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dc.contributor.authorRizzo, Manfredi
dc.date.accessioned2024-06-21T10:34:21Z
dc.date.available2024-06-21T10:34:21Z
dc.date.issued2023-12
dc.identifier.urihttps://repository.mbru.ac.ae/handle/1/1516
dc.description.abstractAbstract: Background: Despite the widespread use of classical cholesterol-lowering drugs to mitigate the adverse impacts of dyslipidaemia on atherosclerosis, many patients still face a substantial residual risk of developing atherosclerotic cardiovascular disease (CVD). This risk is partially attributed to non-traditional pathophysiological pathways. Latest evidence suggests that sodium glucose co-transporter-2 (SGLT2) inhibitors are beneficial for patients suffering from type 2 diabetes mellitus (T2DM) or established CVD by reducing morbidity and mortality. However, the underlying mechanisms of this benefit have not been clearly elucidated. It has been hypothesized that one possible mechanism could be the attenuation of subclinical atherosclerosis (SA) progression. Aim: The objective of this narrative review is to examine the present evidence concerning the impact of SGLT2 inhibitors on markers of SA. Results: The current evidence on the efficacy of SGLT2 on SA, endothelial function and arterial stiffness remains controversial. Findings from observational and randomized studies are quite heterogeneous; however, they converge that the antiatherosclerotic activity of SGLT2 inhibitors is not strong enough to be widely used for prevention of atherosclerosis progression in patients with or without T2DM. Conclusions: Further research is needed to investigate the underlying mechanisms and the possible beneficial impact of SGLT2i on primary and secondary CVD prevention through attenuation of premature atherosclerosis progression.en_US
dc.language.isoenen_US
dc.subjectFMD; IMT; PWVen_US
dc.subjectSGLT-2 inhibitorsen_US
dc.subjectarterial stiffness; endothelial dysfunctionen_US
dc.subjectepicardial adipose tissue.en_US
dc.titleThe effect of sodium-glucose co-transporter-2 inhibitors on markers of subclinical atherosclerosisen_US
dc.typeArticleen_US


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