Diabetic Cardiomyopathy


In large part due to an increase in age, obesity, and diabetes mellitus, heart failure and accompanying morbidity and mortality are rising alarmingly quickly. Patients with diabetes mellitus experience much worse clinical outcomes from heart failure than patients without the condition. The phrase "diabetic cardiomyopathy" refers to the existence of cardiac dysfunction in persons with diabetes mellitus in the absence of overt clinical coronary artery disease, valvular disease, and other traditional cardiovascular risk factors, such as hypertension and dyslipidaemia. Alongside the rise in diabetes mellitus, the prevalence of diabetic cardiomyopathy is also rising. Myocardial fibrosis, dysfunctional remodelling, and concomitant diastolic dysfunction are the early symptoms of diabetic cardiomyopathy. Systolic dysfunction and clinical heart failure are later symptoms.



Impaired mitochondrial and cardiomyocyte calcium handling, inflammation, activation of the renin-angiotensin-aldosterone system, cardiac autonomic neuropathy, endoplasmic reticulum stress, micro vascular dysfunction, and a myriad of other factors contribute to impaired cardiac insulin metabolic signalling, mitochondrial dysfunction, increases in oxidative stress, reduced nitric oxide bioavailability, elevations in advanced glaciation end products, and stiffness of collagen-based Anomalies in AMP-activated protein kinase, peroxisome proliferator-activated receptors, O-linked N-acetyl glucosamine, protein kinase C, microRNA, and exospore pathways are among the molecular mechanisms connected to the underlying pathophysiological alterations. This review's objective is to present a current understanding of these causes of diabetic cardiomyopathy as well as mechanistically based techniques for its prevention and therapy.



 


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