The relationship between plasma endothelin-1, nitric oxide levels, and heart rate variability in patients with coronary slow flow.

Abstract

Coronary slow flow (CSF) is characterized by delayed opacification of coronary arteries in the absence of epicardial occlusive disease. In this study, we aimed to determine endothelin-1 (ET-1), nitric oxide (NOx) levels and time domain heart rate variability (HRV) parameters in patients with CSF and relationship among these parameters. Thirty-three patients with CSF detected in the coronary angiography (17 females; mean age 55 +/- 7) and 19 patients with normal coronary flow (10 females; mean age 54 +/- 11) as a control group were enrolled in the study. Patients were divided into two groups according to exercise testing as if positive (group A, n = 8) or negative (group B, n = 25). Plasma ET-1 levels were higher in the group A patients (28.7 +/- 17.4 pg/ml) than that of group B (15.9 +/- 10.6 pg/ml) and control group (6.0 +/- 5.7 pg/ml); and higher in group B patients than that of control group (P < 0.05). Although groups A and B did not differ according to plasma NOx levels (23.4 +/- 13.5 micromol/L vs. 32.8 +/- 22.7 micromol/L, P > 0.05), NOx levels in group A were lower than the control group (23.4 +/- 13.5 micromol/L versus 42.5 +/- 15.9 micromol/L, P < 0.05). Time domain HRV parameters were decreased in all patient groups. This was more prominent in group A. Additionally, HRV parameters were negatively correlated with ET-1 and TIMI frame counts. TIMI frame count was also significantly correlated with ET-1 and NOx levels (r = 0.61, P < 0.0001, r =-0.30, P < 0.05). Upon intravascular ultrasonography investigation, the common finding was longitudinally extended massive calcification throughout the epicardial arteries. Mean intimal thickness was 0.50 +/- 0.13 mm (group A; 0.58 +/- 0.11 mm, group B 0.47 +/- 0.12 mm, P = 0.029). The present study demonstrated that in patients with CSF, both increased plasma ET-1, decreased plasma NOx and diffuse atherosclerosis may cause the decrease in HRV by effecting myocardial blood flow.