Potential impact of SGLT2 inhibitors on left ventricular diastolic function in patients with diabetes mellitus.

Abstract

The pathogenesis of diabetes mellitus (DM)-related cardiac dysfunction is thought to be multifactorial, and possibly a key factor for the development of heart failure with preserved ejection fraction (HFpEF) in patients with DM and preserved left ventricular (LV) ejection fraction. Currently, there is no effective treatment for HFpEF, which is presented as LV diastolic dysfunction. Furthermore, it is well known that, in addition to DM, hypertension and overweight/obesity are also important factors associated with HFpEF. Sodium glucose cotransporter 2 (SGLT2) inhibitors are a new class of diabetic medications indicated only for the treatment of type 2 DM, and a recent clinical trial showed that patients with this disease and at high risk for cardiovascular events attained cardiovascular benefits from SGLT2 inhibitor in comparison with placebo efficacy. In addition to reduction of glycated hemoglobin levels in patients with type 2 DM, SGLT2 inhibitors are associated with weight loss and reductions in blood pressure. However, despite such intriguing results, it remains uncertain whether SGLT2 inhibitors are beneficial for LV diastolic function in patients with DM. This review deals with the impact of SGLT2 inhibitors on LV diastolic function in patients with DM and their current potential for prevention of the future development of HFpEF in such patients.

• Authors: Hidekazu Tanaka, Ken-Ichi Hirata
• Journal: Heart failure reviews (Heart Fail Rev) Vol. 23 Issue 3 Pg. 439-444 (05 2018) ISSN: 1573-7322 [Electronic] United States
• PMID: 29330646 (Publication Type: Journal Article, Review)

Chemical References

• Sodium-Glucose Transporter 2 Inhibitors

Topics

• Diabetes Mellitus, Type 2 (complications, drug therapy, physiopathology)
• Diastole
• Heart Failure (etiology, physiopathology)
• Humans
• Sodium-Glucose Transporter 2 Inhibitors (pharmacology)
• Stroke Volume (drug effects)
• Ventricular Function, Left (drug effects, physiology)