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BackgroundOnset of postoperative atrial fibrillation (POAF) is a common and costly complication of heart surgery despite major improvements in surgical technique and quality of patient care. The etiology of POAF, and the ability of clinicians to identify and therapeutically target high‐risk patients, remains elusive.Methods and ResultsMyocardial tissue dissected from right atrial appendage (RAA) was obtained from 244 patients undergoing cardiac surgery. Reactive oxygen species (ROS) generation from multiple sources was assessed in this tissue, along with total glutathione (GSHt) and its related enzymes GSH‐peroxidase (GPx) and GSH‐reductase (GR). Monoamine oxidase (MAO) and NADPH oxidase were observed to generate ROS at rates 10‐fold greater than intact, coupled mitochondria. POAF risk was significantly associated with MAO activity (Quartile 1 [Q1]: adjusted relative risk [ARR]=1.0; Q2: ARR=1.8, 95% confidence interval [CI]=0.84 to 4.0; Q3: ARR=2.1, 95% CI=0.99 to 4.3; Q4: ARR=3.8, 95% CI=1.9 to 7.5; adjusted Ptrend=0.009). In contrast, myocardial GSHt was inversely associated with POAF (Quartile 1 [Q1]: adjusted relative risk [ARR]=1.0; Q2: ARR=0.93, 95% confidence interval [CI]=0.60 to 1.4; Q3: ARR=0.62, 95% CI=0.36 to 1.1; Q4: ARR=0.56, 95% CI=0.34 to 0.93; adjusted Ptrend=0.014). GPx also was significantly associated with POAF; however, a linear trend for risk was not observed across increasing levels of the enzyme. GR was not associated with POAF risk.ConclusionsOur results show that MAO is an important determinant of redox balance in human atrial myocardium, and that this enzyme, in addition to GSHt and GPx, is associated with an increased risk for POAF. Further investigation is needed to validate MAO as a predictive biomarker for POAF, and to explore this enzyme's potential role in arrhythmogenesis.

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Brain death often results in a series of hemodynamic alterations that complicate the treatment of potential organ donors before transplantation. The deterioration of myocardial performance after brain death has been described; however, the pathophysiologic process of the myocardial dysfunction that occurs after brain death has not been elucidated. This study was designed to analyze the function of the myocardial beta-adrenergic receptor and the development of left ventricular dysfunction in a porcine model of experimental brain death. Analysis of the beta-receptor included determination of receptor density and adenylate cyclase activity after stimulation independently at the receptor protein, the G protein, and the adenylate cyclase moiety. Myocardial beta-receptor density did not change after the induction of brain death. A decrease in stimulated adenylate cyclase activity was observed within the first hour after brain death at the level of the beta-receptor, the G protein, and the adenylate cyclase moiety, which suggests the occurrence of rapid desensitization of beta-receptor function. Significant deterioration of myocardial performance also occurred within the first hour after brain death, represented by a decrease in preload-recruitable stroke work compared with the baseline value. The deterioration of myocardial performance after brain death correlates temporally with desensitization of the myocardial beta-receptor signal transduction system. The mechanism of impairment appears to be localized to the adenylate cyclase moiety itself.

P ulmonary artery pseudoaneurysms after traumatic injury are a very rare occurrence; only 14 cases have been reported in the literature. Blunt traumatic pulmonary artery pseudoaneurysms constitute a small number of these cases; only three cases have been reported to date. In every reported case of traumatic pulmonary artery pseudoaneurysm since 1920, the pseudoaneurysm was repaired operatively using local resection (aneurysectomy), ligation of vessels, lobectomy, or embolization. 1,2 We report a case of blunt traumatic main pulmonary artery pseudoaneurysm detected on initial computed tomography (CT) that was treated nonoperatively. To our knowledge, this is the first reported pulmonary artery pseudoaneurysm detected immediately on trauma assessment and also the first reported patient with traumatic pulmonary artery pseudoaneurysm treated nonoperatively that survived. CASE REPORTA 57-year-old man who was involved in a head-on motor vehicle collision as the unrestrained passenger presented awake and alert with multiple facial lacerations and unknown loss of consciousness. The patient denied any known drug allergies and took no medications. Medical history was significant for hypertension and diabetes mellitus and there was no surgical history. The patient did admit to regular alcohol and marijuana use but denied any significant family medical history. The primary survey was unremarkable. The airway was patent, Glasgow Coma Scale score was 15, and the patient seemed in no apparent distress. No additional injuries were noted and motor and sensory exams were normal. The usual resuscitation maneuvers were employed.Routine pelvis and chest x-rays were obtained. The chest film revealed minimal widening of the superior mediastinum (measured as 10 cm of 38.5 cm chest width) and tortuosity of the thoracic aorta. The pelvic film was negative. The patient had helical multidetector CT imaging without contrast of the head, face, and c-spine. The head CT was negative for intracranial injury, whereas the CT scan of the face showed minimal medial displacement of the left zygoma. In addition, helical multidetector CT imaging of the chest with intravenous contrast was obtained in addition to the usual abdomen/ pelvis CT with oral and intravenous contrast. The chest CT was added because of widened mediastinum and loss of aortic knob. The chest CT revealed a lobulated contour of the main pulmonary artery with an 18-mm probable pseudoaneurysm along the left superior margin of the main pulmonary artery (Fig. 1). A small amount of mediastinal hematoma was seen although the aorta and great vessels of the arch were intact. There was no evidence of pericardial effusion, pleural effusion, or pneumothorax. The abdomen/pelvis CT scan revealed minimal free fluid in the left upper quadrant inferior to the spleen and in the left paracolic gutter with the absence of identifiable solid organ injury.The patient was then taken for pulmonary angiography, which also revealed a lobulated appearance with a focal contour abnormality along the left anterio...