Diabetic Cardiomyopathy: Evidence, Mechanisms, and Therapeutic Implications
Zhi You Fang,
Johannes B. Prins and
Thomas H. Marwick
University of Queensland, Brisbane, Queensland 4102, Australia
Correspondence: Address all correspondence and requests for reprints to: Prof. T. Marwick, University of Queensland Department of Medicine, Princess Alexandra Hospital, Ipswich Road, Brisbane, Queensland 4012, Australia. E-mail: tmarwick{at}soms.uq.edu.au
The presence of a diabetic cardiomyopathy, independent of hypertensionand coronary artery disease, is still controversial. This systematicreview seeks to evaluate the evidence for the existence of thiscondition, to clarify the possible mechanisms responsible, andto consider possible therapeutic implications.
The existence of a diabetic cardiomyopathy is supported by epidemiologicalfindings showing the association of diabetes with heart failure;clinical studies confirming the association of diabetes withleft ventricular dysfunction independent of hypertension, coronaryartery disease, and other heart disease; and experimental evidenceof myocardial structural and functional changes. The most importantmechanisms of diabetic cardiomyopathy are metabolic disturbances(depletion of glucose transporter 4, increased free fatty acids,carnitine deficiency, changes in calcium homeostasis), myocardialfibrosis (association with increases in angiotensin II, IGF-I,and inflammatory cytokines), small vessel disease (microangiopathy,impaired coronary flow reserve, and endothelial dysfunction),cardiac autonomic neuropathy (denervation and alterations inmyocardial catecholamine levels), and insulin resistance (hyperinsulinemiaand reduced insulin sensitivity).
This review presents evidence that diabetes is associated witha cardiomyopathy, independent of comorbid conditions, and thatmetabolic disturbances, myocardial fibrosis, small vessel disease,cardiac autonomic neuropathy, and insulin resistance may allcontribute to the development of diabetic heart disease.
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