Two morphological features may be seen as a main result of the cardiovascular cell damage caused by cigarette smoking: myocardial cell necrosis and smoke cardiomyopathy that, however, can lead to cell necrosis in case of chronic prolonged exposure to tobacco smoke. Both these pathological patterns recognise hypoxia as the basic mechanism. Cardiovascular cell damage may involve either myocardial cell or coronary artery wall determining a varied but a wide spectrum of alterations. Necrosis may be well defined as a result of those morphological changes which follow cell death in a living tissue or organ with partial or total loss in their function. All infarcts of the heart muscle belong to the group of necrotic lesions, but not all cardiac necroses are necessarily infarcts. Coronarogenic, or non-coronarogenic mechanism following a direct action of tobacco compounds on myocardial cells may induce myocardial cell necrosis. Smoke cardiomyopathy is probably the most typical evidence of cellular damage induced by cigarette smoking on the myocardium. The term cardiomyopathy is used to describe all those forms of degenerative myocardial lesions caused directly by toxics or metabolic substances and, indirectly, by changes in blood flow which are able to induce chronic hypoxia. Initially, smoke cardiomyopathy is not characterised by necrotic phenomena but, instead, by alterations of those intracellular structures RNA- related like mitochondria and ribosomes, which are primarily deputed to carry out metabolic and respiratory pathways of myocardial cells, the function of which strongly depends on oxygen availability. Experimental findings documented undoubtedly either the type of cellular changes or their reproducibility after both acute or chronic exposure to cigarette smoke.