Empagliflozin improves diastolic function in a nondiabetic rodent model of heart failure with preserved ejection fraction
KA Connelly, Y Zhang, A Visram, A Advani… - JACC: Basic to …, 2019 - jacc.org
JACC: Basic to Translational Science, 2019•jacc.org
Recent studies send an unambiguous signal that the class of agents known as sodium-
glucose–linked co-transporter-2 inhibitors (SGLT2i) prevent heart failure hospitalization in
patients with type 2 diabetes. However, the mechanisms remain unclear. Herein the authors
utilize a rodent model of heart failure with preserved ejection fraction (HFpEF), and
demonstrate that treatment with the SGLT2i empagliflozin, reduces left ventricular mass,
improving both wall stress and diastolic function. These findings extend the observation that …
glucose–linked co-transporter-2 inhibitors (SGLT2i) prevent heart failure hospitalization in
patients with type 2 diabetes. However, the mechanisms remain unclear. Herein the authors
utilize a rodent model of heart failure with preserved ejection fraction (HFpEF), and
demonstrate that treatment with the SGLT2i empagliflozin, reduces left ventricular mass,
improving both wall stress and diastolic function. These findings extend the observation that …
Summary
Recent studies send an unambiguous signal that the class of agents known as sodium-glucose–linked co-transporter-2 inhibitors (SGLT2i) prevent heart failure hospitalization in patients with type 2 diabetes. However, the mechanisms remain unclear. Herein the authors utilize a rodent model of heart failure with preserved ejection fraction (HFpEF), and demonstrate that treatment with the SGLT2i empagliflozin, reduces left ventricular mass, improving both wall stress and diastolic function. These findings extend the observation that the main mechanism of action of empagliflozin involves improved hemodynamics (i.e., reduction in preload and afterload) and provide a rationale for upcoming trials in patients with HFpEF irrespective of glycemic status.
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