The coronary angiograms of 120 consecutive patients under 40 years of age were examined. Ten new cases of myocardial infarction with normal coronary arteriogram were identified (group 1) and compared with 30 cases of myocardial infarction and obstructive coronary disease (group 2). Heavy cigarette smoking was the sole major risk factor in group 1. Patients in group 2 smoked as well but most also had hypercholesterolaemia or hypertension. Pre- and postinfarction angina was rare among the patients with myocardial infarction and normal coronary arteriogram, and recanalisation after smoking-induced thrombotic occlusion is thought to be the most likely mechanism. Smoking-induced thrombosis is only likely to be recognised in special circumstances, when it develops in apparently normal coronary arteries, is followed by recanalisation, and is complicated by infarction as a permanent marker of previous obstruction to regional myocardial blood flow. Thrombotic occlusion of a "normal" coronary artery without recanalisation will only be recognised when infarction is fatal. If smoking can predispose to thrombosis in "normal" coronary arteries, it may be even more likely to accelerate thrombosis in atheromatous coronary arteries. The importance of recognising group 1 may well be in relation to the much commoner group 2.
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