It is widely accepted that obesity and type 2 diabetes mellitus (T2DM) increase the risk of heart failure (HF) independently of underlying coronary artery disease. The changes in myocardial structure or function associated with diabetes have been termed diabetic cardiomyopathy. Corresponding to changes in the risk factors for HF, an epidemiologic transition is underway from HF with a reduced ejection fraction to HF with a preserved ejection fraction. Hyperglycemia can damage the myocardium, even before diagnosis of diabetes, but intensive glycemic control has no impact on the risk of HF in patients with T2DM. Recent clinical studies have demonstrated that sodium-glucose cotransporter 2 (SGLT2) inhibitors, which inhibit renal reabsorption of glucose, decrease the risk of HF in T2DM patients. The cardioprotective mechanisms involved appear to be multifactorial and have been the subject of considerable debate. This review focuses on the hemodynamic effects of SGLT2 inhibitors in T2DM patients and the mechanisms by which these drugs decrease the risk of HF.
Keywords: Diuretic effect; Heart failure; Sodium-glucose cotransporter 2 inhibitor; Type 2 diabetes mellitus.