The Relationship Between Myocardial Fibrosis in Hypertensive Patients With Preserved Ejection Fraction and the Severity of Systemic Inflammatory Status Is Mediated by Epicardial Adipose Tissue: A Multicenter Cohort Study

心肌纤维化与全身炎症状态严重程度之间的关系在射血分数保留的高血压患者中由心外膜脂肪组织介导:一项多中心队列研究

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Abstract

This study aims to investigate the impact of exacerbated systemic inflammatory status on the degree of myocardial fibrosis and strain impairment in hypertensive patients with preserved ejection fraction, as well as the role played by epicardial adipose tissue (EAT) in this process. A total of 236 hypertensive patients who underwent cardiovascular magnetic resonance (CMR) and blood routine examinations at two medical centers in China were included. Thirty healthy volunteers were included as the control group. Compared with the low systemic inflammatory response index (SIRI) group, patients in the high SIRI group exhibited greater EAT volume, higher Native T1 value, and increased extracellular volume (ECV) (all p < 0.01). Additionally, significant differences were observed between the two groups in cardiac MRI parameters (all p < 0.001). Hypertensive patients had a significantly higher SIRI than healthy controls (p < 0.001). Binary logistic regression analysis indicated that SIRI and indexed EAT volume were independently associated with high ECV value (SIRI: p < 0.001; indexed EAT volume: p < 0.001), with results remaining stable after adjusting for confounding factors. Furthermore, mediation analysis showed that even after adjusting for confounding factors, EAT continued to play a role in SIRI-mediated changes in ECV (indirect effect: 0.1773 [95% CI 0.0173-0.3147]). HTN may contribute to the increase in systemic inflammatory severity. The relationship between the degree of myocardial fibrosis and the severity of systemic inflammatory status in patients with early HTN is mediated by EAT. Early mitigation of systemic inflammatory status in patients with early-stage HTN can reduce the adverse effects of EAT, thereby alleviating myocardial fibrosis and strain impairment.

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