关键词: Cardiac remodeling Heart failure Hypoglycaemic agent Myocardial infraction NT-proBNP Sodium-glucose transporter 2 inhibitor

Mesh : Humans Natriuretic Peptide, Brain / blood Sodium-Glucose Transporter 2 Inhibitors / therapeutic use Peptide Fragments / blood Myocardial Infarction / drug therapy blood Randomized Controlled Trials as Topic / methods Biomarkers / blood Diabetes Mellitus, Type 2 / drug therapy blood Treatment Outcome

来  源:   DOI:10.1016/j.ijcard.2024.132239

Abstract:
BACKGROUND: Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are anti-hyperglycemic drugs and have been proven to have cardiovascular protective effects for patients with heart failure regardless of their diabetes status. However, the benefit of SGLT2i following myocardial infarction (MI) remains incompletely established. This review aimed to investigate the impact of SGLT2i on NT-proBNP levels and structural changes post-MI.
METHODS: Medline, ClinicalTrial.gov, Scopus, and Directory of open-access journals were searched to retrieve the relevant articles. Eligible studies were randomized clinical trials that assessed NT-proBNP and cardiac structural changes in patients who received SGLT2i compared to placebo following MI. Two reviewers independently screened articles, extracted data, and assessed study quality.
RESULTS: Four studies were included in this review, including patients with and without diabetes. While two studies showed no marked decrease from the baseline in NT-proBNP levels between the SGLT2i group and the control group, two studies reported a substantial reduction. The meta-analysis included three of these studies, with a total of 238 participants. The meta-analysis did not find a statistically significant drop in NT-proBNP levels post-MI in the SGLT2 inhibitors group compared to placebo (pooled SMD = 0.16, 95% CI 0.57-0.26, P 0.45). Furthermore, different echocardiographic parameters were reported in the included trials, yet no meta-analysis could be conducted to assess the influence of SGLT2i on cardiac remodeling post-MI.
CONCLUSIONS: SGLT2i did not result in a statistically significant reduction of NT-proBNP level subsequent to myocardial infarction. A knowledge gap exists regarding the impact of these agents on cardiac remodeling post-MI. Future high-quality clinical trials are needed to provide more robust evidence.
摘要:
背景:钠-葡萄糖共转运蛋白2抑制剂(SGLT2i)是抗高血糖药物,已被证明对心力衰竭患者具有心血管保护作用,无论其糖尿病状态如何。然而,心肌梗死(MI)后SGLT2i的获益仍未完全确定.本文旨在探讨SGLT2i对MI后NT-proBNP水平和结构变化的影响。
方法:Medline,ClinicalTrial.gov,Scopus,并搜索了开放获取期刊目录以检索相关文章。合格的研究是随机临床试验,评估接受SGLT2i的患者与MI后安慰剂相比的NT-proBNP和心脏结构变化。两名审稿人独立筛选文章,提取的数据,并评估研究质量。
结果:这篇综述包括四项研究,包括有和没有糖尿病的患者。虽然两项研究显示SGLT2i组和对照组之间的NT-proBNP水平与基线相比没有明显下降,两项研究报告大幅减少。荟萃分析包括其中三项研究,共有238人参加。荟萃分析未发现与安慰剂相比,SGLT2抑制剂组MI后NT-proBNP水平有统计学意义的下降(合并SMD=0.16,95%CI0.57-0.26,P0.45)。此外,纳入的试验报道了不同的超声心动图参数,然而,无法进行荟萃分析来评估SGLT2i对MI后心脏重构的影响.
结论:SGLT2i并未导致心肌梗死后NT-proBNP水平的显著降低。关于这些药物对MI后心脏重塑的影响存在知识空白。未来需要高质量的临床试验来提供更有力的证据。
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