Abstract 19797: Follistatin-Like 3 is Elevated In Acute Heart Failure Patients
Background: Follistatin-like 3 is an extracellular regulator of the TGF-β superfamily members such as activin A, myostatin, and BMP2. FSTL-3 transcripts have been found to be upregulated in myocardium from patients with severe heart failure (HF), and are associated with severity of the disease. Furthermore, FSTL-3 has been identified as a possible modulator of stress-induced cardiac hypertrophy following pressure overload in mice. In this study, we sought to examine whether: 1) FSTL-3 is elevated in patients with HF vs. age-matched controls, and 2) FSTL-3 is elevated in patients with acute decompensated HF vs. those with chronic HF; and 3) FSTL-3 levels change 5 weeks after an acute HF episode.
Methods and Results: We measured plasma levels of FSLT-3 in: 1) healthy ageing volunteers (n=67, age 68±6 yrs), 2) patients with acute HF (n=45, age 71±13), and 3) patients with chronic HF (n=28, age 71±10). Plasma FSTL-3 levels were significantly higher patients with acute HF (mean 16,220 ± 8645 pg/mL) vs, chronic HF (mean 10,205 ± 5636 pg/mL, p<0.01) patients vs. healthy ageing volunteers (mean 5601 ± 955.4 pg/ml, p<0.001) (one-way ANOVA with Bonferroni post hoc analysis) (Figure 1A). In 27 patients who were admitted to hospital due to acute decompensated HF, blood samples were taken to assess for FSTL3 levels at baseline and 5 weeks after treatment. While there was no difference in NT-proBNP levels in patients with acute HF upon admission vs. 5 weeks of follow-up (medians of 3997 pg/mL vs 2678 pg/mL respectively; p=0.4, Wilcoxon matched pairs rank test); FSTL-3 levels were significantly reduced (mean ±SD, 14,117 ± 7374 pg/mL vs. 12,744 ± 5573 pg/mL, p<0.05, paired t-test).
Conclusions: Plasma levels of FSTL-3 are increased in HF patients with a further incremental increase in those with acute versus chronic HF. These results suggest that FSTL-3 is a potential sensitive biomarker of changes in HF status. Furthermore, FSTL3 appears to be an even earlier and more consistent biomarker of response to anti-failure therapy compared to NT-proBNP.
Author Disclosures: S. Liu: None. B. Assadi-Khansari: None. C. Ajaero: None. S. Chua: None. J.D. Horowitz: None. D.T. Ngo: None. A.L. Sverdlov: None.
- © 2016 by American Heart Association, Inc.