Parental cigarette smoke as a risk factor for early coronary artery disease and sudden unexpected death in perinatal and infant death.

There is also an association between smoke and other pregnancy problems, such as low birth weight and miscarriage. The combustion products of nicotine are heterogeneous and cause specific lesions of the autonomic nervous system. Gaseous combustion products, such as carbon oxide, lead to atherosclerotic plaques in the cardiovascular district and in the sino-atrial and atrio-ventricular arteries. We recorded a high incidence of preatherosclerotic lesions in the coronaries of fetuses with smoker mothers. If the maternal smoking habit persists, juvenile plaques can be observed in the infant. The study population included 22 stillborns, 6 neonates and 49 infants dying suddenly and unexpectedly. Samples of the myocardium and the major coronary arteries were stained with Hematoxylin-eosin and Azan. The cardiac conduction system was removed in two blocks (the sino-atrial node and the atrio-ventricular junction) cut serially at intervals of 40-mm and stained alternately with Hematoxylin-eosin and Azan. In 55% of perinatal and in 67% of infant deaths, multifocal coronary early atherosclerotic lesions of varying entity (from focal plaques with mild myointimal thickening to juvenile soft plaques) were detected. In 45% of stillborns and in 75% of infants with coronary lesions the parents were smokers. A significant correlation was observed between early atherosclerotic lesions and the risk factor considered. The reduction in the coronary lumen can be such as to cause alterations in cardiac blood supply. The harmful effects of cigarette smoking are not confined to the coronaries but also affect the small and medium-caliber arteries, including the sino-atrial and atrio-ventricular arteries. Analysis of our series suggests that parental cigarette smoking has the highest significance among the risk factors considered in the pathogenesis of sudden perinatal and infant death. The nicotine combustion products cause an oxygenation deficit of the common myocardium, as well as developmental abnormalities of the conducting tissue, laying the morphological substrate for arrhythmias. The early atherosclerotic lesions can be attributed to a direct action of the combustion products of nicotine on the smooth muscle cells of the tunica media of the arterial walls and/or on the neurons, interfering with homeostasis and cell differentiation, as well as to an indirect action of hypoxemia induced by arterio- and arteriolosclerosis.