Abstract
Coronary slow-flow phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. Thus, it still remains to be determined whether either microvascular or epicardial diffuse atherosclerotic disease is related to slow flow. In this study, we aimed to determine the carotid artery intima-media thickness, which is a marker of atherosclerosis in patients with coronary slow flow, and its possible relationship with the total homocysteine level. The study population consisted of 88 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. Forty-four patients with angiographically proven coronary slow flow and 44 individuals with normal coronary flow pattern with similar risk profiles were enrolled in the study. Coronary flow patterns of the latter were determined by the thrombolysis in myocardial infarction frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and the right common carotid artery with a 12-MHz linear array transducer. Plasma homocysteine, folate and B12 levels were measured from blood samples. Plasma homocysteine levels (mumol/l) and carotid intima-media thickness (mm) of patients with coronary slow flow were found to be significantly higher than that of controls (12.4+/-4.9 vs. 8.5+/-2.8, P=0.0001; 0.75+/-0.08 vs. 0.69+/-0.06, P=0.0001, respectively). The plasma folate level (ng/ml) was lower in coronary slow-flow patients than in controls (13.8+/-4.4 vs. 16.5+/-5.6, P=0.014). The plasma homocysteine level was significantly positively correlated with the mean thrombolysis in myocardial infarction frame count and intima-media thickness of the carotid artery in correlation analysis (r=0.58, P=0.0001; r=0.41, P=0.0001; respectively). Homocysteine levels and carotid intima-media thickness increased but folate levels decreased in patients with coronary slow flow. The present findings allow us to conclude that the possible disturbance in the metabolism of homocysteine in patients with coronary slow flow may have a role in the etiopathogenesis of this phenomenon by causing generalized atherosclerosis.
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