Abstract
The findings of recent clinical trials have shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors produce effects beyond glucose lowering and have demonstrated beneficial cardiovascular effects that have been observed across a broad range of patients with type 2 diabetes mellitus. In particular, the cardiovascular benefit results largely from substantial and early effects of SGLT2 inhibition on cardiovascular death and hospitalization for heart failure. Recent cardiovascular outcomes trials (CVOTs) have also shown that relative risk reductions in cardiovascular outcomes were observed with SGLT2 inhibition both in patients with current and prior heart failure. Since the observed reductions of cardiovascular outcomes with SGLT2 inhibitor therapy were observed much earlier than would be expected by an anti-atherosclerotic effect, these results have led to speculation about the potential underlying pathways. Suggested mechanisms include natriuresis and osmotic diuresis; reductions in inflammation, oxidative stress, and arterial stiffness; reductions in blood pressure and body weight; and possible renoprotective effects. These effects could produce cardiovascular benefits through a range of cardiac effects, including reduction in left ventricular load, attenuation of cardiac fibrosis and inflammation, and improved myocardial energy production. Other possible mechanisms include inhibition of sodium-hydrogen exchange, increases in erythropoietin levels, and reduction in myocardial ischemia or reperfusion injury. It is likely that a range of mechanisms underlie the observed cardiovascular benefits of SGLT2 inhibitors; further elucidation of these mechanisms will be answered by ongoing research.
Highlights
Patients with type 2 diabetes mellitus have approximately twice the risk of cardiovascular disease compared with those without diabetes.[1]
After 6 months of treatment, epicardial adipose tissue volume was significantly reduced, as were tumor necrosis factor-alpha (TNF-a) and plasminogenactivator inhibitor-1 (PAI-1) levels, in the dapagliflozintreated group compared with the conventional treatment group.[67]
These results suggest this class of drugs might be beneficial for patients with type 2 diabetes mellitus and hyperuricemia.[68]
Summary
Patients with type 2 diabetes mellitus have approximately twice the risk of cardiovascular disease compared with those without diabetes.[1]. 58) trial showed a reduction in hospitalization for osmotic diuresis; reductions in inflammation, oxidative heart failure among patients with type 2 diabetes mellitus stress, and arterial stiffness; reductions in blood pressure with a high cardiovascular risk and who received dapagli- and body weight; and possible renoprotective effects These flozin instead of placebo (17%), but no significant effect on MACE was observed.[6]. Fewer clinical trials of SGLT2 inhibitors in patients with type 2 diabetes mellitus have used ambulatory blood pressure monitoring, as shown in a recent meta-analysis that included 6 such studies.[44] This analysis demonstrated significant reduction in 24-hour ambulatory systolic and diastolic placebo-corrected blood pressure by À 3.76 mm Hg (95% CI À 4.23, À 2.34; I2 = 0.99) and À 1.83 mm Hg (95% CI À 2.35, À 1.31; I2 = 0.76), respectively. These meta-analyses and studies suggest the reductions in seated and ambulatory blood pressure, as well as improvements in vascular function, observed with SGLT2 inhibitors are a class effect
Sign-in/Register to view highlights & summary 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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
