osttraumatic pulmonary arteriovenous fistula (PAVF) is a rare clinical entity. Most PAVFs are congenital and arise in the setting of hereditary hemorrhagic telangiectasia. Acquired PAVFs are rare and have been reported with metastatic thyroid carcinoma, cirrhosis, pulmonary schistosomiasis, actinomycosis, mitral stenosis, Fanconi's syndrome, and trauma. We present a case of acquired PAVF presenting 1 year after a thoracic stab wound injury with a review of the previously reported cases and a discussion. CASE REPORTThe patient is a 27-year-old male who sustained a single stab wound to the right chest in the para-sternal region. His vital signs were stable on initial evaluation and he reported only shortness of breath. A right chest tube was placed with minimal return of blood. Computed tomography of the chest was performed, which revealed a large unevacuated right hemothorax. A second chest tube was placed, without improvement, based on serial chest films.The patient was taken to the operating room for right posterolateral thoracotomy and evacuation of clotted hemothorax. A large amount of clotted blood was evacuated and active chest wall bleeding was controlled with electrocautery. A pulmonary laceration with an associated 5-cm parenchymal hematoma was identified in the right upper lobe. The segment containing the laceration and the hematoma was resected with a single application of a gastrointestinal anastomosis-stapling device. The patient returned to the operating room the following day for significant, persistent bloody chest tube output and a drop in hematocrit to 18%. A right hemothorax was evacuated, but no site of bleeding was identified. The patient was extubated the following day and discharged to home on postoperative day 6.The patient was lost to follow up during the next several months. He presented to an outlying hospital with complaints of progressive weakness, fatigue, shortness of breath, and several episodes of syncope a year after initial surgery. On physical examination, the patient appeared anxious. Jugular venous distension was not present. The chest was clear to auscultation bilaterally and there was no appreciable murmur heard over the precordium. Resting O 2 saturation on room air was 85% and fell to 75% with exertion. Hemoglobin and hematocrit were 19.0 and 55%, respectively. A small right pleural effusion was noted on chest X-ray film. Computed tomography of the chest showed a mild amount of scarring in the right upper lobe and was negative for pulmonary embolism. A transesophageal echocardiogram was performed with a bubble study and this demonstrated a right to left shunt. A pulmonary angiogram was obtained, which revealed a PAVF with significant flow between the inferior division of the right pulmonary artery and the right superior pulmonary vein ( Figs. 1 and 2). Pulmonary function tests were performed and the FEV 1 (forced expiratory volume in 1 sec) was reported at 2.73 (Ͼ40% predicted value).The interventional radiologist ruled out therapeutic embolization based on the large size ...
The cardioprotective effects of an antilipolytic compound, nicotinic acid, on arrested-reperfused myocardium were investigated in the isolated in situ pig heart preparation. Hearts were preperfused for 15 min in the presence of (5-3H)-glucose and (U-14C)-palmitic acid. Half of the hearts were then perfused with 0.08 mM nicotinic acid for an additional 15-min period, while the remaining control hearts received unmodified perfusion. Arrest was then induced in all animals for 2 h using hypothermic K+ cardioplegia, followed by 60 min of normothermic reperfusion. In control hearts, there were significantly greater levels of long-chain acyl Co-A and acyl carnitine and lower levels of membrane phospholipids than in the nicotinic acid group. While nicotinic acid inhibited beta-oxidation during pre-ischemia and reperfusion, it also prevented the degradation of membrane phospholipids. The net result was a reduction of free fatty acid accumulation during arrest and reperfusion in the nicotinic acid group. Glycolysis, as reflected in 3H2O production, was significantly increased by nicotinic acid administration. In the control heart as compared to the nicotinic acid group, the incorporation of 14C-label from palmitate into triglyceride and cholesterol during arrest was enhanced, while incorporation into phospholipids was depressed. The cardioprotective effects of nicotinic acid were demonstrated by decreased release of creatine kinase and improved coronary blood flow, and cardiac contractility in the reperfused myocardium supplemented with nicotinic acid compared to the control group. These results suggest that nicotinic acid significantly protects the arrested-reperfused myocardium by a) preventing elevation of myocardial fatty acid levels, b) stimulating glycolysis by limiting fatty acid oxidation, c) inhibiting degradation of membrane phospholipids, and d) preventing accumulation of fatty acid metabolites with harmful detergent properties.
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