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 mg/ml fibrinogen equivalent units (FEU)) vs. 0.56 (IQR 0.31-1.12 mg/ml FEU), P U 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 mg/ml FEU) vs. 0.53 (IQR 0.29-0.90 mg/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 U 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 U 0.006]. Positive significative correlations between D-dimer and hsCRP levels (R U 0.56, P < 0.001) were found. High levels of admission D-dimer were strongly associated with inhospital 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.

Systemic inflammation biomarkers during angioedema attacks in hereditary angioedema

“…In addition to fibrinolysis contributing to the generation of D-dimer in HAE patients via contact system activation, it is crucial to underscore that inflammatory states trigger the production of fibrinogen in response to interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor (TNF) ( 18 ). This reciprocal interaction suggests that D-dimer and other fibrin degradation products might impact inflammatory and acute-phase responses by promoting neutrophil and monocyte activation, thus facilitating the release of IL-6 ( 22 , 23 ). In HAE attacks, an elevation of IL-6 has been demonstrated ( 26 ), so it is plausible to hypothesize that the activation of the inflammatory cascade and the production of fibrinogen by endothelial and inflammatory cells in HAE patients can contribute to the production of D-dimer ( 18 ).…”

“…Additionally, D-dimer acts as an APR, triggering elevated levels of cytokines such as IL-6. Consequently, this reciprocal interaction suggests that D-dimer and other fibrin degradation products might impact inflammatory and acute-phase responses by fostering neutrophil and monocyte activation, thus stimulating the release of IL-6 ( 21 – 23 ).…”

Omega-3 Fatty Acids and Markers of Thrombosis in Patients with Atrial Fibrillation

“…Model 2 was additionally adjusted for body mass index, physical activity status, smoking and drinking habits, type of AF, hypertension, diabetes mellitus, chronic kidney disease, cancer, previous stroke, previous transient ischemic attack, heart failure, coronary artery disease, major bleeding, aspirin use, statin use, P2Y12 inhibitor use and use of/type of anticoagulant. Finally, due to the well-described relationship of inflammation and thrombogenesis, [ 21 , 22 ] model 3 was adjusted for high-sensitivity C-reactive protein. All analyses were performed in R version 4.2.2 Patched (2022-11-10 r83330) or higher (R Core Team, 2022).…”