Cigarette smoking-related cardiovascular diseases have been described widely. However, the mechanisms of their effects on cardiovascular system were not totally clear. The effects of nicotine and carbon monoxide on blood vessel walls, unfavorable lipid profiles, increased myocardial work and the decreased oxygen carrying capacity of the blood of smokers contribute to the overall effect of cigarette smoking on cardiovascular disease [3J. Of the increased cardiovascular risk caused by smoking, it is estimated that approximately one-tenth of this is due to smoking-induced changes in serum lipid , The majority of studies indicate elevations in serum cholesterol, phospholipids, triglycerides, low-density lipoprotein (LDL) and increased hepatic lipase activity in smokers, with decreased serum high-density lipoprotein (HDL) cholesterol ,
A mechanism to explain the link between smoking and some of the observed changes in serum lipid and lipoprotein concentrations includes the pharmacological effects of nicotine in stimulating sympathetic nervous activity and release of catecholamines. Catecholamines mediate lipolysis, causing an increase in plasma concentrations of free fatty acids and very low-density lipoprotein triglycerides. Free fatty acids stimulate hepatic secretion of very low-density lipoprotein and hence triglycerides and high-density lipoprotein concentrations vary inversely with low-density lipoprotein concentrations in serum , On the other hand, smokers had higher levels of fibrinogen, plasminogen activator inhibitor 1 (PAI-1) activity and fasting and steady-state C-peptide levels during the clamp. They also showed insulin resistance and lipid intolerance with an impaired triglyceride clearance after a mixed test meal. Insulin resistance is an important reason for promoting the increased cardiovascular morbidity in smokers ,
Of thousands of cigarette smoke compounds, many are capable of generating reactive oxygen species (ROS) during metabolism. ROS can initiate a serial of cellular responses, such as activation of nuclear factor kappa B (NF-kB), which plays an important role in the proinflammatory process. NF-kB can induce IL-1 beta, platelet-activating factor (PAF) and tumor necrosis factor (TNF) , IL-1 beta is well known as an inducer of several other proinflammatory enzymes such as the inducible cyclooxygenase-2 (COX-2); PAF is shown to benefit platelet aggregation. These are two factors involved in atherogenesis , TNF may decrease myocardial contraction through enhancing inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production or by inducing myocardial apoptosis ,
In addition, cigarette smoking is associated with unhealthy eating patterns, including increased intakes of alcohol, total fat, cholesterol, saturated fat, a lower consumption of foods with fibers such as fruits and vegetables that may lower cholesterol levels, as well as deficiencies of vitamin C, E and beta-carotene [11,12], These factors make smokers and heavy alcohol users more predisposed to cardiovascular disease.
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