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QT Interval Prolongation and Sudden Cardiac Death in Diabetic Autonomic Neuropathy^*

Department of Internal Medicine, Divisions of Endocrinology and Metabolism and Nuclear Medicine, and the Department of Surgery, University of Michigan Medical Center Ann Arbor, Michigan 48109

Address requests for reprints to: Aaron I. Vinik, M.D., 2922B/0331 Taubman Health Care Center, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109.

Alterations in cardiac sympathetic innervation may result in QT interval prolongation and predispose to sudden arrhythmias and death. Sudden cardiac death occurs in diabetic patients who have autonomic neuropathy, but the cause is uncertain. In 30 patients with insulin-dependent diabetes mellitus who had no evidence of ischemic heart disease, cardiac autonomic neuropathy, determined by clinical tests, was found in 17. The corrected QT interval (QT_c), measured using Bazett’s formula at rest and peak exercise, was prolonged (>440 msec) in 12 of these patients at rest and in 15 at peak exercise. Prolonged QT_c intervals were found only in patients who had definite cardiac autonomic neuropathy. As a group, the QT_c interval (mean ± SD) in the diabetic patients with cardiac autonomic neuropathy was prolonged compared to that in patients without cardiac autonomic neuropathy at rest (447 ± 28 vs. 405 ± 9 ms; P < 0.0001) and peak exercise (468 ± 23 vs. 402 ± 23 ms; P < 0.0001). There was a direct linear relationship between the extent of cardiac autonomic neuropathy and the QT_c interval (r = 0.71; P < 0.001). One of the patients with cardiac autonomic neuropathy and prolonged QTC intervals had a nonuniform loss of adrenergic neurons in his heart demonstrated by meta-iodob-enzyl-guanidine scintigraphy, indicating sympathetic imbalance; he subsequently died unexpectedly. These data suggest that diabetic cardiac autonomic neuropathy may result in sympathetic imbalance and QT_c interval prolongation, predisposing these patients to sudden arrhythmias and death.

^* This work was supported by grants to the Clinical Research Center (5MO1-RR-00042-22) and the Michigan Diabetes Research and Training Center (AM-20572-07), and NIH Grant ROl-AM-21477.

Received September 18, 1986.

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