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Dominique Ashen M.,Johns Hopkins Ciccarone Center for the Prevention of Heart Disease
Current Treatment Options in Cardiovascular Medicine | Year: 2013

Opinion statement: There is growing evidence that consumption of a vegetarian diet as well as specific components of a vegetarian diet lower the incidence of cardiovascular disease (CVD) and death. Vegetarian diets lower the probability of developing CVD, are effective in altering serum lipids, are beneficial in reducing blood pressure, improve glycemic control and insulin sensitivity, reduce weight, and lower mortality. Vascular effects of a vegetarian diet include a thinner carotid IMT and lower brachial artery resistance. Health care providers should be aware of the types of vegetarian diets and their risks and benefits in order to guide patients' dietary habits with the ultimate goal of reducing their CVD risk. While a patient does not have to become a complete vegetarian to reduce their CVD risk, they can make simple changes in their diet that are effective in risk reduction. © 2013 Springer Science+Business Media New York. Source


Patel J.,Johns Hopkins Ciccarone Center for the Prevention of Heart Disease
Current atherosclerosis reports | Year: 2014

Pharmacogenetics uses the genetic variation in metabolic pathways to identify groups of patients who may respond differently in terms of therapeutic and adverse effects. Much clinical interest lies in drug metabolism and the opportunity to improve prescribing efficacy and safety. Owing to widespread use and increasing concern regarding side effects, statins are of significant interest in this area. Among other benefits, statins have been shown to improve lipid profiles and reduce coronary heart disease event rates in many populations. However, variability in drug response exists, and genetic variability may be a contributing factor. Our primary goal is to feature the most important genes involved in lipid metabolism, clinical outcomes, and statin-induced side effects, highlighting genome-wide association studies and the candidate gene approach. Source


Berger J.S.,New York University | Berger J.S.,University of Pennsylvania | Jordan C.O.,University of Minnesota | Lloyd-Jones D.,Northwestern University | Blumenthal R.S.,Johns Hopkins Ciccarone Center for the Prevention of Heart Disease
Journal of the American College of Cardiology | Year: 2010

Cardiovascular disease is the number 1 cause of death in the western world and 1 of the leading causes of death worldwide. The lifetime risk of atherosclerotic cardiovascular disease (CVD) for persons at age 50 years, on average, is estimated to be 52% for men and 39% for women, with a wide variation depending on risk factor burden. Assessing patients' cardiovascular risk may be used for the targeting of preventive treatments of individual patients who are asymptomatic but at sufficiently high risk for the development of CVD. Risk stratifying patients for CVD remains challenging, particularly for those with low or intermediate short-term risk. Several algorithms have been described to facilitate the assessment of risk in individual patients. We describe 6 risk algorithms (Framingham Risk Score for coronary heart disease events and for cardiovascular events, Adult Treatment Panel III, SCORE [Systematic Coronary Risk Evaluation] project, Reynolds Risk Score, ASSIGN [Assessing Cardiovascular Risk to Scottish Intercollegiate Guidelines Network/SIGN to Assign Preventative Treatment], and QRISK [QRESEARCH Cardiovascular Risk Algorithm]) for outcomes, population derived/validated, receiver-operating characteristic, variables included, and limitations. Areas of uncertainty include 10-year versus lifetime risk, prediction of CVD or coronary heart disease end points, nonlaboratory-based risk scores, age at which to start, race and sex differences, and whether a risk score should guide therapy. We believe that the best high-risk approach to CVD evaluation and prevention lies in routine testing for cardiovascular risk factors and risk score assessment. We recommend that health care providers discuss the global cardiovascular risk and lifetime cardiovascular risk score assessment with each patient to better explain each patient's future risk. Appropriate intervention, guided by risk assessment, has the potential to bring about a significant reduction in population levels of risk. © 2010 American College of Cardiology Foundation. Source


Weiss S.A.,University of Chicago | Blumenthal R.S.,Johns Hopkins Ciccarone Center for the Prevention of Heart Disease | Redberg R.F.,University of California at San Francisco | Mora S.,Harvard University
Circulation | Year: 2010

BACKGROUND-: Individuals with exaggerated exercise blood pressure (BP) tend to develop future hypertension. It is controversial whether they have higher risk of death from cardiovascular disease (CVD). METHODS AND RESULTS-: A total of 6578 asymptomatic Lipid Research Clinics Prevalence Study participants (45% women; mean age, 46 years; 74% with untreated baseline BP <140/90 mm Hg [nonhypertensive]) performing submaximal Bruce treadmill tests were followed for 20 years (385 CVD deaths occurred). Systolic and diastolic BP at rest, Bruce stage 2, and maximal BP during exercise were significantly associated with CVD death. When we compared multivariate hazard ratios and 95% confidence intervals per 10/5-mm Hg BP increments, the association was strongest for rest BP (systolic, 1.21 [1.14 to 1.27]; diastolic, 1.20 [1.14 to 1.26]), then Bruce stage 2 BP (systolic, 1.09 [1.04 to 1.14]; diastolic, 1.09 [1.05 to 1.13]), then maximal exercise BP (systolic, 1.06 [1.01 to 1.10]; diastolic, 1.04 [1.01 to 1.08]). Overall, exercise BP was not significant after adjustment for rest BP. However, hypertension status modified the risk associated with exercise BP (Pinteraction=0.03). Among nonhypertensives, whether they had normal BP (<120/80 mm Hg) or prehypertension, Bruce stage 2 BP >180/90 versus ≤180/90 mm Hg carried increased risk independent of rest BP and risk factors (adjusted hazard ratio for systolic, 1.96 [1.40 to 2.74], P<0.001; diastolic, 1.48 [1.06 to 2.06], P=0.02) and added predictive value (net reclassification improvement, systolic, 12.0% [-0.1% to 24.2%]; diastolic, 9.9% [-0.3% to 20.0%]; relative integrated discrimination improvement, 14.3% and 12.0%, respectively). CONCLUSIONS-: In asymptomatic individuals, elevated exercise BP carried higher risk of CVD death but became nonsignificant after accounting for rest BP. However, Bruce stage 2 BP >180/90 mm Hg identified nonhypertensive individuals at higher risk of CVD death. © 2010 American Heart Association, Inc. Source


Martin S.S.,Johns Hopkins Ciccarone Center for the Prevention of Heart Disease | Blumenthal R.S.,Johns Hopkins Ciccarone Center for the Prevention of Heart Disease | Miller M.,University of Maryland, Baltimore
Medical Clinics of North America | Year: 2012

High cholesterol is often a prerequisite for atherosclerotic plaque. Low-density lipoprotein cholesterol (LDL-C) is the focus of the National Cholesterol Education Program Adult Treatment Panel guidelines. LDL-C ranges from 50 to 70 mg/dL in native hunter-gatherers, healthy human neonates, free-living primates, and other wild mammals, who are notably free of atherosclerotic vascular disease. Multiple statin trials and meta-analyses support a treatment target of LDL-C levels less than 70 mg/dL, as this is associated with improved clinical outcomes and atherosclerosis regression. In fact, no threshold has yet been identified below which patients do not benefit from lowering of LDL-C. © 2012 Elsevier Inc. Source

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