Induction of cardiomyopathic changes in hearts of animals rendered insulin deficient is a well-recognized phenomenon. Accordingly, the term ''diabetic cardio- a
& u myopathy'' has been extant for decades. Implicated derangements include impaired function of the sarcoplasmic reticulum, an organelle responsible for the uptake and release of intracellular calcium and, therefore, pivotal in modulating cardiac contractility. However, cardiomyopathy changes may not be related exclusively to metabolic derangements typical of insulin deficiency. They occur also in hearts of patients with type 2 diabetes whose hyperglycemia is well controlled.
Abnormalities in myocardial ultrasonic backscatter are seen in diabetic subjects even when ventricular systolic and diastolic function are normal. Such changes have been attributed to intramyocardial edema, alterations in the nature and deposition of collagen, and accumulation of advanced glycation products.
Patients with diabetes who sustain acute myocardial infarction exhibit greater impairment in ventricular function and more severe congestive heart failure normalized for infarct size than do nondiabetic subjects. Factors implicated in causing such derangements include limitation of energy supply attributable to insulin resistance in the myocardium and diminished availability of intracellular glucose and its metabolites for oxidative phosphorylation, impaired calcium cycling associated with abnormalities in the sarcoplasmic reticulum calcium-sensitive ATPase, and contributions of advanced glycation end products to cross-linking structural proteins and augmenting myocardial stiffness.
Elucidation of specific mechanisms responsible for cardiomyopathic changes associated with diabetes should enhance prevention and treatment of ventricular functional impairment under basal conditions and in response to myo-cardial insults.
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