Diabetic cardiomyopathy: Emerging therapeutic options

Abstract

Diabetic cardiomyopathy (DbCM) is a common but underrecognized compli-cation of patients with diabetes mellitus (DM). Although the pathobiology of other cardiac complications of diabetes such as ischemic heart disease and cardiac autonomic neuropathy are mostly known with reasonable therapeutic options, the mechanisms and management options for DbCM are still not fully understood. In its early stages, DbCM presents with diastolic dysfunction followed by heart failure (HF) with preserved ejection fraction that can progress to systolic dysfunction and HF with reduced ejection fraction in its advanced stages unless appropriately managed. Apart from prompt control of DM with lifestyle changes and antidiabetic medications, disease-modifying therapy for DbCM includes prompt control of hypertension and dyslipidemia inherent to patients with DM as in other forms of heart diseases and the use of treatments with proven efficacy in HF. A basic study by Zhang et al, in a recent issue of the World Journal of Diabetes elaborates the potential pathophysiological alterations and the therapeutic role of teneligliptin in diabetic mouse models with DbCM. Although this preliminary basic study might help to improve our understanding of DbCM and offer a potential new management option for patients with the disease, the positive results from such animal models might not always translate to clinical practice as the pathobiology of DbCM in humans could be different. However, such experimental studies can encourage more scientific efforts to find a better solution to treat patients with this enigmatic disease.

Keywords: Diabetic cardiomyopathy; Diabetic cardiomyopathy; Heart failure; Pathobiology; Teneligliptin

Core Tip: Diabetic cardiomyopathy (DbCM) is a common and underrecognized complication of diabetes mellitus. The pathobiological mechanisms of DbCM are not fully elusive and the therapeutic options are not adequate. Stages of DbCM include diastolic dysfunction followed by heart failure (HF) with preserved ejection fraction, systolic dysfunction and HF with reduced ejection fraction in its order of progression. Zhang et al, in a recent issue of the World Journal of Diabetes, demonstrate the potential pathophysiological changes of DbcM and explore the therapeutic potential of teneligliptin in mouse models of DbCM. Such experimental models might harness better research efforts to find an appropriate therapeutic strategy for DbCM in the near future.