Myocardial Fibroblast Activation in Ischemic and Nonischemic Cardiomyopathy.

作者：S. Joshi, A. Barton, K. Loganath, Neil J. Craig, M. Mahendran, B. Whittington, T. Ramtoola, Michelle C. Williams, E. V. van Beek, Andrew H. Baker, A. Fletcher, T. Clark, Clint Waight, D. Dey, P. Slomka, D. Newby, M. Dweck · 发表于：JAMA cardiology · 年份：2026 · DOI：10.1001/jamacardio.2026.0661 · 被引用次数：2 · 研究领域：Medicine

Importance Adverse myocardial remodeling and fibrosis contribute to heart failure progression and are thought to be driven by activated fibroblasts. Noninvasive assessment of myocardial fibroblast activation may improve phenotyping and risk stratification in heart failure. Objective To evaluate myocardial fibroblast activation in patients with heart failure with reduced ejection fraction using gallium 68-labeled fibroblast activation protein inhibitor 46 ([68Ga]FAPI-46) positron emission tomography (PET) and magnetic resonance imaging (MRI). Design, Setting, and Participants This was a prospective case-control study including patients with heart failure with reduced ejection fraction, patients with prior myocardial infarction without heart failure, and healthy volunteers. A subset of patients with heart failure underwent repeat imaging after more than 6 months. Data analysis was conducted from January 2024 to January 2025. Exposure All participants underwent [68Ga]FAPI-46 PET/MRI. Main Outcomes and Measures Myocardial fibroblast activation quantified using maximum standardized uptake values (SUVmax) of [68Ga]FAPI-46. Results A total of 81 participants were included (mean [SD] age, 66.2 [9.7] years; 22 [27%] female): 42 with heart failure (21 with heart failure due to ischemic cardiomyopathy from a previous myocardial infarction and 21 with a nonischemic etiology; mean [SD] left ventricular ejection fraction, 41% [9%]), 20 with a prior myocardial infarction but prese...