ABSTRACT
Coronary heart disease (CHD) and its manifestations account for approximately half a million deaths annually in the United States, 25% of the nation’s total mortality [1]. Much progress has been made in defining the mechanisms involved in the pathogenesis and progression of CHD, devising new therapeutic approaches for the treatment and prevention of CHD, and identifying factors that promote susceptibility to this disease. Important lifestyle factors affecting CHD risk include exercise, smoking, diet and alcohol consumption [2]. Moderate drinking reduces risk of CHD mortality, and although it is generally accepted that about half of the risk reduction might be due to a beneficial effect of moderate consumption of alcohol or alcoholic beverages on plasma lipids [3-5], the effects of alcohol on other parameters undoubtedly contribute. Although there are many definitions of ‘moderate alcohol consumption’ the United States Departments of Agriculture and Health and Human Services define moderate drinking as ‘no more than one drink per day for women and no more than two drinks per day for men’ (a standard drink contains approximately 12 grams of ethanol, which is the amount present in a 12 oz bottle of beer, a 5 oz serving of table wine, or 1.5 ounces of 80 proof distilled spirits) [6]. The effects of alcohol on platelet aggregation and subsequent thrombus formation have been studied by several laboratories including our own [7-14], and is the topic of the present review. Platelets are of substantial interest because of their role in CHD-related mortality. Myocardial infarction (MI) most often results from thrombotic occlusion of stenosed coronary vessels. In this scenario, the blockage is due to the rupture of an atherosclerotic plaque, which exposes a thrombogenic surface to platelets. Adherence of platelets and subsequent thrombus formation eventually blocks flow through the affected coronary artery, causing ischemia, acute MI and potentially death [15]. An inhibitory effect of alcohol on platelet aggregation is therefore a potential factor in the reduced risk of CHD-related death with moderate drinking. In addition, studies have suggested that alcohol consumption might have a role in inhibiting the progression of atherosclerosis, a process that involves both plasma lipids and platelets [16]. While this chapter focuses mainly on the possibly beneficial aspects of moderate alcohol consumption on the hemostatic system, it is recognized that there are complex issues associated with drinking, which can vary from individual to individual. Some of these are discussed elsewhere in this volume.
