Evaluation of the relationship between markers presenting the severity of acute pulmonary embolism and plasma alpha defensin 1 level

Pulmonary embolism is a life-threatening clinical entity that occurs as a result of partial or total occlusion of the main pulmonary artery and its branches. In clinical practice, risk stratification is mandatory in order to determine the appropiate treatment approach in patients with acute PTE. Hemodynamic instability is the major determinant of poor prognosis as well as short and longterm mortality. Clinical evaluation, biochemical markers and several imaging modalities are utilized to determine prognosis in patients without hemodynamic instability. Alpha defensin 1 is a proinflamatory and prothrombogenic biochemical marker which previously was shown to be prognosticly associated with different cardiovasculer diseases. There is no previous study showing the relationship between alpha defensin 1 level and acute pulmonary embolism. In this study, we aimed to assess serum alpha defensin 1 level in patient diagnosed with acute PTE in emergency room and normal healthy subjects, also to investigate its correlation with short-term mortality markers. We included 65 acute PTE patients and 65 healthy volunteers were included in this observational study. Acute PTE group were categorized according to their clinical status at presentation, presence of right ventricular dysfunction finding detected by echocardiography, and risk stratification using cardiac biomarkers such as brain natriuretic peptid and high sensitive troponin. Alpha defensin 1 level was measured in all paticipants. In our study, no statistically significant difference was found between the acute PTE patients and the control group in term of serum alpha defensin 1 levels. In addition, no significant correlation was found between short-term mortality markers and serum alpha defensin 1 levels in patients with acute PTE. Gender and age distrubution was similar between groups. Hs-troponin T, NT-proBNP, CRP, WBC and D-dimer levels were significantly higher in patients with acute PTE compared to the control group; while sodium, platelet count and hemoglobin levels were significantly low. Right heart dimensions and pulmonary artery pressure were higher in patients with acute PTE; whereas tricuspit annuler plane systolic excursion (TAPSE) was significantly lower. In addition, the number of patients with RV/LV> 1 was more prevelant in the patients group. In addition, there was no significant relationship between serum alpha defensin 1 levels and NT-proBNP, hs-troponin T and D-dimer levels, clinical scores (PESI and s PESI scores) and early mortality risk classification status. Moreover; no significant relationship was detected in patients with and without hypertension, diabetes mellitus, coronary artery diseases, hyperlipidemia and presence of any cancer in terms of serum alpha defensin 1 levels. In conclusion, there was no significant difference between groups in terms of serum alpha defensin 1 levels. Similarly serum alpha defensin 1 levels was not correlated with well established guideline recommended risk stratifiers in patients with PTE. To our knowledge, this was the first study examining serum alpha defensin 1 levels in patients with acute PTE.