Nonischemic heart failure in diabetes mellitus.
OBJECTIVE
Diabetic patients with heart failure have a poor prognosis. Although it has been demonstrated in animal models that metabolic maladaptation plays a pivotal role in contractile dysfunction of the heart, the understanding of 'diabetic cardiomyopathy' and its treatment in humans remains incomplete.


RESULTS
Epidemiological studies show that structural changes in the left ventricle can be demonstrated before onset of clinical diabetes. Diastolic dysfunction is the earliest manifestation that is associated with increasing level of serum-free fatty acids and worsening glycemic control. Spectroscopic and histologic evidence in the human myocardium indicates a maladaptive metabolic response in diabetes, characterized by intramyocellular triglyceride accumulation. Studies also suggest a link between myocardial isoform switching, calcium homeostasis and altered metabolism in the development of heart failure. However, treatment directed at deranged metabolic control in diabetes is effective only in animals, and not in humans.


CONCLUSIONS
Although clinical studies suggest the existence of 'diabetic cardiomyopathy', it is still difficult to prove causality. However, animal models and human studies suggest that systemic metabolic derangements may lead to metabolic, functional and structural maladaptation of the heart. The exact mechanisms of heart failure in diabetes remain elusive.
Guha
Ashrith
A
Department of Internal Medicine, Division of General Medicine, The University of Texas Medical School at Houston, Houston, Texas 77030, USA.
Harmancey
Romain
R
Taegtmeyer
Heinrich
H
D000818:Animals; D009202:Cardiomyopathies / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D048909:Diabetes Complications / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000378:metabolism; D006333:Heart Failure / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D054144:Heart Failure, Diastolic / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D006801:Humans; D009206:Myocardium / Q000378:metabolism / Q000473:pathology