Leukocytes and Systemic Inflammatory Response in PE Patients
Leukocytes and Systemic Inflammatory Response in PE Patients
Hemodynamic status and comorbidities are key factors in the prognosis of pulmonary embolism (PE). In addition to hemodynamic variables, cardiac biomarkers such as troponins and natriuretic peptides are risk factors for patients with acute PE. The PE prognostic prediction model that is based on these variables is widely accepted.
Initial risk stratification of patients with PE is based on the presence of shock or hypotension. If the patient is hemodynamically stable, right ventricular function is then assessed by echocardiography, and cardiac biomarkers are measured. However, these variables are not accurate predictors of PE mortality, especially in hemodynamically stable patients.
The triad of vessel wall injury, venous stasis, and blood hypercoagulability has historically been considered a major risk factor for venous thrombosis. Infection is another established risk factor for PE, and in certain cases, PE has been associated with influenza or cytomegalovirus infection.
In deep vein thrombosis (DVT), an inflammatory reaction triggers endothelial cell dysfunction and results in high serum concentrations of the inflammatory marker C-reactive protein. Such inflammatory reactions frequently induce well-studied DVT risk factors; however, few studies have investigated a prognostic prediction model for PE. Respiratory and pulse rates are included in the representative PE severity index (PESI). Nevertheless, there is a dearth of studies on the potential association between the systemic inflammatory response and PE patient prognosis.
Studies have suggested that leukocytes contribute to venous thrombosis by damaging the endothelium. Animal models have shown that genetic knock-out of the adhesion molecules E- and P-selectin results in a reduction in thrombus size, which is associated with altered leukocyte accumulation in the surrounding vein wall. However, the role of leukocytes in the prognosis of PE has not been well studied. We hypothesize that both a systemic inflammatory response and leukocytosis may be negative prognostic factors in PE patients.
Background
Hemodynamic status and comorbidities are key factors in the prognosis of pulmonary embolism (PE). In addition to hemodynamic variables, cardiac biomarkers such as troponins and natriuretic peptides are risk factors for patients with acute PE. The PE prognostic prediction model that is based on these variables is widely accepted.
Initial risk stratification of patients with PE is based on the presence of shock or hypotension. If the patient is hemodynamically stable, right ventricular function is then assessed by echocardiography, and cardiac biomarkers are measured. However, these variables are not accurate predictors of PE mortality, especially in hemodynamically stable patients.
The triad of vessel wall injury, venous stasis, and blood hypercoagulability has historically been considered a major risk factor for venous thrombosis. Infection is another established risk factor for PE, and in certain cases, PE has been associated with influenza or cytomegalovirus infection.
In deep vein thrombosis (DVT), an inflammatory reaction triggers endothelial cell dysfunction and results in high serum concentrations of the inflammatory marker C-reactive protein. Such inflammatory reactions frequently induce well-studied DVT risk factors; however, few studies have investigated a prognostic prediction model for PE. Respiratory and pulse rates are included in the representative PE severity index (PESI). Nevertheless, there is a dearth of studies on the potential association between the systemic inflammatory response and PE patient prognosis.
Studies have suggested that leukocytes contribute to venous thrombosis by damaging the endothelium. Animal models have shown that genetic knock-out of the adhesion molecules E- and P-selectin results in a reduction in thrombus size, which is associated with altered leukocyte accumulation in the surrounding vein wall. However, the role of leukocytes in the prognosis of PE has not been well studied. We hypothesize that both a systemic inflammatory response and leukocytosis may be negative prognostic factors in PE patients.
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