Current smokers develop more posterior myocardial infarctions probably due to increased tendency to thrombosis

This investigation was carried out to determine whether smokers developed smaller infarcts as assessed by peak enzyme levels and also to what extent smoking could modify infarct localization. The study included 753 patients, of whom 351 had no history of previous coronary heart disease (CHD) (angina pectoris and/or myocardial infarction (MI)). The investigation was designed as an exposed (smoking) versus non-exposed (non-smoking) cohort study. Outcome was infarct size, posterior versus non-posterior MI and non-Q-wave versus Q-wave infarcts. In the total cohort of patients, 312 (41%) were smokers, the corresponding number in the restricted cohort of patients without a previous CHD (CHD-0-pts) was 169 (48%). Smokers were younger than non-smokers, and more of them were males. It was found that infarct size was similar in smokers and in non-smokers (crude and adjusted effects). Crude effects showed that smokers developed significantly more posterior infarcts than non-smokers; odds ratio (OR) for developing a posterior MI was 1.95 (2p < 0.001) (all patients) and 2.34 (2P < 0.001) (CHD-0-pts), respectively. After adjusting for confounders (logistic regression model), OR in the two groups was 1.24 (2p = 0.256) and 1.95 (2p = 0.01), respectively. The study shows that current smokers were younger, and indicates that in those without a previous CHD, significantly more of them developed a posterior MI.