Diabetic cardiomyopathy: the search for a unifying hypothesis.
Although diabetes is recognized as a potent and prevalent risk factor for ischemic heart disease, less is known as to whether diabetes causes an altered cardiac phenotype independent of coronary atherosclerosis. Left ventricular systolic and diastolic dysfunction, left ventricular hypertrophy, and alterations in the coronary microcirculation have all been observed, although not consistently, in diabetic cardiomyopathy and are not fully explained by the cellular effects of hyperglycemia alone. The recent recognition that diabetes involves more than abnormal glucose homeostasis provides important new opportunities to examine and understand the impact of complex metabolic disturbances on cardiac structure and function.
Department of Medicine, Allegheny General Hospital, Pittsburgh, PA 15212, USA.
Indu G
IG
Poornima
Pratik
P
Parikh
Richard P
RP
Shannon
D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology*; D003326:Coronary Circulation; D048909:Diabetes Complications / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000150:complications; D003924:Diabetes Mellitus, Type 2 / Q000150:complications; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006801:Humans; D006943:Hyperglycemia / Q000150:complications; D006946:Hyperinsulinism / Q000150:complications; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D007333:Insulin Resistance; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000209:etiology
D005230:Fatty Acids, Nonesterified; D019869:Phosphatidylinositol 3-Kinases; C494918:AKT1 protein, human; D051057:Proto-Oncogene Proteins c-akt