Abstract
Smoking contributes to the progression of atherosclerotic heart disease by causing endothelial dysfunction. In the present study the effect of smoking on endothelial functions and coronary flow was investigated, as well as the relationship of these factors with oxidative stress parameters, in subjects with normal coronary arteries. The study group comprised 87 patients with angiographically normal coronary arteries (36 smokers, 51 nonsmokers). Coronary flow patterns were determined by the Thrombolysis In Myocardial Infarction (TIMI) frame count method. Endothelial function was evaluated by high-frequency ultrasound imaging of the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the endproduct of lipid peroxidation, malondialdehyde (MDA), were measured as oxidative stress markers. Mean TIMI frame count was significantly higher in smokers than nonsmokers (42.2 +/- 16 vs 29.5 +/- 9.5, p = 0.0001). Endothelium-dependent flow-mediated dilatation was 6.81+/-1.95% in nonsmokers and 5.7 +/- 2.2% in smokers (p = 0.0001). The smokers had dramatically higher levels of SOD and MDA and lower levels of GSH than the nonsmoker group. Smoking induced oxidative stress deteriorates coronary blood flow by disturbing endothelial function.
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