Abstract 11201: Elevated Ratio of Placental Growth Factor to Soluble Fms-Like Tyrosine Kinase-1 Predicts an Adverse Outcome in Patients with Chronic Coronary Artery Disease
Background: Placental growth factor (PlGF) and its endogenous inhibitor, soluble fms-like tyrosine kinase-1 (sFlt-1), play an important role in the pathophysiology of coronary artery disease. We recently demonstrated that plasma sFlt-1 level was negatively correlated with the severity of coronary atherosclerosis, and previous studies showed elevated PlGF level was a marker of poor prognosis in patients with acute coronary syndrome. In this study, we tried to examine whether plasma levels of PlGF and sFlt-1 predict the risk of long-term all-cause death (ACD) and total cardiovascular event (TCVE: ACD, nonfatal myocardial infarction, nonfatal stroke, CCU admission from CHF, introduction of maintenance hemodialysis) in patients with stable coronary artery disease (sCAD).
Methods: ACD and TCVE were investigated on June 2010 in 491 sCAD patients who received coronary angiography from February 2004 to December 2008. Median follow-up period was 3.3 years. Baseline blood samples were collected before coronary angiography (after 20-Unit heparin administration), and plasma levels of PlGF and sFlt-1 were measured using ELISA kits. Cox proportional hazard regression analysis was performed to evaluate the relationship between patients' parameters and events.
Results: A total of 37 ACD and 67 TCVE occurred during follow-up period. Patients with higher PlGF/sFlt-1 ratio (>4.47X10-2) had significantly higher risk of both ACD and TCVE than patients with lower ratio (<4.47X10-2) (HR, 2.99: 95% CI, 1.41-6.34, p=0.004, HR, 2.12: 95% CI, 1.26-3.55, p=0.004, respectively). Kaplan-Mayer curves were shown in Figure. Multivariate analysis showed PlGF/sFlt-1 ratio was an independent predictor for ACD.
Conclusion: The present study demonstrated that baseline PlGF/sFlt1 ratio seems to be an independent predictor of adverse outcome in patients with sCAD in chronic phase, possibly due to the activated atherosclerotic process in patients with higher PlGF/sFlt1 ratio.
- © 2011 by American Heart Association, Inc.