Abstract
Type 2 diabetes mellitus (T2DM) is a known independent risk factor for atherosclerotic cardiovascular disease (CVD) and solid epidemiological evidence points to heart failure (HF) as one of the most common complications of diabetes. For this reason, it is imperative to consider the prevention of CV outcomes as an effective goal for the management of diabetic patients, as important as lowering blood glucose. Endothelial dysfunction (ED) is an early event of atherosclerosis involving adhesion molecules, chemokines, and leucocytes to enhance low-density lipoprotein oxidation, platelet activation, and vascular smooth muscle cell proliferation and migration. This abnormal vascular phenotype represents an important risk factor for the genesis of any complication of diabetes, contributing to the pathogenesis of not only macrovascular disease but also microvascular damage. Gliflozins are a novel class of anti-hyperglycemic agents used for the treatment of Type 2 diabetes mellitus (T2DM) that selectively inhibit the sodium glucose transporter 2 (SGLT2) in the kidneys and have provoked large interest in scientific community due to their cardiovascular beneficial effects, whose underlying pathophysiology is still not fully understood. This review aimed to analyze the cardiovascular protective mechanisms of SGLT2 inhibition in patients T2DM and their impact on endothelial function.
Highlights
Type 2 diabetes mellitus (T2DM) is a well-known independent risk factor for atherosclerotic cardiovascular disease (CVD), including coronary, cerebral, and peripheral vasculopathy, a clinical condition that globally represents the worldwide primary cause of complications and death in diabetic patients [1,2,3,4,5,6,7]
Endothelial dysfunction (ED) is among the first disorders that can be detected in atherogenesis by flow-mediated dilation (FMD) of the brachial artery, one of the most widely used tests of endothelial function in macrocirculation and a useful surrogate endpoint, for short-term pharmacological studies [117]
A favorable effect on highly sensitive C-reactive protein, a biomarker of cardiovascular inflammation, has been observed in a phase 3 trial in T2DM patients treated with dapagliflozin, whereas conflicting results have been obtained in the few clinical studies that have investigated
Summary
Type 2 diabetes mellitus (T2DM) is a well-known independent risk factor for atherosclerotic cardiovascular disease (CVD), including coronary, cerebral, and peripheral vasculopathy, a clinical condition that globally represents the worldwide primary cause of complications and death in diabetic patients [1,2,3,4,5,6,7]. Robust epidemiological evidence indicates heart failure (HF) among the most common CVDs of diabetes, since 1974 when the Framingham study reported a risk of HF in T2DM greater than that of coronary heart disease (CHD) [8,9]. Based on these data, it is imperative to consider the prevention of CV outcomes as an effective goal for the management of diabetic patients, as important as lowering blood glucose. This guidance for the pharmaceutical industry has resulted in the publication, in recent years, of multiple large cardiovascular outcomes trials (CVOTs) that have greatly influenced the diabetes management landscape.
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