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Review
. 2006 Mar 15;22(4):305-8.
doi: 10.1016/s0828-282x(06)70914-x.

Diabetic cardiomyopathy: where are we 40 years later?

V Sharma  1 , John H McNeill
Affiliations
Review

Diabetic cardiomyopathy: where are we 40 years later?

V Sharma et al. Can J Cardiol. .

Abstract
in English, French

Diabetic cardiomyopathy is a cardiac disease that arises as a result of the diabetic state, independent of vascular or valvular pathology. It manifests initially as asymptomatic diastolic dysfunction, which progresses to symptomatic heart failure. The compliance of the heart wall is decreased and contractile function is impaired. The pathophysiology is incompletely understood, but appears to be initiated both by hyperglycemia and changes in cardiac metabolism. These changes induce oxidative stress and activate a number of secondary messenger pathways, leading to cardiac hypertrophy, fibrosis and cell death. Alterations in contractile proteins and intracellular ions impair excitation-contraction coupling, while decreased autonomic responsiveness and autonomic neuropathy impair its regulation. Extensive structural abnormalities also occur, which have deleterious mechanical and functional consequences.

La myocardiopathie diabétique est une maladie cardiaque qui se déclare à cause de l’état diabétique, indépendamment d’une pathologie vasculaire ou valvulaire. Elle se manifeste d’abord sous forme de dysfonction diastolique asymptomatique, puis elle dégénère en insuffisance cardiaque symptomatique. La souplesse de la paroi cardiaque diminue et la fonction contractile se détériore. On ne comprend pas tout à fait sa physiopathologie, mais elle semble être déclenchée tant par l’hyperglycémie que par des modifications au métabolisme cardiaque. Ces modifications induisent un stress oxydatif et activent plusieurs voies messagères secondaires, lesquels provoquent une hypertrophie cardiaque, une fibrose et la mort cellulaire. Des altérations aux protéines contractiles et aux ions intracellulaires compromettent le couplage excitation-contraction, tandis que la diminution de la réactivité et de la neuropathie autonomes nuit à sa régulation. Des anomalies structurelles généralisées se produisent également et ont des conséquences mécaniques et fonctionnelles délétères.

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Figures

Figure 1
Figure 1
Overview of the etiology of diabetic cardiomyopathy. AGE Advanced glycosylation end products; NO Nitric oxide; PKC Protein kinase C; PPAR-α Peroxisome proliferator-activated receptor-alpha; SNS Sympathetic nervous system
See this image and copyright information in PMC

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