Influence of cardiovascular autonomic neuropathy on atherogenesis and heart function in patients with type 1 diabetes

Diabetes Res Clin Pract. 2009 Jan;83(1):26-31. doi: 10.1016/j.diabres.2008.09.007. Epub 2008 Nov 14.

Abstract

Aim: Cardiovascular autonomic neuropathy (CAN) increases mortality of patients with type 1 diabetes (Type 1 DM). We set out to find out whether the presence of CAN in asymptomatic, normotensive Type 1 DM affects endothelial function (marker of atherogenesis) and left ventricle function (marker of cardiomyopathy).

Methods: Twenty-one Type 1 DM with CAN (Group A) and 35 Type 1 DM without CAN (Group B) were enrolled in the study. None of them suffered from any cardiovascular disease nor advanced chronic complications of diabetes. Both groups were comparable in age, glycemic control, BMI, and blood pressure. Markers of endothelial dysfunction and chronic inflammation were used as indicators of incipient atherogenesis. Left ventricle function was evaluated using echocardiography.

Results: Both groups did not differ in any parameter of atherogenesis. However we found a statistically significant difference in values characterizing systolic and diastolic left ventricle functions between the groups.

Conclusions: CAN is not associated with elevation of markers of endothelial dysfunction and chronic inflammation in normotensive asymptomatic Type 1 DM. However CAN is associated with the impairment of systolic and diastolic left ventricle function and can thus be regarded as one of the risk factors of diabetic cardiomyopathy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Atherosclerosis / etiology
  • Atherosclerosis / physiopathology*
  • Autonomic Nervous System Diseases / physiopathology*
  • Cardiomyopathies / physiopathology*
  • Diabetes Mellitus, Type 1 / complications
  • Diabetes Mellitus, Type 1 / physiopathology*
  • Diabetic Neuropathies / physiopathology*
  • Echocardiography
  • Female
  • Humans
  • Male
  • Middle Aged
  • Ventricular Dysfunction, Left / etiology
  • Ventricular Dysfunction, Left / physiopathology*