The objective of this article is to review the role of vitamin E in cardiovascular disease. We begin by describing the general characteristics and metabolism of vitamin E and the pathogenesis of atherosclerosis as it relates to oxidation. We also discuss key in vitro studies, animal studies, observational studies, and clinical trials regarding the potentially cardioprotective effect of vitamin E. Lastly, we outline the current recommendations regarding vitamin E in the prevention and treatment of cardiovascular disease as stated by the American Heart Association. Vitamin E is a fat-soluble antioxidant vitamin and alpha-tocopherol is its most naturally abundant and active form. Oxidation is a key step in atherogenesis. Oxidized low-density lipoprotein stimulates endothelial cells to produce inflammatory markers, is involved in foam cell formation, has cytotoxic effects on endothelial cells, inhibits the motility of tissue macrophages, and inhibits nitric oxide-induced vasodilatation. Vitamin E has been shown to increase oxidative resistance in vitro and prevent atherosclerotic plaque formation in mouse models. Consumption of foods rich in vitamin E has been associated with lower risk of coronary heart disease in middle-aged to older men and women. Clinical studies at large have not demonstrated a benefit of vitamin E in the primary and secondary prevention of cardiovascular disease. Vitamin E supplementation might be associated with an increase in total mortality, heart failure, and hemorrhagic stroke. The American Heart Association does not support the use of vitamin E supplements to prevent cardiovascular disease, but does recommend the consumption of foods abundant in antioxidant vitamins and other nutrients.
We reviewed the roles of both alcohol and red wine in cardiovascular disease by discussing key animal and human studies. Included are studies regarding alcohol's association with coronary heart disease and the proposed mechanisms of action of alcohol. Likewise, studies concerning red wine's cardiovascular benefit and the mechanisms of action of red wine are discussed. Lastly, we reviewed studies on the adverse effects of alcohol and the current consumption recommendations as stated by the American Heart Association. Moderate alcohol consumption (#2 drinks per day) is associated with a reduced risk of coronary heart disease. This is believed to occur through alcohol's antithrombotic properties and its ability to increase high-density lipoprotein levels. It remains unclear whether polyphenol compounds in red wine make it an especially cardioprotective alcoholic beverage. These compounds are proposed to act by inhibiting low-density lipoprotein oxidation and thrombosis independently of alcohol. Moderate alcohol consumption is not associated with any significant morbidity; however, three or more drinks per day is associated with hypertriglyceridemia, cardiomyopathy, hypertension, and stroke. The American Heart Association does not recommend alcohol as a treatment approach and suggests that men drink no more than two drinks per day and women no more than one drink per day.
We reviewed the use of marine-derived omega-3 fatty acids in cardiovascular disease by discussing key epidemiologic and placebo-controlled studies in people with and without prior cardiovascular disease at baseline. In addition, studies on the antitriglyceridemic, antihypertensive, hemostatic, antiarrhythmic, and antiatherogenic properties of omega-3 fatty acids were examined. Lastly, we discussed current dietary and safety recommendations regarding fish and fish oil capsules as stated by the US Food and Drug Administration and the US Environmental Protection Agency. We found that omega-3 fatty acids have shown to significantly reduce coronary mortality and sudden death in people without prior cardiovascular disease and reduce all-cause death and cardiac mortality in secondary prevention studies. Studies on stroke are still unclear and more studies need to focus on stroke subtypes. The beneficial effects of omega-3 fatty acids might be the result of their ability to reduce triglyceride levels, blood pressure, platelet aggregation, arrhythmia, and atherogenesis. Currently, the general public is recommended to consume two fatty fish meals per week (0.3-0.5 grams per day eicosapentaenoic acid and docosahexaenoic acid). Pregnant mothers and children should refrain from eating fish high in methylmercury levels while limiting their consumption of other fish varieties to 12 ounces per week. Patients with coronary heart disease should have 1 g per day of eicosapentaenoic acid and docosahexaenoic acid, whereas patients with hypertriglyceridemia should take 3 to 5 g per day of eicosapentaenoic acid and docosahexaenoic acid under a physician's supervision.
Heart failure is extremely prevalent and is associated with significant mortality, morbidity and cost. Studies have already established mortality benefit with the use of neurohormonal blockade therapy in systolic failure. Unfortunately, physical signs and symptoms of heart failure lack diagnostic sensitivity and specificity, and medication doses proven to improve mortality in clinical trials are often not achieved. Brain natriuretic peptide (BNP) has proven to be of clinical use in the diagnosis and prognosis of heart failure, and recent efforts have been taken to further elucidate its role in guiding heart failure management. Multiple studies have been conducted on outpatient guided management, and although still controversial, there is a trend towards improved outcomes. Inpatient studies are lacking, but preliminary data suggest various BNP cut-off values, as well as percentage changes in BNP, that could be useful in predicting outcomes and improving mortality. In the future, heart failure management will probably involve an algorithm using clinical assessment and a multibiomarker-guided approach.
Abstract:The objective of this document is to review the clinical applicability of coronary artery calcium (CAC) scoring in both asymptomatic and symptomatic patients at risk for cardiovascular disease. We begin by describing the pathological basis of atherosclerosis, the characteristic stages of atherosclerotic plaque development, and the mechanism and role of arterial calcifi cation in advanced atherosclerotic lesions. We also explain the utility of CAC scoring in cardiovascular risk assessment, discuss the most current clinical methods for measuring CAC, and examine major clinical studies reporting CAC scores in both asymptomatic and symptomatic heart patients. Lastly, the current recommendations for CAC scoring as stated by the American College of Cardiology/American Heart Association (ACC/AHA) are outlined, and a number of considerations for future research are provided. Atherosclerosis begins when certain factors cause chronic endothelial injury, which eventually leads to the build up of fi brofatty plaques in the intima of arterial blood vessels. In time, blood vessel walls can weaken, thrombi can form and plaques can send emboli to distal sites. There are six characteristic stages of plaque development. Mature plaques may be calcifi ed in an active process comparable to bone remodeling, where calcium phosphate crystals coalesce among lipid particles inside arterial walls. Calcifi cation is only present in atherosclerotic arteries, and the site and levels of calcium are non-linearly and positively associated with luminal narrowing of coronary vessels. Calcifi cation is also postulated to stabilize vulnerable plaques in atherosclerotic vessels. Recent studies have shown that CAC scoring can improve the management of both asymptomatic and symptomatic heart patients. Electron beam computed tomography (EBCT) and Multidetector computed tomography (MDCT) are two fast cardiac CT methods used to measure CAC. No matter what technique one uses, CAC is scored with either the Agatston or the "volume" score system. The ACC/ AHA currently fi nds it is reasonable for asymptomatic patients with intermediate Framingham risk scores (FRS) to undergo CAC assessment because these patients can be re-stratifi ed into the high risk category if their CAC scores are Ն400. Conversely, CAC measurement in asymptomatic patients with low or high FRS is not warranted. There is also no evidence to suggest that high risk asymptomatic patients with no detectable coronary calcium should not be treated with secondary prevention medical therapy. For symptomatic patients, the ACC/AHA recommends CAC assessment as a second line technique to diagnose obstructive CAD, or when primary testing modalities are not possible or are unclear. Furthermore, they do not recommend the use of CAC measurement to determine the etiology of cardiomyopathy, to help identify patients with acute MI in the emergency room, or to assess the progression or regression of coronary atherosclerosis. Future research needs to incorporate calcium scores with percentile rankings...
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