As well as being an independent risk factor for the development of CHD, cigarette smoking is associated with changes in the lipoprotein distribution and other metabolic factors that promote atherogenesis.
Nicotine stimulation of sympathetic nervous system activity results in elevation of plasma free fatty acids and very low density lipoproteins. Smoking also clearly reduces HDL-cholesterol and may reduce HDL-cholesterol antiatherogenic effects by altering its composition. Smoking cessation trials have documented a significant rise in HDL-cholesterol after smoking cessation. Cigarette smoking in women is associated with earlier menopause and lower estrogen levels, which contribute to an increased CHD risk (Billimoria, 1975 [C]; McBride,1992 [R]; Scheffler, 1992 [C]). |