Autonomic neuropathy tests correlate with left ventricular mass and cardiac diastolic function in normotensive patients with type 2 diabetes mellitus and without left ventricular hypertrophy.

2010 
Proposed causes of diabetic cardiomyopathy include metabolic abnormalities (hyperglycemia and changes in myocardial lipid metabolism), hypertension (HPT) and autonomic neuropathy (AN) (1–4). Diabetes mellitus (DM) is associated with HPT and coronary atherosclerosis (5), which can reduce myocardial performance. There is an attractive hypothesis to explain the pathogenesis of diabetic cardiomyopathy. AN has been associated with a high cardiac mortality rate (6,7), and autopsy studies have found low concentrations of noradrenaline in diabetic patients with cardiomyopathy (8). In addition, Kahn et al (9) compared patients with and without AN, and found that patients with AN had reduced levels of plasma catecholamines; this finding was related to abnormalities in diastolic heart function. We previously reported that good glycemic control in patients with type 2 DM (DM2) and HPT could reverse left ventricular hypertrophy (LVH) (10,11). Unfortunately, we did not evaluate 24 h blood pressure (BP) in the present study. AN has been associated with hyperglycemia (6,7) and a small decrease in nocturnal BP (12,13). Therefore, a reasonable hypothesis is that AN is a means through which hyperglycemia causes preclinical myocardial abnormalities. The purpose of the present study was to evaluate the relationship between AN tests, and left ventricular mass index (LVMI) and cardiac diastolic function (CDF) in normotensive patients with DM2 and without AN symptoms or LVH.
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