Systemic inflammation is associated with myocardial fibrosis in patients with obstructive hypertrophic cardiomyopathy

被引:0
|
作者
Guo, Xinli [1 ]
Zhang, Jian [2 ]
Huang, Manyun [3 ]
Song, Changpeng [1 ]
Nie, Changrong [4 ]
Zheng, Xinxin [1 ]
Wang, Shuiyun [4 ,5 ]
Huang, Xiaohong [1 ]
机构
[1] Chinese Acad Med Sci & Peking Union Med Coll, Fuwai Hosp, Dept Cardiol, Natl Ctr Cardiovasc Dis, Beijing, Peoples R China
[2] Peking Univ First Hosp, Dept Geriatr, Beijing, Peoples R China
[3] Tongji Univ, Shanghai East Hosp, Sch Med, Dept Heart failure, Shanghai, Peoples R China
[4] Chinese Acad Med Sci, Natl Ctr Cardiovasc Dis, Fuwai Hosp, Dept Cardiovasc Surg,Peking Union Med Coll, Beijing, Peoples R China
[5] Chinese Acad Med Sci, Fuwai Hosp, Dept Cardiovasc Surg, Shenzhen, Peoples R China
来源
ESC HEART FAILURE | 2025年 / 12卷 / 01期
关键词
Histopathology; Hypertrophic cardiomyopathy; Inflammatory markers; Myocardial fibrosis; NECROSIS-FACTOR-ALPHA; CYTOKINES; QUANTIFICATION; EXPRESSION; MICE;
D O I
10.1002/ehf2.15109
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims Chronic low-grade inflammation, often observed in hypertrophic cardiomyopathy (HCM), promotes adverse ventricular remodelling. This study aimed to investigate the relationship between inflammatory markers and myocardial fibrosis (MF) in patients with HCM. Methods and results This study included 102 patients with complete baseline data who underwent septal myectomy. Myocardial samples were stained with Masson's trichrome and analysed to determine myocardial collagen content and MF levels. Plasma levels of inflammatory markers were measured using standard laboratory procedures. Univariate and multivariate logistic regression analyses were performed to explore the relationship between the inflammatory markers and MF. Among the 102 participants included in the analysis, the mean age was 48.9 years, with 69 [67.6%] being men. The overall MF ranged from 2.5% to 40.7% (mean = 15.2 +/- 8.1%, median = 13.0%, IQR = 9.9%-18.4%). Participants were divided into two groups based on a median MF of 13%. The high MF group had a larger left atrial diameter and left ventricular ejection fraction. Levels of interleukin (IL)-2, tumour necrosis factor (TNF)-alpha and interferon (IFN)-alpha were significantly higher in patients with high MF compared to those with low MF (2.3 vs. 4.0 pg/mL, 3.1 vs. 3.9 pg/mL, 4.2 vs.4.7 pg/mL, respectively; all P < 0.05). In multivariate models adjusted for age, sex and other clinical features, IL-2, IL-5 and TNF-alpha, were correlated with increased interstitial MF [odds ratio (OR): 1.54, 95% confidence interval (CI): 1.10-2.14; OR: 1.42, 95% CI: 1.02-1.98; OR: 1.33, 95% CI: 1.04-1.70]. After additional adjustment for imaging indicators, IL-2 and TNF-alpha remained significant (OR: 1.49, 95% CI: 1.06-2.09, P = 0.021; OR:1.35, 95% CI: 1.01-1.80, P = 0.044). The correlation analysis between inflammation and replacement fibrosis assessed by CMR in 97 patients revealed that 72 (74.2%) showed late gadolinium enhancement (LGE). No significant correlation was found between inflammatory markers and the presence or extent of LGE. Conclusions Higher levels of IL-2 and TNF-alpha were associated with increased histopathological interstitial MF in patients with HCM. Given the gradual progression of MF in HCM, initiating anti-inflammatory treatment in the early stages may delay its progression.
引用
收藏
页码:582 / 591
页数:10
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