SGLT2-inhibitor therapy significantly increased minimum fibrous cap thickness and reduced the risk of major adverse cardiovascular events by 65% (HR 0.342) at 1 year of follow-up.
Observational (n=369)
Single-blind
Yes
Does SGLT2-I therapy improve fibrous cap thickness and reduce MACEs in T2DM patients with multivessel non-obstructive coronary stenosis?
In diabetic patients with multivessel non-obstructive coronary stenosis, SGLT2-I therapy is associated with increased fibrous cap thickness, reduced plaque inflammation, and a lower risk of MACE at 1 year.
Absolute Event Rate: 170.29% vs 163.19%
p-value: p=0.003
BACKGROUND: Sodium-glucose transporter 2 inhibitors (SGLT2-I) could modulate atherosclerotic plaque progression, via down-regulation of inflammatory burden, and lead to reduction of major adverse cardiovascular events (MACEs) in type 2 diabetes mellitus (T2DM) patients with ischemic heart disease (IHD). T2DM patients with multivessel non-obstructive coronary stenosis (Mv-NOCS) have over-inflammation and over-lipids' plaque accumulation. This could reduce fibrous cap thickness (FCT), favoring plaque rupture and MACEs. Despite this, there is not conclusive data about the effects of SGLT2-I on atherosclerotic plaque phenotype and MACEs in Mv-NOCS patients with T2DM. Thus, in the current study, we evaluated SGLT2-I effects on Mv-NOCS patients with T2DM in terms of FCT increase, reduction of systemic and coronary plaque inflammation, and MACEs at 1 year of follow-up. METHODS: In a multi-center study, we evaluated 369 T2DM patients with Mv-NOCS divided in 258 (69.9%) patients that did not receive the SGLT2-I therapy (Non-SGLT2-I users), and 111 (30.1%) patients that were treated with SGLT2-I therapy (SGLT2-I users) after percutaneous coronary intervention (PCI) and optical coherence tomography (OCT) evaluation. As the primary study endpoint, we evaluated the effects of SGLT2-I on FCT changes at 1 year of follow-up. As secondary endpoints, we evaluated at baseline and at 12 months follow-up the inflammatory systemic and plaque burden and rate of MACEs, and predictors of MACE through multivariable analysis. RESULTS: At 6 and 12 months of follow-up, SGLT2-I users vs. Non-SGLT2-I users showed lower body mass index (BMI), glycemia, glycated hemoglobin, B-type natriuretic peptide, and inflammatory cells/molecules values (p < 0.05). SGLT2-I users vs. Non-SGLT2-I users, as evaluated by OCT, evidenced the highest values of minimum FCT, and lowest values of lipid arc degree and macrophage grade (p < 0.05). At the follow-up end, SGLT2-I users vs. Non-SGLT2-I users had a lower rate of MACEs n 12 (10.8%) vs. n 57 (22.1%); p < 0.05. Finally, Hb1Ac values (1.930, CI 95%: 1.149-2.176), macrophage grade (1.188, CI 95%: 1.073-1.315), and SGLT2-I therapy (0.342, CI 95%: 0.180-0.651) were independent predictors of MACEs at 1 year of follow-up. CONCLUSIONS: SGLT2-I therapy may reduce about 65% the risk to have MACEs at 1 year of follow-up, via ameliorative effects on glucose homeostasis, and by the reduction of systemic inflammatory burden, and local effects on the atherosclerotic plaque inflammation, lipids' deposit, and FCT in Mv-NOCS patients with T2DM.
Sardu et al. (Sat,) conducted a observational in Type 2 diabetes mellitus with inducible myocardial ischemia and multi-vessel non-obstructive coronary artery stenosis (n=369). SGLT2-inhibitors vs. Non-SGLT2-inhibitor oral anti-diabetic medications was evaluated on Minimum fibrous cap thickness (FCT) in µm at 1 year of follow-up (p=0.003). SGLT2-inhibitor therapy significantly increased minimum fibrous cap thickness and reduced the risk of major adverse cardiovascular events by 65% (HR 0.342) at 1 year of follow-up.