Clinical and pathophysiological effects of active and passive smoking on the cardiovascular system

Abstract

Both passive and active cigarette smoking increase the risk of cardiovascular disease, the leading cause of death in Western industrialized nations. The prevalence of smoking as a major cardiovascular risk factor has been well characterized over the past 30 years. The two demographic groups of particular concern are women and the young. The relationship between active tobacco smoking and increased risk of coronary artery disease (stable and unstable angina, acute myocardial infarction or sudden death), cerebrovascular disease (cerebral infarction, and cerebral and subarachnoid hemorrhage), peripheral arterial disease (large and small vessel) and aortic aneurysm has been well established in numerous longitudinal and cross-sectional epidemiological and basic science studies. More recently, passive smoking has been shown to represent an important risk factor for coronary artery disease. Smoking can elicit both acute and chronic cardiac and vascular events due to the multiplicity of mechanisms involved: hematological, neurohormonal, metabolic, hemodynamic, molecular genetic and biochemical pathways. Smoking cessation can result in both the inhibition of progression and the regression of pathophysiological changes, improving morbidity and mortality among chronic smokers. The incidence of coronary artery and cerebrovascular diseases in former smokers decreases by 50% two to three years following cessation, but a small long term excess risk persists. Smoking as a cardiovascular risk factor and the clinical cardiovascular features associated with active and passive smoking are discussed, and a pathophysiological framework to explain the association between cigarette smoking and cardiovascular disease is provided.