Neutrophil/lymphocyte ratio can predict postoperative mortality in patients with chronic thromboembolic pulmonary hypertension

Objective: The aim of our study was to investigate clinical importance of neutrophil/ lymphocyte ratio in patients with Chronic thromboembolic pulmonary hypertension. Methods: 125 consecutive patients with a diagnosis of Chronic thromboembolic pulmonary hypertension were operated pulmonary thromboendarterectomy in our center between February 2011 and August 2013. 106 patients included into the study due to limitations. The patients were classified into two groups as patients discharged alive (Group 1) and those dying in the hospital (Group 2). Baseline neutrophil/lymphocyte ratio level was measured by dividing neutrophil count to lymphocyte count. Results: 84 patients (79%) were in Group 1, 22 patients (21%) were in Group 2. Patients with higher neutrophil/lymphocyte ratio in admission have a significantly higher mortality rate and postoperative pulmonary vascular resistance was found statistically significant variable to predict the mortality. Receiver operator characteristic (ROC) analysis revealed that using a cut-off point of 2.54, admission neutrophil/lymphocyte ratio predicts mortality. Also, correlation analysis showed a significant correlation between preopera-tive pulmonary vascular resistance and neutrophil/lymphocyte ratio. Conclusion: The neutrophil/lymphocyte ratio level may be a useful and noninvasive biomarker for operative risk stratification for mortality after pulmonary thromboendarterectomy

Evaluation of apoptotic molecular pathways for smooth muscle cells isolated from thoracic aortic aneurysms in response to oxidized sterols

WOS: 000349005800018PubMed ID: 25266234Oxysterols, oxygenated derivatives of cholesterol, are found abundantly in the plasma and atherosclerotic plaques, a common risk factor for thoracic aortic aneurysms (TAAs). Among the oxysterols, namely 7-ketocholesterol (7-KC) and 25-hydroxycholesterol (25-OHC), lead both to induction of reactive oxygen species (ROS) in cells and to apoptosis in smooth muscle cells (SMCs) probably due to increased oxidative stress. Since loss of SMCs through apoptosis is a major event in TAA formation, it is important to understand the molecular pathways of apoptosis in response to ROS in TAAs. Very little is known about the effect of oxysterols on TAA SMCs. Therefore, we investigated molecular pathways participating in the oxysterol induced cell death of TAAs. Our results showed that TAA SMCs died mainly as a result of apoptosis as suggested by cellular shrinkage, blebbing, DNA condensation/fragmentation in response to oxysterol treatment. There was no significant difference in oxysterol induced cell death between TAA and control SMCs. Addition of antioxidant molecules prevented cell death, hence ROS appears to be involved in the apoptosis of these cells. While oxysterol treatment increased caspase 3 activity, cell death was not rescued in its absence. Efficient silencing of other targets including apoptotic proteins (p53, Bax), and survival proteins (Akt1, Akt2) showed that apoptosis can occur through p53, and Bax independent pathways. Silencing Akt1 or Akt2 did not lead to further cell death. These results indicate that oxysterols can induce several cell death pathways in TAA SMCs.FP7 Project entitled "Fighting Aneurysmal Disease" (FAD) [200647]Istanbul University Department of Scientific Research Projects [10241]This work was supported by the FP7 Project entitled "Fighting Aneurysmal Disease" (FAD), Grant No: 200647 and Istanbul University Department of Scientific Research Projects, entitled "Investigation of Gene Expressions Related to Oxidative Stress in Human Thoracic Aort Aneurysms", Grant No: 10241