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钠-葡萄糖协同转运蛋白2抑制剂对2型糖尿病合并无症状心力衰竭患者心肌功能的影响

Sodium-dependent glucose transporter 2 inhibitors effects on myocardial function in patients with type 2 diabetes and asymptomatic heart failure.

作者信息

Grubić Rotkvić Petra, Rotkvić Luka, Đuzel Čokljat Ana, Cigrovski Berković Maja

机构信息

Department of Cardiology, University Hospital Centre Zagreb, Zagreb 10000, Croatia.

Department of Cardiology, Magdalena Clinic for Cardiovascular Disease, Krapinske Toplice 49217, Croatia.

出版信息

World J Cardiol. 2024 Aug 26;16(8):448-457. doi: 10.4330/wjc.v16.i8.448.

DOI:10.4330/wjc.v16.i8.448
PMID:39221192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11362810/
Abstract

BACKGROUND

Sodium-dependent glucose transporter 2 inhibitors (SGLT2i) have shown efficacy in reducing heart failure (HF) burden in a very heterogeneous groups of patients, raising doubts about some contemporary assumptions of their mechanism of action. We previously published a prospective observational study that evaluated mechanisms of action of SGLT2i in patients with type 2 diabetes who were in HF stages A and B on dual hypoglycemic therapy. Two groups of patients were included in the study: the ones receiving SGLT2i as an add-on agent to metformin and the others on dipeptidyl peptidase-4 inhibitors as an add-on to metformin due to suboptimal glycemic control.

AIM

To evaluate the outcomes regarding natriuretic peptide, oxidative stress, inflammation, blood pressure, heart rate, cardiac function, and body weight.

METHODS

The study outcomes were examined by dividing each treatment arm into two subgroups according to baseline parameters of global longitudinal strain (GLS), N-terminal pro-brain natriuretic peptide, myeloperoxidase (MPO), high-sensitivity C-reactive protein (hsCRP), and systolic and diastolic blood pressure. To evaluate the possible predictors of observed changes in the SGLT2i arm during follow-up, a rise in stroke volume index, body mass index (BMI) decrease, and lack of heart rate increase, linear regression analysis was performed.

RESULTS

There was a greater reduction of MPO, hsCRP, GLS, and blood pressure in the groups with higher baseline values of mentioned parameters irrespective of the therapeutic arm after 6 months of follow-up. Significant independent predictors of heart rate decrease were a reduction in early mitral inflow velocity to early diastolic mitral annular velocity at the interventricular septal annulus ratio and BMI, while the predictor of stroke volume index increase was SGLT2i therapy itself.

CONCLUSION

SGLT2i affect body composition, reduce cardiac load, improve diastolic/systolic function, and attenuate the sympathetic response. Glycemic control contributes to the improvement of heart function, blood pressure control, oxidative stress, and reduction in inflammation.

摘要

背景

钠-葡萄糖协同转运蛋白2抑制剂(SGLT2i)已在非常异质性的患者群体中显示出减轻心力衰竭(HF)负担的疗效,这引发了人们对其作用机制的一些当代假设的质疑。我们之前发表了一项前瞻性观察性研究,评估了SGLT2i在接受双重降糖治疗的A期和B期HF 2型糖尿病患者中的作用机制。该研究纳入了两组患者:一组将SGLT2i作为二甲双胍的附加药物,另一组因血糖控制不佳将二肽基肽酶-4抑制剂作为二甲双胍的附加药物。

目的

评估利钠肽、氧化应激、炎症、血压、心率、心脏功能和体重方面的结果。

方法

根据整体纵向应变(GLS)、N末端脑钠肽前体、髓过氧化物酶(MPO)、高敏C反应蛋白(hsCRP)以及收缩压和舒张压的基线参数,将每个治疗组分为两个亚组来检查研究结果。为了评估随访期间SGLT2i组观察到的变化的可能预测因素,进行了线性回归分析,以分析每搏输出量指数的增加、体重指数(BMI)的降低和心率无增加情况。

结果

随访6个月后,无论治疗组如何,在上述参数基线值较高的组中,MPO、hsCRP、GLS和血压的降低幅度更大。心率降低的显著独立预测因素是室间隔环处早期二尖瓣流入速度与早期舒张期二尖瓣环速度之比的降低和BMI,而每搏输出量指数增加的预测因素是SGLT2i治疗本身。

结论

SGLT2i影响身体成分,减轻心脏负荷,改善舒张/收缩功能,并减弱交感神经反应。血糖控制有助于改善心脏功能、控制血压、减轻氧化应激和炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/32e0c7995f69/WJC-16-448-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/805677f262de/WJC-16-448-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/212dddf244d0/WJC-16-448-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/36f5a10312f5/WJC-16-448-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/32e0c7995f69/WJC-16-448-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/805677f262de/WJC-16-448-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/212dddf244d0/WJC-16-448-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/36f5a10312f5/WJC-16-448-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a495/11362810/32e0c7995f69/WJC-16-448-g004.jpg

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