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Circulating dipeptidyl peptidase 3 and outcomes in acute heart failure: an analysis of the STRONG-HF and CORTAHF
J Bruno1,2,3, C Edwards4, K Takagi4
1INSERM UMR-S 942, Cardiovascular Markers in Stress Condition (MASCOT), 2 rue Ambroise Paré, Paris 75010, France.
Insights
Circulating dipeptidyl peptidase 3 (cDPP3) in acute heart failure (AHF) patients was mildly elevated and did not predict outcomes. Elevated cDPP3 identified a distinct patient group but did not worsen prognosis during guideline-directed medical therapy optimization.
Area of Science:
- Cardiology
- Biomarkers
- Heart Failure Research
Background:
- Circulating dipeptidyl peptidase 3 (cDPP3) is linked to cardiocirculatory failure and poor outcomes in shock.
- The role of cDPP3 in acute heart failure (AHF) remains unexamined.
Purpose of the Study:
- To investigate the clinical relevance and prognostic value of cDPP3 in patients with AHF.
- To explore the association between cDPP3 levels and outcomes during guideline-directed medical therapy (GDMT).
Main Methods:
- Prospective analysis of two AHF trials (STRONG-HF and CORTAHF).
- Measurement of cDPP3 at baseline and follow-up.
- Evaluation of associations with clinical outcomes and response to GDMT.
Main Results:
- Elevated baseline cDPP3 (≥40 ng/mL) was observed in 23% of AHF patients, who were younger, more often female and Black, with lower NT-proBNP.
- Elevated cDPP3 was not associated with 180-day outcomes in STRONG-HF.
- cDPP3 levels decreased with high-intensity care but changes were not linked to NT-proBNP reduction.
- Mineralocorticoid receptor antagonist use predicted elevated cDPP3, while non-Black ethnicity was associated with lower odds.
Conclusions:
- In AHF, cDPP3 is mildly elevated and not associated with clinical outcomes or congestion relief during GDMT optimization.
- Elevated cDPP3 identifies a distinct clinical phenotype in AHF patients but does not confer an adverse prognosis.
Introduction:
Circulating dipeptidyl peptidase 3 (cDPP3) is implicated in cardiocirculatory failure and elevated concentrations predict poor outcomes in shock states. Its role in acute heart failure (AHF) is unexplored. We assessed the clinical relevance of cDPP3 in AHF.
Methods:
Analyses were performed using two prospective AHF trials: STRONG-HF and CORTAHF. cDPP3 was measured at baseline and follow-up (day 90 in STRONG-HF; day 30 in CORTAHF). Associations with 180-day (STRONG-HF) and 90-day (CORTAHF) outcomes were evaluated according to baseline concentrations. Longitudinal changes during guideline-directed medical therapy (GDMT) optimization and predictors of elevated cDPP3 were analysed.
Results:
In STRONG-HF, 222/973 patients (23%) had cDPP3 ≥ 40 ng/mL. These patients were younger (58 ± 15 vs. 65 ± 13 years, P < .0001), more frequently female (47.7% vs. 35.8%, P = .0013) and Black (42.8% vs. 14.4%, P < .0001), with lower NT-proBNP concentrations (P < .0001). Baseline cDPP3 ≥ 40 ng/mL was not associated with 180-day outcomes. Over 90 days, cDPP3 decreased by -15% with high-intensity care and -8% with usual care (P = .078). Changes in cDPP3 were not associated with NT-proBNP reduction (continuous P = .797; ≥30% responder P = .990). In pooled multivariable analysis, MRA use was independently associated with cDPP3 ≥ 40 ng/mL (OR 3.83; 95% CI 1.47-9.96; P = .006), whereas non-Black ethnicity was associated with lower odds (OR 0.43; 95% CI 0.29-0.64; P < .0001).
Conclusion:
In AHF, cDPP3 was mildly elevated and was not associated with clinical outcomes or congestion relief during GDMT optimization. Elevated cDPP3 identified a distinct clinical phenotype but did not confer adverse prognosis.
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