Abstract 12644: Growth Differentiation Factor-15 (GDF-15) for Risk Stratification in Patients After an Acute Coronary Syndrome: Insights From the SOLID-TIMI 52 trial
Background: Growth differentiation factor (GDF)-15, a stress responsive cytokine, is associated with the risk of CV events after an acute coronary syndrome (ACS). Unlike other established cardiac biomarkers, the level of GDF-15 remains elevated in sub-acute phase after ACS and gradually decreases over time. We evaluated the prognostic utility of GDF-15 in patients after ACS accounting for established markers and risk predictors.
Methods: GDF-15 (R&D Systems) and other established cardiac biomarkers (BNP, hsCRP and hsTnI) were measured at baseline in a randomly selected cohort of 4,968 patients enrolled within 30 days of hospitalization with ACS (median=14d) in SOLID-TIMI 52. Previously defined cutpoints were applied for GDF-15 concentration: <1200 (n=3451), 1200-1800 (n=919), and > 1800 ng/L (n=598). Analyses were adjusted for established risk predictors, days from the ACS event and other markers. MACE was defined as CV death, MI or stroke. Median follow-up was 2.5 years.
Results: Patients with higher GDF-15 tended to be older, more likely to have diabetes, hypertension, history of revascularization, and CKD at baseline. Higher baseline levels of GDF-15 identified patients with higher rates of MACE as well as each individual element (p-trend <0.001 for all endpoints, Fig). The rate of MI was ∼2-fold higher in those with GDF-15 concentration >1800ng/L compared to patients with GDF-15 concentration <1200 ng/L. After adjustment for clinical predictors and other markers, GDF-15 was independently associated with the risk of MACE (HR 1.4, 95% CI 1.1-1.7; HR 1.8, 95% CI 1.4-2.3 for GDF-15 1200-1800, >1800, respectively). Individuals with GDF-15 >1800 ng/L had an increased risk of MI (adj HR 1.4, 95% CI 1.1-2.0) and stroke (adj HR 2.3, 95% CI 1.3-3.9).
Conclusion: In patients after ACS, GDF-15 concentration is associated with the risk of MACE including MI and stroke independent of traditional risk factors and risk markers.
Author Disclosures: E. Toda Kato: None. D.A. Morrow: None. C.P. Cannon: Research Grant; Significant; Boehringer Ingelheim, GlaxoSmithKline, Janssen, Merck&Co., Inc., Takeda. Consultant/Advisory Board; Modest; Boehringer Ingelheim, GlaxoSmithKline, Merck&Co., Inc, Takeda, Bristol-Myers Squibb, CSL Behring, Essentialis, Kowa, Lipimedix, Pfizer, Regeneron, Sanofi. M. Lukas: Employment; Significant; GSK. A. Budaj: Research Grant; Significant; GlaxoSmithKline, AstraZeneca, Bristol Myers Squibb, Pfizer, Sanofi-Aventis, Boehringer Ingelheim, Novartis, Eisai. Other; Modest; GlaxoSmithKline, AstraZeneca, Bristo Myers Squibb, Pfizer. C.W. Hamm: None. P. Jarolim: Other Research Support; Significant; Abbott Laboratories, Amgen Inc, Astra Zeneca LP, Beckman Coulter, Daiichi sankyo, Inc., Glaxo Smith Kline, Merck & Co., Inc., Roche Diagnostics Corporation, Takeda Global Research and Development Center, Waters Technologies Corpoation. K. Im: None. J. Zhou: None. E. Braunwald: Research Grant; Significant; Glaxo Smith Kline. M.L. O’Donoghue: Research Grant; Significant; GSK, Eisai, Merck. Consultant/Advisory Board; Modest; diaDexus.
- © 2015 by American Heart Association, Inc.