Abstract
Adipose tissue dysfunction is a predictor for cardiovascular (CV) events and heart failure (HF) in patient population with obesity, metabolic syndrome, and known type 2 diabetes mellitus. Previous preclinical and clinical studies have yielded controversial findings regarding the role of accumulation of adipose tissue various types in CV risk and HF-related clinical outcomes in obese patients. There is evidence for direct impact of infiltration of epicardial adipocytes into the underlying myocardium to induce adverse cardiac remodeling and mediate HF development and atrial fibrillation. Additionally, perivascular adipocytes accumulation is responsible for release of proinflammatory adipocytokines (adiponectin, leptin, resistin), stimulation of oxidative stress, macrophage phenotype switching, and worsening vascular reparation, which all lead to microvascular inflammation, endothelial dysfunction, atherosclerosis acceleration, and finally to increase in CV mortality. However, systemic effects of white and brown adipose tissue can be different, and adipogenesis including browning of adipose tissue and deficiency of anti-inflammatory adipocytokines (visfatin, omentin, zinc-α2-glycoprotein, glypican-4) was frequently associated with adipose triglyceride lipase augmentation, altered glucose homeostasis, resistance to insulin of skeletal muscles, increased cardiomyocyte apoptosis, lowered survival, and weak function of progenitor endothelial cells, which could significantly influence on HF development, as well as end-organ fibrosis and multiple comorbidities. The exact underlying mechanisms for these effects are not fully understood, while they are essential to help develop improved treatment strategies. The aim of the review is to summarize the evidence showing that adipocyte dysfunction may induce the onset of HF and support advance of HF through different biological mechanisms involving inflammation, pericardial, and perivascular adipose tissue accumulation, adverse and electrical cardiac remodeling, and skeletal muscle dysfunction. The unbalancing effects of natriuretic peptides, neprilysin, and components of renin–angiotensin system, as exacerbating cause of altered adipocytokine signaling on myocardium and vasculature, in obesity patients at high risk of HF are disputed. The profile of proinflammatory and anti-inflammatory adipocytokines as promising biomarker for HF risk stratification is discussed in the review.
Highlights
Abdominal obesity (AO) and diabetes mellitus (DM) remain global public health problems that are associated with a high risk of premature death and disabilities in the general population [1]
Previous studies have revealed that increased serum levels of resistin were associated with the insulin resistance (IR), type 2 DM (T2DM), AO, and CV diseases [226, 227], while there were no significant correlations between resistin levels and echocardiographic parameters including LVEF, Gensini score index, angiographic parameters, and severity of atherosclerosis [228]
heart failure (HF) is common complication of AO and T2DM often occurring as a result of adipocyte dysfunction and adipose tissue expansion
Summary
Abdominal obesity (AO) and diabetes mellitus (DM) remain global public health problems that are associated with a high risk of premature death and disabilities in the general population [1]. A meta-analysis of 77 prospective studies, which included patients with DM, AO, and HF, has shown that individuals with DM were at an increased risk of developing HF, and there was evidence of increased HF risk even within the prediabetic range of blood glucose among AO patients [11]. Despite that both AO and DM predominantly corresponded to HF with preserved (≥50%) ejection fraction (HFpEF), the prevalence of both conditions among patients having HF with reduced (
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