Key result
Acute heart failure is associated with significantly decreased plasma fibroblast activation protein levels (22.58 ng/ml) compared to healthy controls (31.79 ng/ml), despite its upregulation in cardiac tissue.
Why the study?
Fibroblast activation protein plays an emerging role in HF, but a paradoxical reduction occurs in acute conditions. Investigators sought to examine FAP cardiac expression and signaling, and compare plasma levels in acute versus chronic HF.
Are FAP levels altered in cardiac tissue and plasma of patients with acute and chronic heart failure compared to controls?
Observational (n=140)
No
Are FAP levels altered in cardiac tissue and plasma of patients with acute and chronic heart failure compared to controls?
Absolute Event Rate: 22.58% vs 31.79%
p-value: p=<0.05
Despite upregulation in cardiac tissue, plasma FAP levels are paradoxically decreased in acute heart failure, suggesting it may be a complex biomarker for cardiac fibrosis.
Tissue-plasma FAP discordance in HF cautions against simple biomarker use; leaves open its fibrosis role pending prospective studies.
BACKGROUND: Cardiac fibroblast activation protein (FAP) has an emerging role in heart failure (HF). A paradoxical reduction in its levels in pathological conditions associated with acute processes has been observed. We aimed to identify FAP cardiac tissue expression and its relationship with the main cardiac fibrosis-related signaling pathways, and to compare plasma FAP levels in acute and chronic HF patients. METHODS: Transcriptomic changes were assessed via mRNA/ncRNA-seq in left ventricle tissue from HF patients (n = 57) and controls (n = 10). Western blotting and immunohistochemistry were used to explore FAP protein levels and localization in cardiac tissue. ELISA was performed to examine plasma FAP levels in acute HF (n = 48), chronic HF (n = 15) and control samples (n = 7). RESULTS: FAP overexpression in cardiac tissue is related to the expression of molecules directly involved in cardiac fibrosis, such as POSTN, THBS4, MFAP5, COL1A2 and COL3A1 (P < 0.001), and is directly and inversely related to pro- and antifibrotic microRNAs, respectively. The observed FAP overexpression is not reflected in plasma. Circulating FAP levels were lower in acute HF patients than in controls (P < 0.05), while chronic HF patients did not show significant changes. The clinical variables analyzed, such as functional class or etiology, do not affect plasma FAP concentrations. CONCLUSIONS: We determined that in HF cardiac tissue, FAP is related to the main cardiac fibrosis signaling pathways as well as to pro- and antifibrotic microRNAs. Additionally, an acute phase of HF decreases plasma FAP levels despite the upregulation observed in cardiac tissue and regardless of other clinical conditions.
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Delgado‐Arija et al. (2024) conducted an observational in Heart failure (n=140). Acute heart failure vs. Healthy controls and chronic heart failure was evaluated on Plasma FAP levels (ng/ml) (p=<0.05). Acute heart failure is associated with significantly decreased plasma fibroblast activation protein levels (22.58 ng/ml) compared to healthy controls (31.79 ng/ml), despite its upregulation in cardiac tissue.
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