Cigarette Smoking as a Risk Factor of Coronary Artery Disease and its Effects on Platelet Function
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Vol. 2, No. 1: 27-33 (2004) © PTID Society
Cigarette Smoking as a Risk Factor of Coronary Artery Disease and its Effects on Platelet Function Teruo Inoue Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Koshigaya, Saitama, Japan ABSTRACT: It has been well established that cigarette smoking is a powerful risk factor for coronary artery disease. A number of epidemiologic studies have shown a strong association between cigarette smoking and atherosclerosis, myocardial infarction and death from coronary artery disease. In addition to active smoking, passive smoking can also carry a risk of coronary artery disease. Although the detailed mechanism through which cigarette smoking is associated with cardiovascular disease has not yet been clarified, it is suggested that cigarette smoking is related to thrombogenesis, as well as atherogenesis, and blood platelet behavior is thought to be prominent among the proposed mechanisms involved in atherogenesis and thrombogenesis. The following is a review of evidence that cigarette smoking affects platelet function. PLATELET ACTIVATION BY CIGARETTE SMOKING Platelet aggregation studies The most common approach to studying the effect of cigarette smoking on platelet function has been to measure the platelet aggregation response to agonists ex vivo, e.g. adenosine diphosphate (ADP), collagen, thrombin, platelet activating factor, etc. The relationship between platelet aggregation and cigarette smoking was examined by a large number of studies. These studies suggest that smoking has two effects on platelets, i.e., a significant acute potentiation of platelet activation occurring shortly after smoking a cigarette, and a chronic desensitization of the cell to activating agents occurring during the period between cigarettes. Although there are numerous longitudinal investigations of the acute effects of smoking on platelet aggregation, the results produced have been conflicting. Some have demonstrated increased platelet aggregability immediately after smoking [1-4] while others have found no such change [5-7]. Blache and colleagues [4] observed that platelet aggregation to thrombin and ADP
increased significantly 10 minutes after inhalation of one cigarette smoke. However, Siess and colleagues [5] demonstrated that cigarette smoke inhalation did not enhance platelet aggregation stimulated by ADP, epinephrine, and collagen. On the other hand, regarding the effects of chronic smoking, there have also been conflicting reports of increased, decreased and unaltered platelet aggregation response to agonists ex vivo by conventional platelet aggregometric methods [8-10]. The cross sectional results from the Caerphilly Collaborative Heart Disease Study [11] show that the ADPinduced platelet aggregation response was increased among habitual smokers, but the finding was mainly seen in the subjects who had smoked cigarettes shortly before venisection. Conversely, Foo and colleagues [9] demonstrated that in habitual smokers platelet aggregability to aggregating age
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