OBJECTIVE: It has previously been observed that coronary diameter may increase following relief of flow-limiting obstruction. Flow mediated dilatation (FMD) is a fundamental adaptive mechanism for arteries, which is dependent on intact endothelial function. We thus aimed to characterize whether the degree of this flow-mediated dilatation was related to risk factors, which may impair endothelial function. DESIGN: We measured coronary diameter with quantitative angiography before and after relief of chronic total or subtotal (>or=99%) occlusion in 171 patients, in which TIMI-0 or TIMI-1 flow was rapidly restored to TIMI-3 (with attendant increase in flow hypothesized to result in FMD). PATIENTS: Of the 171 patients, 73% were male, 62% were current or ex-smokers, 47% were diabetic, 53% had hypertension, 64% had dyslipidemia (documented hypercholesterolemia or total cholesterol >5.0 mg/dL) and 65% were taking statin therapy. RESULTS: Mean vessel diameter was 2.8 +/- 0.7 mm and flow-mediated dilatation measured 15.1% +/- 20.1% in target vessel, compared with 1.6 +/- 3.1 in control vessels (P < 0.05). FMD was strongly and inversely related to baseline vessel diameter (r = -0.48, P < 0.001). The degree of vessel dilation correlated negatively with the presence of diabetes (r = -0.33, P < 0.001), smoking (r = -0.30, P < 0.001) and extent of coronary artery disease (CAD, r = -0.17, P = 0.01) and positively with the use of statins (r = 0.27, P = 0.001). These factors, apart from extent of CAD, remained significant predictors of FMD on multivariate analysis. CONCLUSIONS: FMD occurs in human coronary arteries following restoration of flow. The magnitude of FMD appears related to vascular risk factors and their treatment. (c) 2008 Wiley-Liss, Inc.
OBJECTIVE: It has previously been observed that coronary diameter may increase following relief of flow-limiting obstruction. Flow mediated dilatation (FMD) is a fundamental adaptive mechanism for arteries, which is dependent on intact endothelial function. We thus aimed to characterize whether the degree of this flow-mediated dilatation was related to risk factors, which may impair endothelial function. DESIGN: We measured coronary diameter with quantitative angiography before and after relief of chronic total or subtotal (>or=99%) occlusion in 171 patients, in which TIMI-0 or TIMI-1 flow was rapidly restored to TIMI-3 (with attendant increase in flow hypothesized to result in FMD). PATIENTS: Of the 171 patients, 73% were male, 62% were current or ex-smokers, 47% were diabetic, 53% had hypertension, 64% had dyslipidemia (documented hypercholesterolemia or total cholesterol >5.0 mg/dL) and 65% were taking statin therapy. RESULTS: Mean vessel diameter was 2.8 +/- 0.7 mm and flow-mediated dilatation measured 15.1% +/- 20.1% in target vessel, compared with 1.6 +/- 3.1 in control vessels (P < 0.05). FMD was strongly and inversely related to baseline vessel diameter (r = -0.48, P < 0.001). The degree of vessel dilation correlated negatively with the presence of diabetes (r = -0.33, P < 0.001), smoking (r = -0.30, P < 0.001) and extent of coronary artery disease (CAD, r = -0.17, P = 0.01) and positively with the use of statins (r = 0.27, P = 0.001). These factors, apart from extent of CAD, remained significant predictors of FMD on multivariate analysis. CONCLUSIONS:FMD occurs in human coronary arteries following restoration of flow. The magnitude of FMD appears related to vascular risk factors and their treatment. (c) 2008 Wiley-Liss, Inc.