^99mTc-HFAPi SPECT imaging predicts left ventricular remodeling after acute myocardial infarction

Despite improved treatments for acute myocardial infarction (AMI), myocardial fibrosis remains a key driver of adverse left ventricular (LV) remodeling and increased mortality. Fibroblast activation and proliferation significantly contribute to this process by enhancing cardiac fibrosis, which can lead to detrimental changes in LV structure. This study evaluates the effectiveness of ^99mTc-labeled fibroblast activation protein inhibitor (^99mTc-HFAPi) SPECT imaging in predicting LV remodeling over 12 months in post-AMI patients.

A cohort of 58 AMI patients (46 males, median age 61 [53, 67] years) underwent baseline ^99mTc-HFAPi imaging (5 ± 2 days post-MI), perfusion imaging (6 ± 2 days post-MI), and echocardiography (2 ± 2 days post-MI). Additionally, 15 patients had follow-up ^99mTc-HFAPi and perfusion imaging, while 30 patients had follow-up echocardiography. Myocardial ^99mTc-HFAPi activity was assessed at the patient level. LV remodeling was defined as a ≥10% increase in LV end-diastolic diameter (LVEDD) or LV end-systolic diameter (LVESD) from baseline to follow-up echocardiography.

AMI patients displayed localized but non-uniform ^99mTc-HFAPi uptake, exceeding perfusion defects. Baseline ^99mTc-HFAPi activity exhibited significant correlations with BNPmax, LDHmax, cTNImax, and WBCmax, inversely correlating with LVEF. After 12 months, 11 patients (36.66%) experienced LV remodeling. Univariate regression analysis demonstrated an association between baseline ^99mTc-HFAPi uptake extent and LV remodeling (OR = 2.14, 95%CI, 1.04, 4.39, P = 0.038).

^99mTc-HFAPi SPECT imaging holds promise in predicting LV remodeling post-MI, providing valuable insights for patient management and prognosis.