Decreased Myocardial Perfusion Reserve in Diabetic Autonomic Neuropathy

Abstract

The pathophysiological mechanisms responsible for increased cardiovascular mortality in diabetic autonomic neuropathy are unknown. To investigate the effect of autonomic neuropathy on myocardial function, we performed dynamic contrast-enhanced magnetic resonance perfusion imaging during baseline conditions and after Dipyridamole-induced vasodilatation in nine type 1 diabetic patients with autonomic neuropathy (AN+), defined by cardiovascular tests, as well as in 10 type 1 diabetic patients without autonomic neuropathy (AN−) and 10 healthy control subjects. Baseline myocardial perfusion index (Ki) was similar in the three groups (AN+ 88.6 ± 8.7 ml · 100 g−1 · min−1, AN− 82.6 ± 7.2, control subjects 93.7 ± 9.0) (means ± SE). Ki during Dipyridamole vasodilatation was significantly lower in the patients with autonomic neuropathy (P < 0.001) than in the other groups (AN+ 131.1 ± 13.0 ml · 100 g−1 · min−1, AN− 177.3 ± 8.6, control subjects 197.2 ± 8.9). Mean blood pressure was unchanged during Dipyridamole infusion in AN− and control subjects, whereas a significant blood pressure decrease was found in AN+ (15.6 ± 2.6 mmHg, P < 0.025). There was a significant correlation between blood pressure response to Dipyridamole and myocardial perfusion reserve index. We conclude that type 1 diabetic patients with autonomic neuropathy have a decreased myocardial perfusion reserve capacity when challenged with a vasodilatator, a finding that may in part be the pathophysiological substrate for the increase in mortality in these patients. The underlying mechanism may be defective myocardial sympathetic vasodilatation, a lack of ability to maintain blood pressure during vasodilatation, or both.