Abstract
Diabetic cardiomyopathy is defined as ventricular dysfunction initiated by alterations in cardiac energy substrates in the absence of coronary artery disease and hypertension. In addition to the demonstrated burden of cardiovascular events associated with diabetes, diabetic cardiomyopathy partly explains why diabetic patients are subject to a greater risk of heart failure and a worse outcome after myocardial ischemia. The raising prevalence and accumulating costs of cardiovascular disease in diabetic patients underscore the deficiencies of tertiary prevention and call for a shift in medical treatment. It is becoming increasingly clearer that the effective prevention and treatment of diabetic cardiomyopathy require measures to regulate the metabolic derangement occurring in the heart rather than merely restoring suitable systemic parameters. Recent research has provided deeper insight into the metabolic etiology of diabetic cardiomyopathy and numerous heart-specific targets that may substitute or reinforce current strategies. From both experimental and translational perspectives, in this review we first discuss the progress made with conventional therapies, and then focus on the need for prospective metabolic targets that may avert myocardial vulnerability and functional decline in next-generation diabetic care.
Highlights
As of 2013, one in ten individuals living in Western countries was diagnosed with diabetes mellitus (DM), and three in ten were obese [1]
Diabetic cardiomyopathy (DCM) encompasses the group of diabetic patients who, while being otherwise free of cardiovascular events, display echocardiographic abnormalities ranging from mild diastolic impairment to overt heart failure, and prevalence of DCM may be over 50% among patients in clinical and preclinical stages [3,4]
Hyperglycemia and hyperlipidemia, DCM brings out the damage of the myocardium due to
Summary
As of 2013, one in ten individuals living in Western countries was diagnosed with diabetes mellitus (DM), and three in ten were obese [1]. Epidemiological studies have long recognized diabetes to be an independent risk factor for heart failure (HF) and a worse prognosis after myocardial infarction (MI) [2]. Imaging studies have shown that diabetic patients are prone to ventricular hypertrophy, diastolic dysfunction, and decreased myocardial strain. Diabetic cardiomyopathy (DCM) encompasses the group of diabetic patients who, while being otherwise free of cardiovascular events, display echocardiographic abnormalities ranging from mild diastolic impairment to overt heart failure, and prevalence of DCM may be over 50% among patients in clinical and preclinical stages [3,4]. The failure of the therapy approaches employed to date calls for accelerating efforts towards the development of Fuentes-Antrás et al Cardiovascular Diabetology (2015) 14:17 new therapeutic strategies capable of preserving heart function while contributing to the overall care of diabetes. Growing experimental research emphasizes the prospective utility of correcting the metabolic imbalance that occurs in the diabetic heart
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