Role of systemic inflammation in the development of venous thromboembolism in patients with ischemic stroke

Aim. To determine the role of systemic inflammation in the development of venous thromboembolism (VTE) in patients with ischemic stroke.

Material and methods. This single-center prospective study included 94 patients with confirmed ischemic stroke and significant mobility impairment (Rivermead Mobility Index ≤3). VTE was diagnosed based on paired ultrasound examinations of the lower extremity veins at 3±1 and 10±1 days of hospitalization and CT pulmonary angiography performed in patients with deep vein thrombosis (DVT). Laboratory markers of systemic inflammation included white blood cell (WBC) count, relative lymphocyte count, relative mid cell count in the complete blood count at admission, leukocyte-lymphocyte ratio, and C-reactive protein levels.

Results. Forty-six (49%) patients were diagnosed with venous thromboembolism (VTE). In 26 cases, DVT was detected by lower extremity vein ultrasound on day 3±1 of hospitalization (early DVT), and in 20 cases, thrombosis was detected on day 10±1 (late DVT). All patients had C-reactive protein levels above reference values on day 3 of hospitalization. An association was established between blood concentrations of inflammatory markers and stroke severity indicators, decreased venous flow velocity, and D-dimer levels. No association was found between systemic inflammation detected during ischemic stroke and underlying chronic inflammatory diseases or acute inhospital infectious complications. Patients with VTE were characterized by significantly more pronounced changes in inflammatory biomarkers. An increase in WBC >12×109/L (area under the receiver operating characteristic curve (AUC) 0,677, p=0,012), a leukocyte-lymphocyte ratio >6,5 (AUC 0,694, p=0,006), and a decrease in the relative lymphocyte content <15% (AUC 0,690, p=0,007) at the time of hospital admission were predictors of early thrombosis.

Conclusion. Ischemic stroke induces a systemic inflammatory response, the severity of which is determined by both the severity of brain injury and the individual characteristics of the patient's inflammatory response. Systemic inflammation has a modulating effect on the pathogenesis of venous thromboembolism (VTE) in patients with ischemic stroke. High inflammatory activity contributes to an earlier (3±1 day) onset of VTE. In patients with moderate inflammation, VTE is preceded by a longer exposure to the main risk factors, and thrombosis develops later (10±1 day). Pronounced inflammatory response in patients with ischemic stroke and significant mobility impairments can be considered as an additional criterion for the early administration of anticoagulants for VTE prevention.

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