Journal
HERZ
Volume 41, Issue 3, Pages 201-207Publisher
URBAN & VOGEL
DOI: 10.1007/s00059-016-4415-7
Keywords
Heart failure; Diabetes mellitus; Diabetic cardiomyopathy; Fibrosis; Therapy
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Heart failure (HF) affects approximately 1-2 % of the adult population. Diabetes mellitus (DM) is one of the most frequent comorbidities in HF, portending a worse prognosis. DM is associated with an increased risk of artery disease, and consequently of post-ischemic HF, but it may also alter directly the myocardial structure and function. Insights into the pathophysiological mechanisms of diabetic cardiomyopathy have been provided by both experimental and clinical investigations. In recent years, it has emerged that the fibrotic process is a result of the convergence of multiple neurohormonal alterations in diabetic cardiomyopathy at the basis of disease progression and phenotype determination: HF with reduced or preserved ejection fraction. Therapies for HF and DM should demonstrate an improved prognosis and have a neutral effect on glucose homeostasis and the risk of HF development.
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