Influence of smoking status on progression of endothelial dysfunction

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Abstract
Background: Cigarette smoking is a major risk factor for developing coronary artery disease and is associated with increased coronary morbidity and mortality in patients with established atherosclerosis. This report describes the influence of smoking on coronary endothelial function in normotensive patients with coronary artery disease, but without left ventricular dysfunction, severe hypercholesterolemia, or insulin‐dependent diabetes mellitus. Methods: Placebo‐treated patients (n = 54) from a larger study assessing coronary endothelial function were classified at baseline as smokers or nonsmokers for this subgroup analysis. Patients underwent coronary angiography at baseline and again after 6‐month follow‐up. Results: At baseline, there was a trend for a greater decrease in target segment diameter (n = 54) in smokers compared with nonsmokers (‐ 17.2 ± 5.3% vs. ‐8.0 ± 2.5%, acetylcholine 10−4 mol/1). All measured coronary artery segments (n = 202) showed similar responses (‐ 7.3 ± 2.7% vs. ‐ 3.8 ± 1.3%, acetylcholine 10−4 mmol/1, for smokers vs. nonsmokers, respectively). After 6 months, smokers showed an even greater vasoconstrictor response to acetylcholine whereas nonsmokers did not (‐ 21.7 ± 5.3% vs. ‐ 8.3 ± 2.5%, acetylcholine 10−4 mmol/1). The vasodilatory response to nitroglycerin was similar in smokers and nonsmokers. Conclusions: In current smokers, a marked decline in endothelium‐dependent vasomotor response was observed over a 6‐month period.