학술논문
Immune Activation Mediates the Association of Advanced Hepatic Fibrosis With Adverse Outcomes in Patients With Coronary Artery Disease
Document Type
article
Author
Vardhmaan Jain; Anurag Mehta; Terence B. Lee; Chang Liu; Nicholas W. S. Chew; Yi‐An Ko; Matthew E. Gold; Daniel A. Gold; Nishant Vatsa; Shivang R. Desai; Jonathan H. Kim; Alireza Rahbar; Yazan Haroun; Kiran Ejaz; Salim S. Hayek; Mohammad S. Siddiqui; Fadi N. Salloum; Laurence S. Sperling; Arun J. Sanyal; Arshed A. Quyyumi
Source
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 12, Iss 24 (2023)
Subject
Language
English
ISSN
2047-9980
Abstract
Background Literature suggests a bidirectional association between advanced hepatic fibrosis (AHF) and coronary artery disease (CAD). We evaluated the association of AHF with immune activation, systemic inflammation, and adverse outcomes in patients with CAD. Methods and Results A fibrosis‐4 index cutoff value ≥2.67 was used to define AHF. Circulating levels of soluble urokinase plasminogen activator receptor and hsCRP (high‐sensitivity C‐reactive protein) were measured as markers for immune activation and systemic inflammation, respectively. The relationship of AHF with soluble urokinase plasminogen activator receptor, hsCRP, and adverse cardiovascular outcomes was evaluated. Among 3406 participants with CAD, 479 had AHF. Participants with AHF were older; were less likely to be Black individuals; and had a lower body mass index, worse renal function, and a prior history of heart failure. In multivariable linear regression models adjusted for clinical and demographic confounders, participants with AHF had 15.6% higher soluble urokinase plasminogen activator receptor and 24.0% higher hsCRP levels. They were more likely to experience the following adverse outcomes: all‐cause death (adjusted hazard ratio [HR], 1.57 ([95% CI, 1.29–1.92]; P