supplements can preserve left ventricular function and reduce interstitial fibrosis.
The question is: Is it sufficient to give dietary recommendations of an increased fish consumption, or do we need to take purified pharmaceutical supplements such as those tested in trials? In other words, shall we have to go to the fish market or to the pharmacy to elevate our circulating levels of omega-3 fatty acids and, in this way, to try to prevent (or treat) HF?
The answer, at least in part, lies in additional large, randomized clinical trials that test high doses of omega-3 fatty acids along and combined with pharmacological and nonpharmacological treatments. Considering the very favorable tolerability and safety profile of this therapeutic approach, any positive results of these trials could provide us with an additional strategy to improve the outcomes of patients with HF or at high risk to develop it.
Aldo P. Maggioni, MD, of the ANMCO Research Center Heart Care Foundation, in Florence, Italy, made these remarks in an editorial. He disclosed honoraria for participation in committees of studies sponsored by Bayer, Novartis, and Fresenius.
Higher levels of eicosapentaenoic acid, a type of omega-3 polyunsaturated fatty acid, were associated with a significantly reduced risk of heart failure in a large, multi-ethnic cohort of adults in the United States.
Despite the potential benefits of omega-3s eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for heart health, their use has been controversial, although data in a mouse model showed that dietary EPA was protective against heart failure, wrote Robert C. Block, MD, of the University of Rochester (N.Y.), and colleagues. Their report is in the Journal of the American College of Cardiology.
To examine the impact of EPA on heart failure in humans, the researchers used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a longitudinal cohort study of U.S. adults, including those who are African American, Hispanic, Asian, and white.
The researchers included 6,562 MESA participants aged 45-84 years from six communities. Participants underwent a baseline exam between July 2000 and July 2002 that included phospholipid measurements used to identify plasma EPA percentage, and they completed study visits approximately every other year for a median follow-up of 13 years.
A total of 292 heart failure events occurred during the follow-up period: 128 with reduced ejection fraction (EF less than 45%), 110 with preserved ejection fraction (EF at least 45%), and 54 with unknown EF status.
The percent EPA for individuals without heart failure was significantly higher compared with those with heart failure (0.76% vs. 0.69%, P =.005). The association remained significant after the researchers controlled for age, sex, race, body mass index, smoking, diabetes, blood pressure, lipids and lipid-lowering drugs, albuminuria, and the lead fatty acid (defined as the fatty acid with the largest in-cluster correlation).
An EPA level greater than 2.5% was considered sufficient to prevent heart failure based on prior definitions. A total of 73% of the participants had insufficient EPA (less than 1.0%), 2.4% had marginal levels (1.0%-2.5%), and 4.5% had sufficient levels. However, given that EPA levels can be easily and safely increased with the consumption of seafood or fish oil capsules, increasing EPA is a feasible heart failure prevention strategy, the researchers said.
The study included 2,532 white, 1,794 black, 1,442 Hispanic, and 794 Chinese participants. Overall, the fewest Hispanic participants met the criteria for sufficient EPA (1.4%), followed by black (4.4%), white (4.9%), and Chinese participants (9.8%).
The study findings were limited by several factors, including relatively few participants with preserved ejection fractions and sufficient EPA levels, as well as the inability to account for changes in omega-3 levels and other risk factors over time, the researchers noted.
“We consider this study to strongly determine a benefit of EPA exists, but insufficient to determine whether a threshold for %EPA exists near 3%,” they said. They proposed a follow-up study including individuals with higher levels of EPA to better detect a protective effect.
Lead author Dr. Block had no financial conflicts to disclose. Several coauthors received honoraria from Amarin Pharmaceuticals. The study was funded in part by the National Heart, Lung, and Blood Institute.
Higher levels of eicosapentaenoic acid, a type of omega-3 polyunsaturated fatty acid, were associated with a significantly reduced risk of heart failure in a large, multi-ethnic cohort of adults in the United States.
Despite the potential benefits of omega-3s eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for heart health, their use has been controversial, although data in a mouse model showed that dietary EPA was protective against heart failure, wrote Robert C. Block, MD, of the University of Rochester (N.Y.), and colleagues. Their report is in the Journal of the American College of Cardiology.
To examine the impact of EPA on heart failure in humans, the researchers used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a longitudinal cohort study of U.S. adults, including those who are African American, Hispanic, Asian, and white.
The researchers included 6,562 MESA participants aged 45-84 years from six communities. Participants underwent a baseline exam between July 2000 and July 2002 that included phospholipid measurements used to identify plasma EPA percentage, and they completed study visits approximately every other year for a median follow-up of 13 years.
A total of 292 heart failure events occurred during the follow-up period: 128 with reduced ejection fraction (EF less than 45%), 110 with preserved ejection fraction (EF at least 45%), and 54 with unknown EF status.
The percent EPA for individuals without heart failure was significantly higher compared with those with heart failure (0.76% vs. 0.69%, P =.005). The association remained significant after the researchers controlled for age, sex, race, body mass index, smoking, diabetes, blood pressure, lipids and lipid-lowering drugs, albuminuria, and the lead fatty acid (defined as the fatty acid with the largest in-cluster correlation).
An EPA level greater than 2.5% was considered sufficient to prevent heart failure based on prior definitions. A total of 73% of the participants had insufficient EPA (less than 1.0%), 2.4% had marginal levels (1.0%-2.5%), and 4.5% had sufficient levels. However, given that EPA levels can be easily and safely increased with the consumption of seafood or fish oil capsules, increasing EPA is a feasible heart failure prevention strategy, the researchers said.
The study included 2,532 white, 1,794 black, 1,442 Hispanic, and 794 Chinese participants. Overall, the fewest Hispanic participants met the criteria for sufficient EPA (1.4%), followed by black (4.4%), white (4.9%), and Chinese participants (9.8%).
The study findings were limited by several factors, including relatively few participants with preserved ejection fractions and sufficient EPA levels, as well as the inability to account for changes in omega-3 levels and other risk factors over time, the researchers noted.
“We consider this study to strongly determine a benefit of EPA exists, but insufficient to determine whether a threshold for %EPA exists near 3%,” they said. They proposed a follow-up study including individuals with higher levels of EPA to better detect a protective effect.
Lead author Dr. Block had no financial conflicts to disclose. Several coauthors received honoraria from Amarin Pharmaceuticals. The study was funded in part by the National Heart, Lung, and Blood Institute.
FROM JACC
Key clinical point: Adults with high levels of eicosapentaenoic acid had significantly lower risk of heart failure than did those with lower levels of EPA.
Major finding: The percent EPA was 0.76% for individuals without heart failure vs. 0.69% for those who suffered heart failure (P = .005).
Study details: An analysis of 6,562 adults aged 45-84 years in the Multi-Ethnic Study of Atherosclerosis.
Disclosures: Lead author Dr. Block had no financial conflicts to disclose. Several coauthors received honoraria from Amarin Pharmaceuticals. The study was funded in part by the National Heart, Lung, and Blood Institute.
New findings cast more doubt on ‘fat-but-fit’ theory
SAN FRANCISCO – Can you be “fat but fit” if you’re obese but don’t suffer from metabolic syndrome? Some advocates have claimed you can, but new findings presented at the annual scientific sessions of the American Diabetes Association provide more evidence that those extra pounds translate to extra cardiac risk.
Fat-but-fit is a misnomer, Yvonne Commodore-Mensah, PhD, RN, assistant professor at Johns Hopkins School of Nursing, Baltimore, said in an interview. “The metabolically healthy obese are not so healthy. [We found] they had a higher risk of heart disease than people who were metabolically healthy and nonobese.”
Studies began supporting the fat-but-fit “paradox” in the late 1990s. They showed “that all-cause and CVD [cardiovascular] mortality risk in obese individuals, as defined by body mass index (BMI), body fat percentage, or waist circumference, who are fit (i.e., cardiorespiratory fitness level above the age-specific and sex-specific 20th percentile) is not significantly different from their normal-weight and fit counterparts” (Br J Sports Med. 2018;52[3]:151-3).
However, a 2017 study had found that “metabolically healthy obese individuals had a higher risk of coronary heart disease, cerebrovascular disease, and heart failure [compared with] normal weight, metabolically healthy individuals” (J Am Coll Cardiol. 2017;70[12]:1429-37). And a 2016 meta-analysis of 22 studies had produced similar results but also found that metabolically healthy obese individuals were better off, cardiac-health–wise, than those of normal weight who were metabolically unhealthy (Eur J Prev Cardiol. 2016;23[9]:956-66).
Dr. Commodore-Mensah and colleagues sought to establish through their study whether there was evidence of subclinical heart disease in people who are considered obese but metabolically healthy (Abstract 272-OR).
They tracked 11,884 participants in the Atherosclerosis Risk in Communities Study (ARIC) from 1990-1992 to 2016-2018. The study, which continues today, includes participants in suburban Minneapolis; Jackson, Miss.; Forsyth County, N.C.; and Washington County, Md.
None of the participants had previous cardiovascular disease at baseline (1990-1992). The researchers divided the participants into four groups at baseline: Nonobese (with metabolic syndrome, 20% of the total number of participants; or without metabolic syndrome, 51%) and obese (with metabolic syndrome, 20%; or without metabolic syndrome, 9%).
The average age range in the groups was 56-57 years. The percentage of women in the groups ranged from 53% to 58%, except for the obese and metabolically healthy group (73%). The percentage of black participants in the groups ranged from 17% (nonobese, metabolically unhealthy) to 45% (obese, metabolically healthy).
“People who were younger, women, and black were more likely to be classified as metabolically healthy obese,” Dr. Commodore-Mensah said.
According to one adjusted model with a median follow-up of 16 years and a total of 3,560 events, obese participants had a higher risk of incident cardiovascular disease, compared with their nonobese counterparts, regardless of whether they had metabolic syndrome.
When compared with the nonobese, metabolically healthy group, the risk grew in the nonobese, metabolically unhealthy group (hazard ratio, .24; 95% confidence interval, 1.12-1.36), as well as in the obese, metabolically healthy (HR, 1.33; 95% CI, 1.15-1.53) and the obese, metabolically unhealthy (HR, 2.11; 95% CI, 1.90-2.35) groups.
The researchers also focused on the cardiac biomarker known as high-sensitive cardiac troponin T (hs-cTnT), which indicates chronic myocardial damage. “This biomarker provides us with a window to the heart,” Dr. Commodore-Mensah said.
According to previous findings reported in 2014, ARIC participants who had hs-cTnT levels of 14 ng/L or higher were much more likely than were those with undetectable levels to suffer from heart failure, death from any cause, and coronary heart disease (JACC Heart Fail. 2014;2[6]:600-7).
Based on an analysis of the hs-cTnT levels in the present study, the researchers believe obese, metabolically healthy participants fell in the intermediate range of excess subclinical myocardial damage, between the nonobese and the obese participants who are also metabolically unhealthy.
“This group is not protected from heart disease,” Dr. Commodore-Mensah said. “They should be targeted, and they would benefit from behavioral changes, such as modifying their diet and increasing physical activity levels.”
The study is funded by the National Institutes of Health. Dr. Commodore-Mensah and six coauthors reported no relevant disclosures. Two coauthors reported various disclosures.
SAN FRANCISCO – Can you be “fat but fit” if you’re obese but don’t suffer from metabolic syndrome? Some advocates have claimed you can, but new findings presented at the annual scientific sessions of the American Diabetes Association provide more evidence that those extra pounds translate to extra cardiac risk.
Fat-but-fit is a misnomer, Yvonne Commodore-Mensah, PhD, RN, assistant professor at Johns Hopkins School of Nursing, Baltimore, said in an interview. “The metabolically healthy obese are not so healthy. [We found] they had a higher risk of heart disease than people who were metabolically healthy and nonobese.”
Studies began supporting the fat-but-fit “paradox” in the late 1990s. They showed “that all-cause and CVD [cardiovascular] mortality risk in obese individuals, as defined by body mass index (BMI), body fat percentage, or waist circumference, who are fit (i.e., cardiorespiratory fitness level above the age-specific and sex-specific 20th percentile) is not significantly different from their normal-weight and fit counterparts” (Br J Sports Med. 2018;52[3]:151-3).
However, a 2017 study had found that “metabolically healthy obese individuals had a higher risk of coronary heart disease, cerebrovascular disease, and heart failure [compared with] normal weight, metabolically healthy individuals” (J Am Coll Cardiol. 2017;70[12]:1429-37). And a 2016 meta-analysis of 22 studies had produced similar results but also found that metabolically healthy obese individuals were better off, cardiac-health–wise, than those of normal weight who were metabolically unhealthy (Eur J Prev Cardiol. 2016;23[9]:956-66).
Dr. Commodore-Mensah and colleagues sought to establish through their study whether there was evidence of subclinical heart disease in people who are considered obese but metabolically healthy (Abstract 272-OR).
They tracked 11,884 participants in the Atherosclerosis Risk in Communities Study (ARIC) from 1990-1992 to 2016-2018. The study, which continues today, includes participants in suburban Minneapolis; Jackson, Miss.; Forsyth County, N.C.; and Washington County, Md.
None of the participants had previous cardiovascular disease at baseline (1990-1992). The researchers divided the participants into four groups at baseline: Nonobese (with metabolic syndrome, 20% of the total number of participants; or without metabolic syndrome, 51%) and obese (with metabolic syndrome, 20%; or without metabolic syndrome, 9%).
The average age range in the groups was 56-57 years. The percentage of women in the groups ranged from 53% to 58%, except for the obese and metabolically healthy group (73%). The percentage of black participants in the groups ranged from 17% (nonobese, metabolically unhealthy) to 45% (obese, metabolically healthy).
“People who were younger, women, and black were more likely to be classified as metabolically healthy obese,” Dr. Commodore-Mensah said.
According to one adjusted model with a median follow-up of 16 years and a total of 3,560 events, obese participants had a higher risk of incident cardiovascular disease, compared with their nonobese counterparts, regardless of whether they had metabolic syndrome.
When compared with the nonobese, metabolically healthy group, the risk grew in the nonobese, metabolically unhealthy group (hazard ratio, .24; 95% confidence interval, 1.12-1.36), as well as in the obese, metabolically healthy (HR, 1.33; 95% CI, 1.15-1.53) and the obese, metabolically unhealthy (HR, 2.11; 95% CI, 1.90-2.35) groups.
The researchers also focused on the cardiac biomarker known as high-sensitive cardiac troponin T (hs-cTnT), which indicates chronic myocardial damage. “This biomarker provides us with a window to the heart,” Dr. Commodore-Mensah said.
According to previous findings reported in 2014, ARIC participants who had hs-cTnT levels of 14 ng/L or higher were much more likely than were those with undetectable levels to suffer from heart failure, death from any cause, and coronary heart disease (JACC Heart Fail. 2014;2[6]:600-7).
Based on an analysis of the hs-cTnT levels in the present study, the researchers believe obese, metabolically healthy participants fell in the intermediate range of excess subclinical myocardial damage, between the nonobese and the obese participants who are also metabolically unhealthy.
“This group is not protected from heart disease,” Dr. Commodore-Mensah said. “They should be targeted, and they would benefit from behavioral changes, such as modifying their diet and increasing physical activity levels.”
The study is funded by the National Institutes of Health. Dr. Commodore-Mensah and six coauthors reported no relevant disclosures. Two coauthors reported various disclosures.
SAN FRANCISCO – Can you be “fat but fit” if you’re obese but don’t suffer from metabolic syndrome? Some advocates have claimed you can, but new findings presented at the annual scientific sessions of the American Diabetes Association provide more evidence that those extra pounds translate to extra cardiac risk.
Fat-but-fit is a misnomer, Yvonne Commodore-Mensah, PhD, RN, assistant professor at Johns Hopkins School of Nursing, Baltimore, said in an interview. “The metabolically healthy obese are not so healthy. [We found] they had a higher risk of heart disease than people who were metabolically healthy and nonobese.”
Studies began supporting the fat-but-fit “paradox” in the late 1990s. They showed “that all-cause and CVD [cardiovascular] mortality risk in obese individuals, as defined by body mass index (BMI), body fat percentage, or waist circumference, who are fit (i.e., cardiorespiratory fitness level above the age-specific and sex-specific 20th percentile) is not significantly different from their normal-weight and fit counterparts” (Br J Sports Med. 2018;52[3]:151-3).
However, a 2017 study had found that “metabolically healthy obese individuals had a higher risk of coronary heart disease, cerebrovascular disease, and heart failure [compared with] normal weight, metabolically healthy individuals” (J Am Coll Cardiol. 2017;70[12]:1429-37). And a 2016 meta-analysis of 22 studies had produced similar results but also found that metabolically healthy obese individuals were better off, cardiac-health–wise, than those of normal weight who were metabolically unhealthy (Eur J Prev Cardiol. 2016;23[9]:956-66).
Dr. Commodore-Mensah and colleagues sought to establish through their study whether there was evidence of subclinical heart disease in people who are considered obese but metabolically healthy (Abstract 272-OR).
They tracked 11,884 participants in the Atherosclerosis Risk in Communities Study (ARIC) from 1990-1992 to 2016-2018. The study, which continues today, includes participants in suburban Minneapolis; Jackson, Miss.; Forsyth County, N.C.; and Washington County, Md.
None of the participants had previous cardiovascular disease at baseline (1990-1992). The researchers divided the participants into four groups at baseline: Nonobese (with metabolic syndrome, 20% of the total number of participants; or without metabolic syndrome, 51%) and obese (with metabolic syndrome, 20%; or without metabolic syndrome, 9%).
The average age range in the groups was 56-57 years. The percentage of women in the groups ranged from 53% to 58%, except for the obese and metabolically healthy group (73%). The percentage of black participants in the groups ranged from 17% (nonobese, metabolically unhealthy) to 45% (obese, metabolically healthy).
“People who were younger, women, and black were more likely to be classified as metabolically healthy obese,” Dr. Commodore-Mensah said.
According to one adjusted model with a median follow-up of 16 years and a total of 3,560 events, obese participants had a higher risk of incident cardiovascular disease, compared with their nonobese counterparts, regardless of whether they had metabolic syndrome.
When compared with the nonobese, metabolically healthy group, the risk grew in the nonobese, metabolically unhealthy group (hazard ratio, .24; 95% confidence interval, 1.12-1.36), as well as in the obese, metabolically healthy (HR, 1.33; 95% CI, 1.15-1.53) and the obese, metabolically unhealthy (HR, 2.11; 95% CI, 1.90-2.35) groups.
The researchers also focused on the cardiac biomarker known as high-sensitive cardiac troponin T (hs-cTnT), which indicates chronic myocardial damage. “This biomarker provides us with a window to the heart,” Dr. Commodore-Mensah said.
According to previous findings reported in 2014, ARIC participants who had hs-cTnT levels of 14 ng/L or higher were much more likely than were those with undetectable levels to suffer from heart failure, death from any cause, and coronary heart disease (JACC Heart Fail. 2014;2[6]:600-7).
Based on an analysis of the hs-cTnT levels in the present study, the researchers believe obese, metabolically healthy participants fell in the intermediate range of excess subclinical myocardial damage, between the nonobese and the obese participants who are also metabolically unhealthy.
“This group is not protected from heart disease,” Dr. Commodore-Mensah said. “They should be targeted, and they would benefit from behavioral changes, such as modifying their diet and increasing physical activity levels.”
The study is funded by the National Institutes of Health. Dr. Commodore-Mensah and six coauthors reported no relevant disclosures. Two coauthors reported various disclosures.
REPORTING FROM ADA 2019
Could some elderly skip statins based on negative risk markers?
Older individuals with certain negative risk markers have a very low risk of atherosclerotic cardiovascular disease, raising the possibility that some could forgo preventive treatment even if it’s indicated by current standards of risk assessment.
Low levels of coronary artery calcification (CAC), low galectin-3 levels, and absence of carotid plaque were all linked to a lower likelihood of disease than might be expected based on traditional risk assessment, according to the authors of analysis of a large, contemporary cohort of elderly individuals published in the Journal of the American College of Cardiology.
“Our results hold the potential to markedly improve statin allocation in elderly individuals by de-escalating or even withholding preventive therapy in elderly individuals at truly low atherosclerotic cardiovascular disease risk despite advancing age,“ wrote Martin Bødtker Mortensen, MD, PhD, of Aarhus (Denmark) University Hospital.
Most elderly individuals now qualify for lifelong preventive statin treatment, based on the broader indication for treatment in recent guidelines, and the substantial impact that age has when risk is being calculated, Dr. Mortensen and coauthors said in their report.
“Because frailty, comorbidity, and polypharmacy are increasing concerns in elderly individuals and have been proposed to increase the risk for adverse effects, the appropriateness of treating almost all elderly individuals is questionable,” they said in the report.
In their study, Dr. Mortensen and colleagues evaluated a set of 13 biomarkers or imaging tests that they though had potential to “downgrade” risk of coronary heart disease (CHD) and cardiovascular disease (CVD). They based their analysis on 5,805 patients in the BioImage Study, a prospective cohort study of elderly men and women with no atherosclerotic cardiovascular disease at the time of enrollment in 2008 and 2009. The mean age at the time of enrollment was 69 years, and the mean follow-up in this analysis was 2.7 years.
The overall rate of CHD was 6.1 per 1,000 person-years, though looking at negative risk markers, the event rate was just 0.9 for individuals with CAC of 0 and also 0.9 for those with a CAC of 10 or less, followed by 1.7 for absence of carotid plaque, and 2.6 for galectin-3 in the bottom 25th percentile, according to Dr. Mortensen and coinvestigators. Similarly, the rate of CVD was 9.2 per 1,000 person-years overall, and just 3.2 for a CAC of 0, 2.8 for a CAC of 10 or lower, 4.4 for no carotid plaque, and 4.0 for low galectin-3.
Results were less impressive for other negative risk markers, including normal ankle-brachial index (ABI) test, lack of family history, and low levels of circulating biomarkers such as high-sensitivity C-reactive protein and lipoprotein (a).
Investigators also calculated diagnostic likelihood ratios (DLR), a measure they said assesses the value of performing a diagnostic test, with values lower than 1 indicating a specific marker has value for downgrading risk.
Zero or low CAC exerted the greatest downward change in pre- to post-test risk, according to the investigators, with a multivariable-adjusted DLR of 0.20 for CHD, translating into an 80% relative risk reduction. Similarly, the adjusted DLRs for zero or low CAC for CVD were 0.48 and 0.41, respectively, translating into a 59% risk reduction.
Low galectin-3 also resulted in significant downward change in that pre- to post-test risk, investigators added.
The BioImage Study was funded by Abbott, AstraZeneca, Merck, Philips, and Takeda. Dr. Mortensen had no disclosures related to the present analysis. Coauthors provided disclosures related to G3 Pharmaceuticals, Abbott Laboratories, AstraZeneca, Bayer, Bristol-Myers Squibb, CSL Behring, Eli Lilly/DSI, Medtronic, Novartis Pharmaceuticals, OrbusNeich, and PLC/Renal Guard, among others.
SOURCE: Mortensen MB et al. J Am Coll Cardiol. 2019 Jul 1. doi: 10.1016/j.jacc.2019.04.049.
This study suggests that atherosclerosis imaging tests are the strongest negative risk factors identified to date in cardiovascular medicine. The results are clinically actionable and should shape our approach to these tests in clinical practice.
Atherosclerosis imaging tests could be important in preventing overuse of pharmacotherapy for primary prevention in older adults, nearly all of whom would be considered at elevated risk by current standards.
Results for other candidate markers in the study were generally unimpressive, though the finding that low galectin-3 levels predicted low cardiovascular risk is novel, highly interesting, and deserving of further study.
Meanwhile, guidelines are already taking notice of an emerging consensus on the value of imaging studies as a negative risk factor.
The 2018 prevention guidelines from the American College of Cardiology/American Heart Association recommend coronary artery calcium (CAC) testing to guide individualized patient decision-making in certain adults between the ages of 40 and 75 years who are at borderline to intermediate risk, and that using CAC results to reclassify risk is reasonable in those aged 76-80 years, they said.
For the first time, the ACC/AHA guidelines devoted a section to negative risk factors, specifically highlighting the value of CAC = 0 and stating that intensive statin therapy is of less value in such patients and can potentially be avoided.
Likewise, 2017 guidelines from the Society of Cardiovascular Computed Tomography say that aspirin for primary prevention can almost always be forgone in patients with a CAC of 0.
“The bar for preventive therapy has justifiably fallen, reaching a point where many patients will qualify based on their age alone,” the authors said.
In light of that development, negative risk factors might meaningfully downgrade risk and help identify individuals who can safely focus on lifestyle therapies and defer preventive medication.
Michael J. Blaha, MD, MPH, and Khurram Nasir, MD, MPH are with the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease in Baltimore; Dr. Nasir also is affiliated with the Center for Outcomes Research and Evaluation, Yale University, New Haven, Conn. Ron Blankstein, MD, is with the cardiovascular division, department of medicine, Brigham and Women’s Hospital, Boston. These comments are adapted from their editorial (J Am Coll Cardiol. 2019 Jul 1. doi: 10.1016/j.jacc.2019.05.032 ). Dr. Blankstein reported research funding/grant support from Amgen and Astellas; Dr. Blaha and Dr. Nasir said they had no disclosures to report.
This study suggests that atherosclerosis imaging tests are the strongest negative risk factors identified to date in cardiovascular medicine. The results are clinically actionable and should shape our approach to these tests in clinical practice.
Atherosclerosis imaging tests could be important in preventing overuse of pharmacotherapy for primary prevention in older adults, nearly all of whom would be considered at elevated risk by current standards.
Results for other candidate markers in the study were generally unimpressive, though the finding that low galectin-3 levels predicted low cardiovascular risk is novel, highly interesting, and deserving of further study.
Meanwhile, guidelines are already taking notice of an emerging consensus on the value of imaging studies as a negative risk factor.
The 2018 prevention guidelines from the American College of Cardiology/American Heart Association recommend coronary artery calcium (CAC) testing to guide individualized patient decision-making in certain adults between the ages of 40 and 75 years who are at borderline to intermediate risk, and that using CAC results to reclassify risk is reasonable in those aged 76-80 years, they said.
For the first time, the ACC/AHA guidelines devoted a section to negative risk factors, specifically highlighting the value of CAC = 0 and stating that intensive statin therapy is of less value in such patients and can potentially be avoided.
Likewise, 2017 guidelines from the Society of Cardiovascular Computed Tomography say that aspirin for primary prevention can almost always be forgone in patients with a CAC of 0.
“The bar for preventive therapy has justifiably fallen, reaching a point where many patients will qualify based on their age alone,” the authors said.
In light of that development, negative risk factors might meaningfully downgrade risk and help identify individuals who can safely focus on lifestyle therapies and defer preventive medication.
Michael J. Blaha, MD, MPH, and Khurram Nasir, MD, MPH are with the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease in Baltimore; Dr. Nasir also is affiliated with the Center for Outcomes Research and Evaluation, Yale University, New Haven, Conn. Ron Blankstein, MD, is with the cardiovascular division, department of medicine, Brigham and Women’s Hospital, Boston. These comments are adapted from their editorial (J Am Coll Cardiol. 2019 Jul 1. doi: 10.1016/j.jacc.2019.05.032 ). Dr. Blankstein reported research funding/grant support from Amgen and Astellas; Dr. Blaha and Dr. Nasir said they had no disclosures to report.
This study suggests that atherosclerosis imaging tests are the strongest negative risk factors identified to date in cardiovascular medicine. The results are clinically actionable and should shape our approach to these tests in clinical practice.
Atherosclerosis imaging tests could be important in preventing overuse of pharmacotherapy for primary prevention in older adults, nearly all of whom would be considered at elevated risk by current standards.
Results for other candidate markers in the study were generally unimpressive, though the finding that low galectin-3 levels predicted low cardiovascular risk is novel, highly interesting, and deserving of further study.
Meanwhile, guidelines are already taking notice of an emerging consensus on the value of imaging studies as a negative risk factor.
The 2018 prevention guidelines from the American College of Cardiology/American Heart Association recommend coronary artery calcium (CAC) testing to guide individualized patient decision-making in certain adults between the ages of 40 and 75 years who are at borderline to intermediate risk, and that using CAC results to reclassify risk is reasonable in those aged 76-80 years, they said.
For the first time, the ACC/AHA guidelines devoted a section to negative risk factors, specifically highlighting the value of CAC = 0 and stating that intensive statin therapy is of less value in such patients and can potentially be avoided.
Likewise, 2017 guidelines from the Society of Cardiovascular Computed Tomography say that aspirin for primary prevention can almost always be forgone in patients with a CAC of 0.
“The bar for preventive therapy has justifiably fallen, reaching a point where many patients will qualify based on their age alone,” the authors said.
In light of that development, negative risk factors might meaningfully downgrade risk and help identify individuals who can safely focus on lifestyle therapies and defer preventive medication.
Michael J. Blaha, MD, MPH, and Khurram Nasir, MD, MPH are with the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease in Baltimore; Dr. Nasir also is affiliated with the Center for Outcomes Research and Evaluation, Yale University, New Haven, Conn. Ron Blankstein, MD, is with the cardiovascular division, department of medicine, Brigham and Women’s Hospital, Boston. These comments are adapted from their editorial (J Am Coll Cardiol. 2019 Jul 1. doi: 10.1016/j.jacc.2019.05.032 ). Dr. Blankstein reported research funding/grant support from Amgen and Astellas; Dr. Blaha and Dr. Nasir said they had no disclosures to report.
Older individuals with certain negative risk markers have a very low risk of atherosclerotic cardiovascular disease, raising the possibility that some could forgo preventive treatment even if it’s indicated by current standards of risk assessment.
Low levels of coronary artery calcification (CAC), low galectin-3 levels, and absence of carotid plaque were all linked to a lower likelihood of disease than might be expected based on traditional risk assessment, according to the authors of analysis of a large, contemporary cohort of elderly individuals published in the Journal of the American College of Cardiology.
“Our results hold the potential to markedly improve statin allocation in elderly individuals by de-escalating or even withholding preventive therapy in elderly individuals at truly low atherosclerotic cardiovascular disease risk despite advancing age,“ wrote Martin Bødtker Mortensen, MD, PhD, of Aarhus (Denmark) University Hospital.
Most elderly individuals now qualify for lifelong preventive statin treatment, based on the broader indication for treatment in recent guidelines, and the substantial impact that age has when risk is being calculated, Dr. Mortensen and coauthors said in their report.
“Because frailty, comorbidity, and polypharmacy are increasing concerns in elderly individuals and have been proposed to increase the risk for adverse effects, the appropriateness of treating almost all elderly individuals is questionable,” they said in the report.
In their study, Dr. Mortensen and colleagues evaluated a set of 13 biomarkers or imaging tests that they though had potential to “downgrade” risk of coronary heart disease (CHD) and cardiovascular disease (CVD). They based their analysis on 5,805 patients in the BioImage Study, a prospective cohort study of elderly men and women with no atherosclerotic cardiovascular disease at the time of enrollment in 2008 and 2009. The mean age at the time of enrollment was 69 years, and the mean follow-up in this analysis was 2.7 years.
The overall rate of CHD was 6.1 per 1,000 person-years, though looking at negative risk markers, the event rate was just 0.9 for individuals with CAC of 0 and also 0.9 for those with a CAC of 10 or less, followed by 1.7 for absence of carotid plaque, and 2.6 for galectin-3 in the bottom 25th percentile, according to Dr. Mortensen and coinvestigators. Similarly, the rate of CVD was 9.2 per 1,000 person-years overall, and just 3.2 for a CAC of 0, 2.8 for a CAC of 10 or lower, 4.4 for no carotid plaque, and 4.0 for low galectin-3.
Results were less impressive for other negative risk markers, including normal ankle-brachial index (ABI) test, lack of family history, and low levels of circulating biomarkers such as high-sensitivity C-reactive protein and lipoprotein (a).
Investigators also calculated diagnostic likelihood ratios (DLR), a measure they said assesses the value of performing a diagnostic test, with values lower than 1 indicating a specific marker has value for downgrading risk.
Zero or low CAC exerted the greatest downward change in pre- to post-test risk, according to the investigators, with a multivariable-adjusted DLR of 0.20 for CHD, translating into an 80% relative risk reduction. Similarly, the adjusted DLRs for zero or low CAC for CVD were 0.48 and 0.41, respectively, translating into a 59% risk reduction.
Low galectin-3 also resulted in significant downward change in that pre- to post-test risk, investigators added.
The BioImage Study was funded by Abbott, AstraZeneca, Merck, Philips, and Takeda. Dr. Mortensen had no disclosures related to the present analysis. Coauthors provided disclosures related to G3 Pharmaceuticals, Abbott Laboratories, AstraZeneca, Bayer, Bristol-Myers Squibb, CSL Behring, Eli Lilly/DSI, Medtronic, Novartis Pharmaceuticals, OrbusNeich, and PLC/Renal Guard, among others.
SOURCE: Mortensen MB et al. J Am Coll Cardiol. 2019 Jul 1. doi: 10.1016/j.jacc.2019.04.049.
Older individuals with certain negative risk markers have a very low risk of atherosclerotic cardiovascular disease, raising the possibility that some could forgo preventive treatment even if it’s indicated by current standards of risk assessment.
Low levels of coronary artery calcification (CAC), low galectin-3 levels, and absence of carotid plaque were all linked to a lower likelihood of disease than might be expected based on traditional risk assessment, according to the authors of analysis of a large, contemporary cohort of elderly individuals published in the Journal of the American College of Cardiology.
“Our results hold the potential to markedly improve statin allocation in elderly individuals by de-escalating or even withholding preventive therapy in elderly individuals at truly low atherosclerotic cardiovascular disease risk despite advancing age,“ wrote Martin Bødtker Mortensen, MD, PhD, of Aarhus (Denmark) University Hospital.
Most elderly individuals now qualify for lifelong preventive statin treatment, based on the broader indication for treatment in recent guidelines, and the substantial impact that age has when risk is being calculated, Dr. Mortensen and coauthors said in their report.
“Because frailty, comorbidity, and polypharmacy are increasing concerns in elderly individuals and have been proposed to increase the risk for adverse effects, the appropriateness of treating almost all elderly individuals is questionable,” they said in the report.
In their study, Dr. Mortensen and colleagues evaluated a set of 13 biomarkers or imaging tests that they though had potential to “downgrade” risk of coronary heart disease (CHD) and cardiovascular disease (CVD). They based their analysis on 5,805 patients in the BioImage Study, a prospective cohort study of elderly men and women with no atherosclerotic cardiovascular disease at the time of enrollment in 2008 and 2009. The mean age at the time of enrollment was 69 years, and the mean follow-up in this analysis was 2.7 years.
The overall rate of CHD was 6.1 per 1,000 person-years, though looking at negative risk markers, the event rate was just 0.9 for individuals with CAC of 0 and also 0.9 for those with a CAC of 10 or less, followed by 1.7 for absence of carotid plaque, and 2.6 for galectin-3 in the bottom 25th percentile, according to Dr. Mortensen and coinvestigators. Similarly, the rate of CVD was 9.2 per 1,000 person-years overall, and just 3.2 for a CAC of 0, 2.8 for a CAC of 10 or lower, 4.4 for no carotid plaque, and 4.0 for low galectin-3.
Results were less impressive for other negative risk markers, including normal ankle-brachial index (ABI) test, lack of family history, and low levels of circulating biomarkers such as high-sensitivity C-reactive protein and lipoprotein (a).
Investigators also calculated diagnostic likelihood ratios (DLR), a measure they said assesses the value of performing a diagnostic test, with values lower than 1 indicating a specific marker has value for downgrading risk.
Zero or low CAC exerted the greatest downward change in pre- to post-test risk, according to the investigators, with a multivariable-adjusted DLR of 0.20 for CHD, translating into an 80% relative risk reduction. Similarly, the adjusted DLRs for zero or low CAC for CVD were 0.48 and 0.41, respectively, translating into a 59% risk reduction.
Low galectin-3 also resulted in significant downward change in that pre- to post-test risk, investigators added.
The BioImage Study was funded by Abbott, AstraZeneca, Merck, Philips, and Takeda. Dr. Mortensen had no disclosures related to the present analysis. Coauthors provided disclosures related to G3 Pharmaceuticals, Abbott Laboratories, AstraZeneca, Bayer, Bristol-Myers Squibb, CSL Behring, Eli Lilly/DSI, Medtronic, Novartis Pharmaceuticals, OrbusNeich, and PLC/Renal Guard, among others.
SOURCE: Mortensen MB et al. J Am Coll Cardiol. 2019 Jul 1. doi: 10.1016/j.jacc.2019.04.049.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Key clinical point: Low or no coronary artery calcification (CAC), low galectin-3 levels, and absence of carotid plaque were all linked to a lower likelihood of atherosclerotic cardiovascular disease in elderly patients, suggesting pharmacotherapy might be avoidable in a certain proportion of them.
Major finding: The diagnostic likelihood ratios (DLR) were low for those negative risk markers, e.g., 0.20 for no or low CAC, indicating a relative risk reduction of about 80%.
Study details: Analysis of data from the BioImage Study, a prospective cohort study of 5,805 older men and women who had no atherosclerotic cardiovascular disease at the time of enrollment.
Disclosures: The BioImage Study was funded by Abbott, AstraZeneca, Merck, Philips, and Takeda. Authors of the present analysis provided disclosures related to G3 Pharmaceuticals, Abbott Laboratories, AstraZeneca, Bayer, Bristol-Myers Squibb, CSL Behring, Eli Lilly/DSI, Medtronic, Novartis Pharmaceuticals, OrbusNeich, and PLC/Renal Guard, among others.
Source: Mortensen MB et al. J Am Coll Cardiol. 2019 Jul 1. doi: j.jacc.2019.04.049.
Siblings of bipolar disorder patients at higher cardiometabolic disease risk
The siblings of patients with bipolar disorder have a higher prevalence of dyslipidemia and higher rates of ischemic stroke than do controls, results of a longitudinal cohort study suggest.
, wrote Wen-Yen Tsao, MD, of the department of psychiatry at Taipei Veterans General Hospital in Taiwan, and associates. Previous research has identified several overlapping genes between cardiometabolic diseases and mood disorders. In addition, polymorphisms of several genes tied to obesity have been associated with bipolar disorder.
In the current study, Dr. Tsao and associates analyzed the Taiwan National Health Insurance Research Database, which includes health care data from more than 99% of the Taiwanese population (J Affect Disord. 2019 Jun 15. doi: 10.1016/j.jad.2019.04.094). Adults born before 1990 who had no psychiatric disorders, a sibling with bipolar disorder, and a metabolic disorder were enrolled as the study cohort. A control group was identified randomly. By way of ICD-9-CM codes, people with type 2 diabetes, hypertension, dyslipidemia, and obesity were identified in both cohorts. The investigators followed the metabolic status of 7,225 unaffected siblings of bipolar disorder patients and 28,900 controls from 1996 to 2011.
Dr. Tsao and associates found that the family members who had siblings with bipolar disorder had a higher prevalence of dyslipidemia (5.4% vs. 4.5%; P = .001), compared with controls. The group with siblings with bipolar disorder also were diagnosed with type 2 diabetes at a younger age (34.81 vs. 37.22; P = .024), and had a higher prevalence of any stroke (1.5 vs. 1.1%; P = .007) and ischemic stroke (0.7% vs. 0.4%, P = .001), compared with controls.
A subanalysis showed that the higher risk of any stroke (odds ratio, 1.38; 95% confidence interval, 1.02-1.85) and ischemic stroke (OR, 2.43; 95% CI, 1.60-3.70) pertained only to male siblings. That gender-specific finding might be attributed to differences in plasma triglyceride clearance between men and women, the researchers wrote.
The findings might not be generalizable to other populations, the investigators noted. In addition, they said, the prevalence of cardiometabolic disease in the groups studied might be underestimated.
“Our results may motivate additional studies to evaluate genetic factors, psychosocial factors, and other pathophysiology of bipolar disorder,” they wrote.
The study was funded by Taiwan’s Ministry of Science and Technology, and Taipei Veterans General Hospital. The researchers cited no conflicts of interest.
The siblings of patients with bipolar disorder have a higher prevalence of dyslipidemia and higher rates of ischemic stroke than do controls, results of a longitudinal cohort study suggest.
, wrote Wen-Yen Tsao, MD, of the department of psychiatry at Taipei Veterans General Hospital in Taiwan, and associates. Previous research has identified several overlapping genes between cardiometabolic diseases and mood disorders. In addition, polymorphisms of several genes tied to obesity have been associated with bipolar disorder.
In the current study, Dr. Tsao and associates analyzed the Taiwan National Health Insurance Research Database, which includes health care data from more than 99% of the Taiwanese population (J Affect Disord. 2019 Jun 15. doi: 10.1016/j.jad.2019.04.094). Adults born before 1990 who had no psychiatric disorders, a sibling with bipolar disorder, and a metabolic disorder were enrolled as the study cohort. A control group was identified randomly. By way of ICD-9-CM codes, people with type 2 diabetes, hypertension, dyslipidemia, and obesity were identified in both cohorts. The investigators followed the metabolic status of 7,225 unaffected siblings of bipolar disorder patients and 28,900 controls from 1996 to 2011.
Dr. Tsao and associates found that the family members who had siblings with bipolar disorder had a higher prevalence of dyslipidemia (5.4% vs. 4.5%; P = .001), compared with controls. The group with siblings with bipolar disorder also were diagnosed with type 2 diabetes at a younger age (34.81 vs. 37.22; P = .024), and had a higher prevalence of any stroke (1.5 vs. 1.1%; P = .007) and ischemic stroke (0.7% vs. 0.4%, P = .001), compared with controls.
A subanalysis showed that the higher risk of any stroke (odds ratio, 1.38; 95% confidence interval, 1.02-1.85) and ischemic stroke (OR, 2.43; 95% CI, 1.60-3.70) pertained only to male siblings. That gender-specific finding might be attributed to differences in plasma triglyceride clearance between men and women, the researchers wrote.
The findings might not be generalizable to other populations, the investigators noted. In addition, they said, the prevalence of cardiometabolic disease in the groups studied might be underestimated.
“Our results may motivate additional studies to evaluate genetic factors, psychosocial factors, and other pathophysiology of bipolar disorder,” they wrote.
The study was funded by Taiwan’s Ministry of Science and Technology, and Taipei Veterans General Hospital. The researchers cited no conflicts of interest.
The siblings of patients with bipolar disorder have a higher prevalence of dyslipidemia and higher rates of ischemic stroke than do controls, results of a longitudinal cohort study suggest.
, wrote Wen-Yen Tsao, MD, of the department of psychiatry at Taipei Veterans General Hospital in Taiwan, and associates. Previous research has identified several overlapping genes between cardiometabolic diseases and mood disorders. In addition, polymorphisms of several genes tied to obesity have been associated with bipolar disorder.
In the current study, Dr. Tsao and associates analyzed the Taiwan National Health Insurance Research Database, which includes health care data from more than 99% of the Taiwanese population (J Affect Disord. 2019 Jun 15. doi: 10.1016/j.jad.2019.04.094). Adults born before 1990 who had no psychiatric disorders, a sibling with bipolar disorder, and a metabolic disorder were enrolled as the study cohort. A control group was identified randomly. By way of ICD-9-CM codes, people with type 2 diabetes, hypertension, dyslipidemia, and obesity were identified in both cohorts. The investigators followed the metabolic status of 7,225 unaffected siblings of bipolar disorder patients and 28,900 controls from 1996 to 2011.
Dr. Tsao and associates found that the family members who had siblings with bipolar disorder had a higher prevalence of dyslipidemia (5.4% vs. 4.5%; P = .001), compared with controls. The group with siblings with bipolar disorder also were diagnosed with type 2 diabetes at a younger age (34.81 vs. 37.22; P = .024), and had a higher prevalence of any stroke (1.5 vs. 1.1%; P = .007) and ischemic stroke (0.7% vs. 0.4%, P = .001), compared with controls.
A subanalysis showed that the higher risk of any stroke (odds ratio, 1.38; 95% confidence interval, 1.02-1.85) and ischemic stroke (OR, 2.43; 95% CI, 1.60-3.70) pertained only to male siblings. That gender-specific finding might be attributed to differences in plasma triglyceride clearance between men and women, the researchers wrote.
The findings might not be generalizable to other populations, the investigators noted. In addition, they said, the prevalence of cardiometabolic disease in the groups studied might be underestimated.
“Our results may motivate additional studies to evaluate genetic factors, psychosocial factors, and other pathophysiology of bipolar disorder,” they wrote.
The study was funded by Taiwan’s Ministry of Science and Technology, and Taipei Veterans General Hospital. The researchers cited no conflicts of interest.
FROM THE JOURNAL OF AFFECTIVE DISORDERS
CVD risk upped in postmenopausal breast cancer survivors
according to a new study of nearly 300 women.
Previous studies have shown that cardiovascular risk is greater among postmenopausal women treated for breast cancer compared with those without cancer, but specific risk factors have not been well studied, wrote Daniel de Araujo Brito Buttros, MD, of Paulista State University, Sao Paulo, Brazil, and colleagues.
In a study published in Menopause, the researchers evaluated several CVD risk factors in 96 postmenopausal women with breast cancer and 192 women without breast cancer, including metabolic syndrome, subclinical atherosclerosis, and heat shock proteins (HSP) 60 and 70.
Overall, breast cancer patients had significantly higher HSP60 levels and lower HSP70 levels than those of their cancer-free peers. These two proteins have an antagonistic relationship in cardiovascular disease, with HSP60 considered a risk factor for CVD, and HSP70 considered a protective factor. Average HSP60 levels for the breast cancer and control groups were 35 ng/mL and 10.8 ng/mL, respectively; average HSP70 levels were 0.5 ng/mL and 1.3 ng/mL, respectively.
Both diabetes and metabolic syndrome were significantly more common among breast cancer patients vs. controls (19.8% vs. 6.8% and 54.2% vs. 30.7%, respectively). Carotid artery plaque also was more common in breast cancer patients vs. controls (19.8% vs. 9.4%, respectively, P = 0.013).
In addition, systolic and diastolic blood pressure levels were significantly higher among the breast cancer patients, as were triglycerides and glucose.
The findings were limited by several factors including the cross-sectional design that could not prove a causal relationship between CVD risk and breast cancer, the researchers noted.
However, the results demonstrate the increased CVD risk for breast cancer patients, and “[therefore], women diagnosed with breast cancer might receive multidisciplinary care, including cardiology consultation at the time of breast cancer diagnosis and also during oncologic follow-up visits,” they said.
“Heart disease appears more commonly in women treated for breast cancer because of the toxicities of chemotherapy, radiation therapy, and use of aromatase inhibitors, which lower estrogen. Heart-healthy lifestyle modifications will decrease both the risk of recurrent breast cancer and the risk of developing heart disease,” JoAnn Pinkerton, MD, executive director of the North American Menopause Society, said in a statement. “Women should schedule a cardiology consultation when breast cancer is diagnosed and continue with ongoing follow-up after cancer treatments are completed,” she emphasized.
The researchers had no financial conflicts to disclose.
SOURCE: Buttros DAB et al. Menopause. 2019. doi: 10.1097/GME.0000000000001348.
according to a new study of nearly 300 women.
Previous studies have shown that cardiovascular risk is greater among postmenopausal women treated for breast cancer compared with those without cancer, but specific risk factors have not been well studied, wrote Daniel de Araujo Brito Buttros, MD, of Paulista State University, Sao Paulo, Brazil, and colleagues.
In a study published in Menopause, the researchers evaluated several CVD risk factors in 96 postmenopausal women with breast cancer and 192 women without breast cancer, including metabolic syndrome, subclinical atherosclerosis, and heat shock proteins (HSP) 60 and 70.
Overall, breast cancer patients had significantly higher HSP60 levels and lower HSP70 levels than those of their cancer-free peers. These two proteins have an antagonistic relationship in cardiovascular disease, with HSP60 considered a risk factor for CVD, and HSP70 considered a protective factor. Average HSP60 levels for the breast cancer and control groups were 35 ng/mL and 10.8 ng/mL, respectively; average HSP70 levels were 0.5 ng/mL and 1.3 ng/mL, respectively.
Both diabetes and metabolic syndrome were significantly more common among breast cancer patients vs. controls (19.8% vs. 6.8% and 54.2% vs. 30.7%, respectively). Carotid artery plaque also was more common in breast cancer patients vs. controls (19.8% vs. 9.4%, respectively, P = 0.013).
In addition, systolic and diastolic blood pressure levels were significantly higher among the breast cancer patients, as were triglycerides and glucose.
The findings were limited by several factors including the cross-sectional design that could not prove a causal relationship between CVD risk and breast cancer, the researchers noted.
However, the results demonstrate the increased CVD risk for breast cancer patients, and “[therefore], women diagnosed with breast cancer might receive multidisciplinary care, including cardiology consultation at the time of breast cancer diagnosis and also during oncologic follow-up visits,” they said.
“Heart disease appears more commonly in women treated for breast cancer because of the toxicities of chemotherapy, radiation therapy, and use of aromatase inhibitors, which lower estrogen. Heart-healthy lifestyle modifications will decrease both the risk of recurrent breast cancer and the risk of developing heart disease,” JoAnn Pinkerton, MD, executive director of the North American Menopause Society, said in a statement. “Women should schedule a cardiology consultation when breast cancer is diagnosed and continue with ongoing follow-up after cancer treatments are completed,” she emphasized.
The researchers had no financial conflicts to disclose.
SOURCE: Buttros DAB et al. Menopause. 2019. doi: 10.1097/GME.0000000000001348.
according to a new study of nearly 300 women.
Previous studies have shown that cardiovascular risk is greater among postmenopausal women treated for breast cancer compared with those without cancer, but specific risk factors have not been well studied, wrote Daniel de Araujo Brito Buttros, MD, of Paulista State University, Sao Paulo, Brazil, and colleagues.
In a study published in Menopause, the researchers evaluated several CVD risk factors in 96 postmenopausal women with breast cancer and 192 women without breast cancer, including metabolic syndrome, subclinical atherosclerosis, and heat shock proteins (HSP) 60 and 70.
Overall, breast cancer patients had significantly higher HSP60 levels and lower HSP70 levels than those of their cancer-free peers. These two proteins have an antagonistic relationship in cardiovascular disease, with HSP60 considered a risk factor for CVD, and HSP70 considered a protective factor. Average HSP60 levels for the breast cancer and control groups were 35 ng/mL and 10.8 ng/mL, respectively; average HSP70 levels were 0.5 ng/mL and 1.3 ng/mL, respectively.
Both diabetes and metabolic syndrome were significantly more common among breast cancer patients vs. controls (19.8% vs. 6.8% and 54.2% vs. 30.7%, respectively). Carotid artery plaque also was more common in breast cancer patients vs. controls (19.8% vs. 9.4%, respectively, P = 0.013).
In addition, systolic and diastolic blood pressure levels were significantly higher among the breast cancer patients, as were triglycerides and glucose.
The findings were limited by several factors including the cross-sectional design that could not prove a causal relationship between CVD risk and breast cancer, the researchers noted.
However, the results demonstrate the increased CVD risk for breast cancer patients, and “[therefore], women diagnosed with breast cancer might receive multidisciplinary care, including cardiology consultation at the time of breast cancer diagnosis and also during oncologic follow-up visits,” they said.
“Heart disease appears more commonly in women treated for breast cancer because of the toxicities of chemotherapy, radiation therapy, and use of aromatase inhibitors, which lower estrogen. Heart-healthy lifestyle modifications will decrease both the risk of recurrent breast cancer and the risk of developing heart disease,” JoAnn Pinkerton, MD, executive director of the North American Menopause Society, said in a statement. “Women should schedule a cardiology consultation when breast cancer is diagnosed and continue with ongoing follow-up after cancer treatments are completed,” she emphasized.
The researchers had no financial conflicts to disclose.
SOURCE: Buttros DAB et al. Menopause. 2019. doi: 10.1097/GME.0000000000001348.
FROM MENOPAUSE