Epicardial adipose tissue mediated the relationship between systemic inflammation and myocardial fibrosis (ECV) in hypertensive patients (indirect effect 0.1773; 95% CI 0.0173-0.3147).
Cohort (n=266)
Yes
Does systemic inflammatory status correlate with myocardial fibrosis and strain impairment in hypertensive patients with preserved ejection fraction, and is this mediated by epicardial adipose tissue?
In hypertensive patients with preserved ejection fraction, systemic inflammation is associated with myocardial fibrosis, a relationship that is mediated by epicardial adipose tissue.
Effect estimate: Indirect effect 0.1773 (95% CI 0.0173-0.3147)
p-value: p=<0.001
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.
Wang et al. (Sat,) conducted a cohort in Hypertension with preserved ejection fraction (n=266). High systemic inflammatory response index (SIRI) vs. Low SIRI group and healthy controls was evaluated on Extracellular volume (ECV) as a measure of myocardial fibrosis (Indirect effect 0.1773, 95% CI 0.0173-0.3147, p=<0.001). Epicardial adipose tissue mediated the relationship between systemic inflammation and myocardial fibrosis (ECV) in hypertensive patients (indirect effect 0.1773; 95% CI 0.0173-0.3147).