Abstract

The relationship between inflammation and venous thrombosis is not well understood. An inflammatory response may be both the cause and consequence of venous thromboembolism (VTE). In fact, several risk factors of VTE modulate thrombosis through inflammatory markers. Acute pulmonary embolism (PE) is burdened by a remarkable mortality rate, up to 34% in severely ill patients presenting with hemodynamic instability. Initial mortality risk stratification is based on hemodynamic instability. Patients with a situation of hemodynamic stability require immediate further risk assessment based on clinical, imaging, and circulating biomarkers, as well as the presence of comorbidities. Some inflammatory biomarkers have shown potential usefulness in the risk stratification of patients with VTE, especially acute PE. C-reactive protein on admission is associated with 30-day mortality and bleeding in VTE patients. P-selectin is associated with right ventricle dysfunction in PE patients and might be associated with VTE recurrences and the extension of thrombosis. Tissue factor microparticles are associated with VTE recurrence in cancer-associated thrombosis. Other inflammatory biomarkers present scarce evidence (inflammatory cytokines, erythrocyte sedimentation rate, fibrinogen, leukocyte count). In this manuscript, we will review the prognostic role of different inflammatory biomarkers available both for clinical practice and research in VTE patients.

Highlights

  • Introduction published maps and institutional affilDeep vein thrombosis (DVT) and pulmonary embolism (PE) are the main manifestations of venous thromboembolism (VTE)

  • Most of them are involved in different mechanisms, which reduces their specificity [36]

  • In the past 15 years, only a few studies evaluating the prognostic role of inflammatory biomarkers in patients with VTE have been published, with indefinite results

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Summary

Inflammation in VTE

Little is known about the relationship between inflammation and venous thrombosis [13]. Similar prothrombotic mechanisms could operate in other inflammatory states characterized by both elevated cytokines known to induce TF expression (e.g., TNF-a, Il-6, Il-1b) and VTE development [22] Examples of such states include Behçet disease [29], AIDS [30], cancer [31], systemic viral infections (notably CMV infection) [32], and surgery [33]. Some inflammatory elements are essential for the proper resolution of VTE [15]

Inflammatory Biomarkers in VTE
P-Selectin
Inflammatory Cytokines
Fibrinogen
Leukocytes
Prognostic Biomarkers for Bleeding Risk during Anticoagulation in VTE
Findings
Conclusions
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