Abstract

In patients with heart failure, empagliflozin offers significant cardiovascular benefits. However, its exact mode of action is unknown. Understanding the way by which empagliflozin works in heart failure may uncover additional therapeutic targets or identify other classes of drugs that may be useful to clinicians and patients. This literature review aims to unravel the mysteries by which empagliflozin reduces cardiovascular death, cardiovascular events, and heart failure hospitalization in diabetic and non-diabetic patients. Three researchers conducted the data collection. We incorporated research that used human models, animal models, patients with diabetes, and patients without diabetes. Pathology, pathophysiology, metabolism, physiology, empagliflozin, heart failure, and cardiovascular were the search terms used to probe the mesh database on PubMed. This study showed that the mechanisms by which empagliflozin could lead to positive clinical outcomes in heart failure (HF) are as follows: down-regulation of the mammalian target of rapamycin complex 1 signaling (mTORC), decreasing sarcoplasmic reticulum calcium loss, increasing cytosolic calcium loss, inducing electrolyte-free osmotic diuresis, improving fuel efficiency, and protecting the endothelial glycocalyx. These findings were inconsistent, with no generally accepted hypotheses within the scientific community. Hence we conclude that further research is required to determine the function of Empagliflozin in heart failure and the degree to which theaforementioned mechanisms of action contribute to cardiac protection.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call