Coronary Flow Reserve Abnormalities in Patients with Diabetes Mellitus Who Have End-stage Renal Disease and Normal Epicardial Coronary Arteries

Background: Diabetic nephropathy is associated with increased cardiovascular events. Coronary atherosclerosis is responsible for many of these events, but other mechanisms such as impaired flow reserve may be involved. The purpose of this study was to define the prevalence and mechanism of abnormal coronary velocity reserve (CVR) in patients with diabetes mellitus who have nephropathy and a normal coronary artery.

Methods: Patients undergoing catheterization for clinical purposes were enrolled. CVR was measured with a Doppler ultrasound scanning wire in a normal coronary in 32 patients without diabetes mellitus, 11 patients with diabetes mellitus who did not have renal failure, and 21 patients with diabetes mellitus who had nephropathy. A CVR <2.0 was considered to be abnormal.

Results: Patients with diabetes mellitus who had renal failure had a higher incidence of hypertension and left ventricular hypertrophy. The average peak velocity (APV) at baseline was higher in patients with diabetes mellitus who had renal failure. At peak hyperemia, APV increased in all 3 groups, with no difference between groups. The mean CVR for patients without diabetes was 2.8 +/- 0.8 and was not different from that in patients with diabetes mellitus who did not have renal failure (2.7 +/- 0.7), but was lower than that in patients with diabetes mellitus who had renal failure (1.6 +/- 0.5; P < 0.001). Abnormal CVR was observed in 9% of patients without diabetes mellitus, 18% of patients with diabetes mellitus who did not have renal failure, and 57% of patients with diabetes mellitus who had renal failure, and abnormal CVR was caused by an elevation of baseline APV in 66% of these cases. The baseline heart rate and the presence of diabetes mellitus with renal failure were independent predictors of abnormal CVR by multivariable analysis.

Conclusions: Patients with diabetic nephropathy have abnormalities in CVR in the absence of angiographically evident coronary disease.