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Invited Reviews

Cardiovascular benefit of SGLT2 inhibitors

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Pages 142-155 | Received 08 Jul 2021, Accepted 11 Oct 2021, Published online: 17 Nov 2021
 

Abstract

Patients with type 2 diabetes mellitus (T2D) are at increased risk of cardiovascular (CV) disease. Sodium glucose cotransporter 2 (SGLT2) inhibitors, also known as gliflozins, are a class of medications used to treat T2D by preventing the reabsorption of glucose filtered through the kidney and thereby facilitating glucose excretion in the urine. Over the past 5 years, many cardiovascular outcome trials (CVOTs) have evaluated the safety and efficacy of SGLT2 inhibitors in preventing CV events. The results of 7 CVOTs have provided solid evidence that the use of SGLT2 in patients with T2D and at high CV risk significantly reduced the risk of death from CV causes. Moreover, in patient with heart failure with reduced ejection fraction, regardless of the presence or absence of T2D, SGLT2 inhibitors use significantly reduced the risk of worsening heart failure and death from CV causes. Although the exact mechanism of the cardiorenal benefit of SGLT2 inhibitors is still unknown, studies have shown that the beneficial effect of these drugs cannot be exclusively explained by their glucose lowering effect, and several possible mechanisms have been proposed. This review will explore the changing role of SGLT2 inhibitors from a diabetes drug to clinical practice guideline-supported therapy for the prevention and treatment of CV diseases, including heart failure.

Disclosure statement

Dr. Januzzi is a Trustee of the American College of Cardiology; is a board member of Imbria Pharmaceuticals; has received grant support from Abbott Diagnostics, Applied Therapeutics, Innolife and Novartis; has received consulting income from Abbott Diagnostics, Boehringer-Ingelheim, Janssen, Novartis, Roche Diagnostics; and participates in clinical endpoint committees/data safety monitoring boards for AbbVie, Siemens, Takeda and Vifor.

Additional information

Funding

Dr. Januzzi is supported by the Hutter Family Professorship.

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