Chinese Ethnicity and Cardiac Remodeling in Obesity and Dysglycemia
The Importance of Understanding Differences to Find Commonalities
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See Article by Lin et al
Type 2 diabetes mellitus (T2DM) and obesity-induced cardiac remodeling occur independently of the presence of coronary disease, hypertension, or valvular disease.1 Importantly, both conditions are associated with an increased risk for developing heart failure and other adverse clinical outcomes,2,3 leading to substantial morbidity, mortality, and costs to the healthcare system.4 Furthermore, epidemiological studies have shown that individuals with an hemoglobin A1c in the range of 6.0% to 6.4% have a high risk for the future development of T2DM, supporting the use of this range to define pre–diabetes mellitus.5
Multiple pathophysiological processes contribute to the myocardial impairment seen in diabetes mellitus and pre–diabetes mellitus, including, but not limited to, hyperglycemia and hyperinsulinemia states, the increased uptake of free fatty acids into cardiomyocytes along with impaired glucose metabolism, myocardial triglyceride accumulation, and oxidative stress.1,2,4 These multifactorial metabolic, proinflammatory, and neurohormonal alterations collectively induce the process of pathological cardiac remodeling, which may manifest as different cardiac phenotypes.1 In patients with T2DM, cardiac remodeling such as the hypertrophic response may occur as a result of, but also independent of, the degree of left ventricular (LV) afterload. Potential pathogenesis include excess epicardial fat, along with the dysregulation of myocardial substrate oxidation leading to a reliance on free fatty acid oxidation.1 Mechanisms of remodeling in T2DM also occur in response to hyperinsulinemia and insulin resistance (eg, growth factor upregulation, such as Akt), along with altered calcium handling and myocardial apoptosis, which remain one of several mechanisms that may ultimately lead to diffuse and focal fibrosis.6 Importantly, even in …