Concomitant Persistent Atelectasis following TEVAR Due to a Descending Aortic Aneurysm: Hybrid Endovascular Repair and ECMO Therapy.

Many thoracic aortic aneurysms are discovered incidentally, and most develop without symptoms. Symptoms are usually due to sudden expansion of the aneurysm, which can cause a vague pain in the back, or sometimes a sharp pain that may denote the presence of impending rupture. Other symptoms are related to pressure on adjacent structures, such as pressure on the bronchus that can cause respiratory distress, or pressure on the laryngeal nerve causing vocal hoarseness. Pressure on the esophagus can cause difficulty in swallowing. Currently, open surgery and thoracic endovascular aneurysm repair (TEVAR) are the choices of treatment for descending thoracic aneurysms (DTA). The decision to intervene on a DTA depends on its size, location, rate of growth and symptoms, and the overall medical condition of the patient. The indications for TEVAR should not differ from those for open surgery and typically include aneurysms larger than 6 cm in diameter. Saccular and symptomatic aneurysms are often repaired at a smaller size. It is also suggested that aneurysms with a growth rate more than 1 cm per year, or 0.5 cm in 6 months should be considered for early repair.Despite the close proximity of the aorta and left main bronchus, atelectasis caused by thoracic aortic aneurysms is rare. We review the case report of a patient with concomitant persistent left pulmonary atelectasis causing acute respiratory distress due to complete compression of the left main bronchus after TEVAR of a descending thoracic aortic aneurysm.

[Which cut-off value of high sensitivity C- reactive protein is more valuable for determining long- term prognosis in patients with acute coronary syndrome?]. / Akut koroner sendromlu hastalarda yüksek duyarli C-reaktif proteinin uzun dönem prognozu belirlemede hangi kestirim degeri daha degerlidir?

OBJECTIVE: The aim of this study to investigate prognostic efficacy of high sensitivity C-reactive protein (hs-CRP) in patients with acute coronary syndrome (ACS) and to identify the most valuable cut-off value of hs-CRP for determining long term prognosis. METHODS: A total of 240 ACS patients presenting within 6 h after the onset of chest pain were included to the study. Admission levels of hs-CRP were analyzed. Patients were followed for 1 year. Primary end-point of the study was new coronary event (NCE), defined as the combination of cardiac death, nonfatal myocardial infarction and recurrent rest angina. Risk factors for NCE were determined by logistic regression analysis. ROC-curve analysis was used to identify cut-off values of the risk factors. The prognostic efficacy of the cut-off value of hs-CRP was compared to other values determined from other studies. Kaplan Meier and log rank tests were used in survival analyses. Factors determining event-free survival were investigated by Cox regression analysis. RESULTS: During the follow-up period, 65 NCEs occurred. In multivariate analysis, hs-CRP was strongly associated with the occurrence of NCE (OR=4.79, 95% CI=2.10-10.44, p<0.001). Cut-off value of hs-CRP for NCE was 1.1 mg/dl (AUC=0.68, 95% CI=0.62-0.74, p<0.001). Compared to other values of different studies, hs-CRP>1.1 mg/dl had the optimal positive and negative predictive values. In the Cox regression analysis, hs-CRP was emerged as the most important parameter for determining event-free survival (RR=3.44, 95% CI=1.91-6.21, p<0.001). CONCLUSION: Admission levels of hs-CRP were emerged as the most important parameter for prognosis and the cut-off value of hs-CRP for predicting NCE was found as 1.1 mg/dl in this cohort of the study population. Further studies are required to confirm the most risky cut off value of hs-CRP for predicting long term prognosis among ACS patients and in general population.

Protective effects of clopidogrel on oxidant damage in a rat model of acute ischemia.

Reperfusion injury is a consequence of inadequate energy supply and acidosis in ischemic tissues and a chain of events triggered by oxygen-derived free radicals released in response to exposure of oxygen. In this study, we aimed to assess the effects of clopidogrel, an antithrombotic agent, on experimental ischemia-reperfusion model in rats. The ischemia was performed by blockade of the circulation of right lower extremity at trochanter major level for 6 hours. Then, the extremity was reperfused for 4 hours. Another group of rats pretreated with clopidogrel (0.2 mg/kg/day) for 10 days prior to ischemia-reperfusion. After the reperfusion period, all rats were anesthetized with ketamine. Blood and tissue samples from the gastrocnemius muscle, liver and lungs were taken for the measurement of malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD) activity. The results revealed that clopidogrel prevented the increase in MDA level and the decrease in GSH level and SOD activity caused by ischemia-reperfusion both in tissue samples and plasma. These findings suggest that clopidogrel is beneficial in prevention of ischemia-reperfusion injury probably via its effects on inflammatory cells, platelets, and endothelial cells.