Diabetic cardiomyopathy: from the pathophysiology of the cardiac myocytes to current diagnosis and management strategies

Abstract

Diabetic cardiomyopathy (DCM), although a distinct clinical entity, is also a part of the diabetic atherosclerosis process. It may be independent of the coexistence of ischemic heart disease, hypertension, or other macrovascular complications. Its pathological substrate is characterized by the presence of myocardial damage, reactive hypertrophy, and intermediary fibrosis, structural and functional changes of the small coronary vessels, disturbance of the management of the metabolic cardiovascular load, and cardiac autonomic neuropathy. These alterations make the diabetic heart susceptible to ischemia and less able to recover from an ischemic attack. Arterial hypertension frequently coexists with and exacerbates cardiac functioning, leading to the premature appearance of heart failure. Classical and newer echocardiographic methods are available for early diagnosis. Currently, there is no specific treatment for DCM; targeting its pathophysiological substrate by effective risk management protects the myocardium from further damage and has a recognized primary role in its prevention. Its pathophysiological substrate is also the objective for the new therapies and alternative remedies.

Ginsenoside Rg1 ameliorates oxidative stress and myocardial apoptosis in streptozotocin-induced diabetic rats

“…Apoptosis due to oxidative stress may be by ways of the mitochondrial, death receptor, or endoplasmic reticulum stress pathways (Aneja et al, 2008;Voulgari et al, 2010). Throughout the process of apoptosis, proteins of the caspase and Bcl-2 families have crucial roles.…”

“…The specific myocardial damage known as diabetic cardiomyopathy exists independent of factors such as coronary heart disease or hypertension (Voulgari et al, 2010;Falcão-Pires and Leite-Moreira, 2012). Many potential mechanisms underlying the pathogenesis of diabetic cardiomyopathy that could eventually lead to cardiac diastolic and systolic dysfunction have been suggested, including inflammation, cardiac fibrosis, oxidative stress, and myocardial apoptosis (Aneja et al, 2008;Voulgari et al, 2010;Falcão-Pires and Leite-Moreira, 2012).…”

Do We Need A Wider Therapeutic Paradigm For Heart Failure With Comorbidities?: A Remote Australian Perspective

“…Diuretics effect on extracellular K+ and non-selective ββ effect on glycemic control are concerns. Combination of calcium blocker e.g amlodipine or vasodilating ββ or lower strength diuretic with potent RAAS blockade can negate this risk [6,21,29,31,[62][63][64][65][66][67][68][69]. Finally, cashing in on post-op weight loss with extended rehab and support are factors to discuss at unit case conferences, and when all options fail bariatric surgery in selected patients [15,70,71].…”

The detection of early myocardial changes in asymptomatic diabetic individuals by 99mTc – Myoview gated-SPET and heart rate variability measurement

“…Based on the results of experimental, pathological and epidemiological studies, it is well established that hypertension and coronary heart disease are not the exclusive underlying causes of diabetic cardiomyopathy (1). Under the conditions of long-term hyperglycaemia, microvascular damage occurs as a consequence of oxidative stress, activation of proteinkinase C and infl ammation associated with endothelial dysfunction (2).…”

“…Hyperglycaemia results in the release of local infl ammatory mediators and activation of coagulation cascade leading to acceleration of atherosclerosis (4). Cardiovascular disease is a common complication of diabetes responsible for 80 % of the mortality in the diabetic population (1).…”