Diabetic cardiomyopathy: a clinical entity or a cluster of molecular heart changes?
BACKGROUND
Although the increasing rate of cardiovascular mortality in patients with diabetes is thought to be due to the coronary atherosclerosis caused mainly by compounding factors such as dyslipidaemia and hypertension, it is now well documented that diabetes alone can lead to a vast array of molecular changes in the heart.


METHODS
The aim of this article was to comprehensively review the pathophysiological and molecular changes leading to diabetic cardiomyopathy (DCM), as well as to critically analyse the literature that offers evidence in favour and against the existence of the overt clinical expression of this entity.


RESULTS
We included in the discussion studies that have revealed the existence of diabetic cardiomyopathy with unique remodelling pattern when compared to other types of cardiomyopathies. On the other hand, several studies debate the existence of clinically discernible cardiomyopathy caused only by diabetes and were also presented and discussed in details.


CONCLUSIONS
Clinicians should be aware of DCM when facing patients with diabetes in order both to recognize on time relevant symptoms and to intensively look for and treat other compounding factors, apart from optimal glucose control. Furthermore, the elucidation of the pathophysiological mechanisms leading to DCM could provide new therapeutic targets for heart disease, which will be wonderful for the good of our patients.
Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece.
Maria
M
Mizamtsidi
Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece.
Stavroula A
SA
Paschou
Department of Cardiovascular Sciences, Imperial College of London, London, UK.
Julia
J
Grapsa
Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece. mahi_vr@hotmail.com.
Andromachi
A
Vryonidou
D016923:Cell Death / Q000502:physiology; D003094:Collagen / Q000378:metabolism; D058065:Diabetic Cardiomyopathies / Q000175:diagnosis / Q000209:etiology*; D003928:Diabetic Nephropathies / Q000150:complications; D003971:Diastole / Q000502:physiology; D004719:Endomyocardial Fibrosis / Q000150:complications; D005230:Fatty Acids, Nonesterified / Q000502:physiology; D006801:Humans; D006943:Hyperglycemia / Q000150:complications; D006946:Hyperinsulinism / Q000150:complications; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000209:etiology; D050356:Lipid Metabolism / Q000502:physiology; D008929:Mitochondria, Heart / Q000502:physiology; D028361:Mitochondrial Diseases / Q000150:complications; D018384:Oxidative Stress / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology
D005230:Fatty Acids, Nonesterified; D003094:Collagen
Cardiomyopathy; cardiovascular; diabetes; hyperglycemia; myocardium; oxidative stress