Association of hemostasis and inflammation biomarkers with outcomes in acute coronary syndromes

Abstract

Plaque rupture triggers a prothrombotic response that is counterbalanced by a fibrinolytic response. d-dimer serves as a marker of both processes. Inflammatory mediators are also released, evidenced with the rise of high-sensitive C reactive protein (hsCRP). Current evidence with these biomarkers has shown conflicting results. Determine an association between d-dimer and hsCRP within hospital and 1-year mortality in patients with acute coronary syndromes. In total, 127 patients were included. In-hospital mortality was 5.7%, and 1-year all-cause and cardiovascular mortality were 14.6 and 9.7%, respectively. The median of admission d-dimer for patients who died during hospital stay was higher than those who survived [4.59 (interquartile ranges (IQR) 1.94–6.05 μg/ml fibrinogen equivalent units (FEU)) vs. 0.56 (IQR 0.31–1.12 μg/ml FEU), P = 0.001]. At 1-year follow-up, the median of admission d-dimer for patients who died was significantly higher than those who survived: 1.55 (IQR 0.91–5.08 μg/ml FEU) vs. 0.53 (IQR 0.29–0.90 μg/ml FEU), P < 0.001. Positive d-dimer vs. negative d-dimer at admission analysis evidenced that almost 25% of the positive patients were dead at 1-year follow-up (22.4 vs. 2.4% negative d-dimer, P = 0.011). Multivariate logistic regression analysis showed that d-dimer has an independent association with 1-year mortality [odds ratio 1.06 (95% confidence interval 1.02–1.10), P = 0.006]. Positive significative correlations between d-dimer and hsCRP levels (R = 0.56, P < 0.001) were found. High levels of admission d-dimer were strongly associated with in-hospital and 1-year mortality. Significant correlations with hsCRP could explain the inflammatory nature that led to poorer outcomes. d-dimer could be useful in risk stratification in acute coronary syndromes; however, a specific threshold should be defined for this type of patient.