Abstract
Heart failure is an important manifestation of diabetic heart disease. Before the development of symptomatic heart failure, as much as 50% of patients with type 2 diabetes mellitus (T2DM) develop asymptomatic left ventricular dysfunction including left ventricular hypertrophy (LVH). Left ventricular hypertrophy (LVH) is highly prevalent in patients with T2DM and is a strong predictor of adverse cardiovascular outcomes including heart failure. Importantly regression of LVH with antihypertensive treatment especially renin angiotensin system blockers reduces cardiovascular morbidity and mortality. However, this approach is only partially effective since LVH persists in 20% of patients with hypertension who attain target blood pressure, implicating the role of other potential mechanisms in the development of LVH. Moreover, the pathophysiology of LVH in T2DM remains unclear and is not fully explained by the hyperglycemia-associated cellular alterations. There is a growing body of evidence that supports the role of inflammation, oxidative stress, AMP-activated kinase (AMPK) and insulin resistance in mediating the development of LVH. The recognition of asymptomatic LVH may offer an opportune target for intervention with cardio-protective therapy in these at-risk patients. In this article, we provide a review of some of the key clinical studies that evaluated the effects of allopurinol, SGLT2 inhibitor and metformin in regressing LVH in patients with and without T2DM.
Highlights
Diabetic cardiomyopathy (DCM) is defined as cardiac dysfunction, characterised by abnormal structural, functional and metabolic changes in the myocardium, that occurs in the absence of significant coronary, valvular or hypertensive diseases in individuals with diabetes [1]
Genome wide association studies (GWAS) have reported substantial heritability for left ventricular hypertrophy (LVH) in diverse populations including diabetic patients [29, 30]. In this mini-review, we summarise the epidemiology of LVH in type 2 diabetes mellitus (T2DM) and the key pathophysiological mechanisms and provide a review of some of the key studies that evaluated the effects of different classes drugs on LVH regression
Variable myocyte hypertrophy and inflammatory cell infiltration with activation of nuclear factor kappa B (NF-κB) have been identified in endomyocardial tissue of patients with Hypertrophic cardiomyopathy (HCM) while the levels of in interleukins (IL1β, IL-1RA, IL-6, IL-10) and high-sensitivity C-reactive protein have been found to be significantly higher in patients with HCM than in control subjects [49]. These suggest that a low-grade inflammatory response may play an important role in the development of cardiac hypertrophy in patients with HCM and support the causative significance of inflammatory signalling in hypertrophic heart disease, demonstrating the feasibility of therapeutic targeting of inflammation in heart failure
Summary
Diabetic cardiomyopathy (DCM) is defined as cardiac dysfunction, characterised by abnormal structural, functional and metabolic changes in the myocardium, that occurs in the absence of significant coronary, valvular or hypertensive diseases in individuals with diabetes [1]. In the early stages of its progression, DCM is usually asymptomatic and is characterised by subclinical structural and functional abnormalities including left ventricular hypertrophy (LVH), reduced LV compliance, LVH in Diabetic Cardiomyopathy. Genome wide association studies (GWAS) have reported substantial heritability for LVH in diverse populations including diabetic patients [29, 30] In this mini-review, we summarise the epidemiology of LVH in T2DM and the key pathophysiological mechanisms and provide a review of some of the key studies that evaluated the effects of different classes drugs on LVH regression
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