Cigarette Smoking and Platelet Function: Relation to Nicotine, Carbon Monoxide and Saturated Fat

Abstract

Smoking has been associated with myocardial infarction, independently of its association with atherosclerotic lesions (1). Since coronary thrombosis is the proximate cause of acute myocardial infarction (2) as confirmed recently by the success of thrombolysis to reopen coronary arteries (3), smoking could act directly on the predisposition to thrombosis. Platelet reactivity seems to play a key role in the thrombotic tendency since, in a recent prospective study on 2500 subjects in Wales (5), aspirin significantly reduced acute coronary events (4) and platelet hyperaggregability to ADP was significantly related to the prevalent cases of myocardial infarction. Thus, it is important to determine whether smoking increases platelet reactivity and additionally which smoke components could be involved in this effect. Finally, in the Seven Country Study (6), smoking was less of a risk factor for heart attacks in Southern Europe and Japan than in the USA and northern Europe. Since the consumption of saturated fats was much lower in Japan (3% of calories) and southern Europe (7–10%) than in the USA (18%) and northern Europe (19–22%), the effect of smoking on platelets could be additive to that of saturated fats which are known to markedly increase their reactivity (7). Results of our studies on the effect of smoking, smoke components and saturated fats on platelet function tests are briefly reviewed hereafter.