Smoking accelerates the onset of acute coronary disease.Smoker’s paradoxis the term applied to the observations that the short-term prognosis following an acute myocardial infarction is better in the smoker than in the nonsmoker. Efforts to explain these surprising observations have not been successful. The approach used in this study was to compare the pathologic findings in the coronary arteries following a complete histologic examination of the major branches of the epicardial coronary tree in smokers and nonsmokers. I found many ulcerated plaques in both smokers and nonsmokers, often without associated luminal stenosis or luminal thrombosis. These ulcerated plaques were discovered only on histologic examination and were consistently associated with dense foci of adventitial inflammatory cells. Based on these findings, the following hypothesis is proposed: Smoking injures the coronary artery endothelium, causing erosions, ulcerations, and a chronic inflammatory response in the arterial adventitia. These ulcerated plaques persist as chronically active, open ulcerations, constantly exposed to flowing blood, leading to increasing luminal stenosis as long as smoking continues. These ulcerated plaques eventually form the substrate for occlusive thrombosis and acute coronary events and are components of active, progressive, inflammatory, atherosclerotic disease. Premature acute coronary disease in the young smoker is due to accelerated plaque ulceration, luminal stenosis, and occlusive thrombosis. Smoker’s paradox can be explained by rapid resolution and healing of these potentially unstable ulcerated plaques when the patient is required to stop smoking during hospitalization for the acute myocardial infarction event.
