4.3 Article

Determinants of reduction of coronary flow reserve in patients with type 2 diabetes mellitus or arterial hypertension without angiographically determined epicardial coronary stenosis

Journal

AMERICAN JOURNAL OF HYPERTENSION
Volume 20, Issue 12, Pages 1283-1290

Publisher

OXFORD UNIV PRESS
DOI: 10.1016/j.amjhyper.2007.08.005

Keywords

diabetes mellitus; arterial hypertension; Doppler echocardiography; coronary flow reserve; left-ventricular mass

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Background: Coronary flow reserve (CFR) may be reduced even in the absence of coronary artery disease. We investigated the determinants of CFR impairment in Type 2 diabetes mellitus (DM2) and in arterial hypertension (HTN) without epicardial coronary artery stenosis. Methods: Twenty-eight patients with DM2 and 27 with HTN, both with normal coronary angiography, and 18 healthy controls underwent transthoracic echocardiography, including Doppler recording of the distal left anterior descending artery, at rest as well as after high-dose dipyridamole. Coronary flow reserve was calculated as the hyperemic to resting coronary diastolic peak velocities ratio. Results: The three groups were comparable for sex, age, and heart rate. Systolic and mean blood pressures were higher in DM2 and HTN patients than in control subjects. Diabetic and hypertensive patients had a higher left-ventricular mass index (LVMi) and relative wall thickness, impaired diastolic indexes, and lower CFR compared with control subjects (P =.02 and P =.03, respectively) because of lower hyperemic coronary velocity (P =.005 and P =.004, respectively). After a multi-linear regression analysis (using age, sex, HTN status, DM2 status, smoking, total cholesterol/HDL-cholesterol ratio, and LVMi as potential determinants), the LVMi increase was the main predictor of the reduction of CFR, adjusted for mean BP (P <.0001), in the pooled population, with a minor contribution of age (P =.03), HTN status (P =.02), and DM2 status (P =.03). Conclusions: In Type 2 DM and HTN without epicardial coronary stenosis, an impairment of CFR is demonstrable. This is partly explained by an increased left-ventricular mass, able to condition the hyperemic stimulation of myocardial blood flow. Am J Hypertens 2007;20:1283-1290 (c) 2007 American Journal of Hypertension, Ltd.

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