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

Maurizio Galderisi, Brunella Capaldo, Milena Sidiropulos, Arcangelo D'Errico, Luigi Ferrara, Annamelia Turco, Pasquale Guarini, Gabriele Riccardi, Oreste de Divitiis

Journal: American journal of hypertension 2008;20(12):1283-90

PMID: 18047918

Abstract

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 multilinear 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.

Address: Department of Clinical and Experimental Medicine, Federico II University Hospital of Naples, Naples, Italy. [email protected]
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