Lipid effects of smoking

Abstract

Cigarette smoking is believed to cause harmful cardiovascular and atherogenic effects resulting from changes in lipid metabolism. Intravenous nicotine and smoking raise plasma free fatty acid (FFA) levels through enhanced lipolysis resulting from sympathoadrenal stimulation. The study reported here investigated FFA-stimulated myocardial oxygen consumption (Mvo 2) in intact dogs. It was found that about half of the nicotine-induced rise in Mvo 2 resulted from metabolic stimulation by high concentration of FFA, and the remander was a result of enhanced mechanical activity of the heart directly produced by nicotine. In intact dogs, the increase in myocardial oxygen requirement resulting from excess myocardial FFA uptake also increased the severity of myocardial ischemic injury after acute coronary occlusion. Human studies with men who had smoked for more than 10 years showed that smokers had lower plasma high-density lipoprotein cholesterol fractions 2 and 3. High-density lipoprotein fraction 2 is reported to be antiatherogenic. Thus smoking appears to have at least two lipid effects that may promote coronary heart disease and atherosclerosis: increased plasma FFA and decreased plasma high-density lipoprotein cholesterol fraction.