Key result
Higher myocardial 99mTc-HFAPi activity in non-ischemic HF predicts poor cardiac function improvement at 3 months.
Why the study?
Activated myocardial fibroblasts drive progression toward heart failure, but the characteristics of myocardial fibroblast activation imaging and its predictive value for improved cardiac function in non-ischemic heart failure were uncharacterized.
Does 99mTc-HFAPi imaging predict cardiac functional improvement in patients with non-ischemic heart failure?
Cohort (n=74)
Yes
Does 99mTc-HFAPi imaging predict cardiac functional improvement in patients with non-ischemic heart failure?
99mTc-HFAPi imaging reveals intense, heterogeneous fibroblast activation in non-ischemic heart failure, which negatively correlates with baseline systolic function and predicts poor functional improvement.
Answers are grounded in this paper and cite their sources.
May identify non-ischemic HF patients unlikely to recover; leaves open prospective validation before clinical adoption.
Activated myocardial fibroblasts are key contributors to cardiac fibrosis and drive progression toward heart failure (HF). This study aimed to investigate the characteristics of myocardial fibroblast activation imaging and its predictive value for improved cardiac function in non-ischemic HF. This double-center prospective study enrolled 38 patients who underwent 99m Tc-labeled-hydrazinonicotinamide-fibroblast activation protein inhibitor-04 ( 99m Tc-HFAPi) and cardiac magnetic resonance (CMR) imaging. For comparison, 18 healthy volunteers were recruited to undergo 99m Tc-HFAPi imaging as controls, while another 18 controls were selected from the CMR database. Myocardial 99m Tc-HFAPi activity was quantified by intensity, extent, and amount. CMR-derived T1 values, extracellular volume (ECV), and strain were analyzed. Baseline and follow-up echocardiographic data were used to evaluate improved cardiac function. All patients exhibited intense but inhomogeneous 99m Tc-HFAPi uptake in the left ventricular (LV) myocardium, and the intensity was higher than that of controls (4.1 ± 1.8 vs. 1.2 ± 0.1, p < 0.001). LV 99m Tc-HFAPi amount negatively correlated with LVEF (r = -0.43, p = 0.008). At the segmental level, abnormal 99m Tc-HFAPi uptake was present in 79.8 % of segments, exceeding the prevalence of increased native T1 values (66.1 %) (p < 0.001). At median follow-up of 3 months, patients without improved cardiac function demonstrated significantly higher intensity (5.0 ± 2.0 vs. 3.5 ± 1.6, p = 0.022). Patients with non-ischemic HF showed intense but heterogeneous 99m Tc-HFAPi activity. The 99m Tc-HFAPi activity was negatively correlated with baseline cardiac systolic function and associated with poor improvement in cardiac function during follow-up.
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Su et al. (2025) conducted a cohort in non-ischemic heart failure (n=74). 99mTc-HFAPi imaging vs. Healthy controls was evaluated on 99mTc-HFAPi intensity in patients without vs. with improved cardiac function (p=0.022). Myocardial 99mTc-HFAPi activity was higher in non-ischemic HF patients than controls (4.1 vs 1.2, p<0.001) and higher intensity predicted poor cardiac function improvement at 3 months (p=0.022).
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