Low-grade systemic inflammation and left ventricular dysfunction in hypertensive compared to non-hypertensive hypertrophic cardiomyopathy

医学 肥厚性心肌病 内科学 心脏病学 舒张期 全身炎症 心肌病 利钠肽 队列 炎症 人口 血压 心力衰竭 环境卫生
作者
David Zach,Nora Schwegel,Viktoria Santner,Larissa Winkelbauer,Viktoria Hoeller,Ewald Kolesnik,Johannes Gollmer,Hubert Seggewiß,Angelika Batzner,Sabine Perl,Markus Wallner,Ursula Reiter,Peter P. Rainer,Andreas Zirlik,Klemens Ablasser,Nicolas Verheyen
出处
期刊:International Journal of Cardiology [Elsevier BV]
卷期号:399: 131661-131661 被引量:1
标识
DOI:10.1016/j.ijcard.2023.131661
摘要

BackgroundArterial hypertension (HTN) is associated with excess mortality in hypertrophic cardiomyopathy (HCM), but underlying mechanisms are largely elusive. The objective of this study was to investigate the association between HTN and markers of left ventricular (LV) dysfunction and low-grade systemic inflammation in a HCM cohort.MethodsThis was a single-center cross-sectional case-control study comparing echocardiographic and plasma-derived indices of LV dysfunction and low-grade systemic inflammation between 30 adult patients with HCM and HTN (HTN+) and 30 sex- and age-matched HCM patients without HTN (HTN-). Echocardiographic measures were assessed using post-processing analyses by blinded investigators.ResultsMean age of the study population was 55.1 ± 10.4 years, 30% were women. Echocardiographic measures of systolic and diastolic dysfunction, including speckle-tracking derived parameters, did not differ between HTN+ and HTN-. Moreover, levels of N-terminal pro B-type natriuretic peptide were balanced between cases and controls. Compared with HTN-, HTN+ patients exhibited a higher white blood cell count [8.1 ± 1.8 109/l vs. 6.4 ± 1.6 109/l; p < 0.001] as well as higher plasma levels of interleukin-6 [2.8 pg/ml (2.0, 5.4) vs. 2.1 pg/ml (1.5, 3.4); p = 0.008] and high-sensitivity C-reactive protein [2.6 mg/l (1.4, 6.5) vs. 1.1 mg/l (0.9, 2.4); p = 0.004].ConclusionThis study demonstrates that HTN is associated with indices of low-grade systemic inflammation among HCM patients. Moreover, this analysis indicates that the adverse impact of HTN in HCM patients is a consequence of systemic effects rather than alterations of cardiac function, as measures of LV systolic and diastolic dysfunction did not differ between HTN+ and HTN-.

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