Increased left ventricular mass in normotensive type 1 diabetic patients with diabetic nephropathy.

OBJECTIVE

Diabetic nephropathy increases the risk of premature cardiovascular disease and sudden death, particularly in type 1 diabetic patients. One possible mechanism for this risk may be left ventricular hypertrophy. In our study, we aimed to evaluate left ventricular structure and function in normotensive type 1 diabetic patients with and without nephropathy.

RESEARCH DESIGN AND METHODS

M-mode and Doppler echocardiography was performed in 17 type 1 diabetic patients with nephropathy (albuminuria [median (range)], 345 (135-2,846) mg/24 h) and compared with 34 normotensive, normoalbuminuric (10 [3-30] mg/24 h) type 1 diabetic patients matched for arterial blood pressure (mean +/- SD) ([134/77] +/- [13/7] vs. [129/78] +/- [12/7] mmHg), age (40 +/- 11 vs. 42 +/- 10 years), duration of diabetes (28 +/- 7 vs. 28 +/- 6 years), and BMI (24.2 +/- 4.2 vs. 24.6 +/- 2.4 kg/m2).

RESULTS

Left ventricular mass (LVM) index was significantly higher in patients with nephropathy compared with patients with normoalbuminuria (100.8 +/- 10.3 vs. 88.2 +/- 21.0 g/m2, respectively; P = 0.02). Greater ventricular septum width was demonstrated in the nephropathic group compared with the control group (9.4 +/- 1.0 vs. 8.2 +/- 1.3 mm, respectively; P = 0.002). No significant difference in posterior wall thickness was apparent. The nephropathic group tended to have reduced diastolic function (E/A ratio, 1.2 +/- 0.3 vs. 1.4 +/- 0.4; P = 0.09). Fractional shortening was normal and about the same in the two groups. The groups did not differ with respect to serum creatinine or hemoglobin, while metabolic control (assessed by HbA1c) and plasma renin and prorenin levels were elevated in the nephropathic group compared with the normoalbuminuric group.

CONCLUSIONS

A blood pressure-independent increase in LVM may contribute to the increased cardiac morbidity and mortality in normotensive type 1 diabetic patients with diabetic nephropathy. Glycemic abnormalities and activation of the renin-angiotensin system may lead to the ventricular enlargement.