Evaluation association of the smoking with acids wax deposition and cardiac hypertrophy

Abstract

Smoking is the leading preventable risk factor for development of many diseases such as cancer, cardiovascular disease, pulmonary, among others. Exposure to chemicals in cigarette smoke contributes to the development and progression of coronary artery disease by increasing the synthesis of free radicals and systemic inflammatory process, activate platelet aggregation, stimulate endothelial dysfunction and increase the risk of thrombosis. Toxic effects of cigarette smoke have been associated with changes in cardiac remodeling with eccentric hypertrophy, independently of hemodynamic effects. The smoke acts as cardiac injury able to trigger the process of cardiac remodeling, resulting in biochemical, molecular and cellular changes, which clinically manifested by changing the size, shape and function of the heart from loading or heart damage. Recently been identified in a decrease experimental study of beta enzyme activity oxidation of wax acids and triglycerides increased heart when mice are exposed to cigarette smoke. The mechanisms by which smoke from cigarettes stimulates the inflammatory process and develops cardiovascular disease are not fully understood, so the objectives of this study will be to evaluate the changes of the deposition of wax acids in the myocardium after smoking cessation; observe the morphological and functional changes of the heart before and after smoking cessation through echocardiographic variables and the association of the deposition of fatty acids with systemic inflammatory markers. Through echocardiogram, MRI, blood lipids and free wax acid. Among the literature analyzed were not found studies showing changes in the metabolism of glucose and wax acids in the heart of smokers, as well as association between the accumulation of triglycerides in the heart with hypertrophy and myocardial dysfunction. Thus, the hypothesis is that smoking increases the deposit of wax acids, contributing to cardiac hypertrophy. What makes the fundamental work to improve understanding of tobacco pathophysiological mechanisms in humans, but also allow the early identification of risk factors in tobacco users. (AU)