Late manifestation of coarctation of the aorta after arterial switch operation for D-transposition of the great arteries with intact ventricular septum.

We describe an infant with D-transposition of the great arteries with an intact ventricular septum who developed coarctation of the aorta 13 days after arterial switch operation. A mildly hypoplastic aortic isthmus was present on echocardiogram at the time of the arterial switch operation, but there was no echocardiographic or clinical evidence of coarctation of the aorta.

Factors affecting outcome in proximal abdominal aortic aneurysm repair.

Sixty-five consecutive patients undergoing nonemergent repair of an abdominal aortic aneurysm (AAA) originating above the visceral and/or renal arteries were studied to determine operative results and identify factors influencing outcome of proximal AAA repair. Factors associated with postoperative morbidity were analyzed using multivariate analysis. There were no postoperative deaths, paraplegia/paraparesis, or symptomatic visceral ischemia. Proximal AAA repair can be accomplished with acceptable mortality. If renal artery bypass or reimplantation is anticipated, cold renal perfusion may protect against renal dysfunction. Postoperative pulmonary dysfunction can be reduced by avoiding radial division of the diaphragm.

Analysis of coagulation changes associated with supraceliac aortic crossclamping using thromboelastography.

INTRODUCTION: The etiology of the coagulation changes seen with supraceliac (SC) aortic crossclamping (AXC) remains controversial; both primary fibrinolysis and clotting factor consumption have been implicated. The cause of these changes was investigated with thromboelastography (TEG), a test that measures the viscoelastic properties of thrombus to dynamically assess coagulation and fibrinolysis. METHODS: Eight pigs underwent SC AXC for 30 min; 5 pigs undergoing 30 min of infrarenal (IR) aortic clamping served as controls. Blood was drawn before AXC, before unclamping, and 5 and 60 min after unclamping. Thromboelastography and standard coagulation tests [prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and platelet count] were performed. Measured TEG parameters included fibrinolytic index (a measure of fibrinolysis), r value (a reflection of intrinsic coagulation cascade activity), and the alpha angle and K values (measures of the speed of solid clot formation). Repeated measures ANOVA and t test were used for statistical analysis. RESULTS: There was no difference in the fibrinolytic index at any time point between the two groups. Increased activity of the intrinsic coagulation cascade during SC clamping was reflected by a lower R value just before unclamping (12.6 +/- 3.0 vs 20.0 +/- 3.0, P = 0.048) compared to IR AXC. Decreased speed of solid clot formation was noted 5 min after unclamping in the SC group but not the IR group [as defined by an increased K value (ANOVA, P = 0.010) and a decreased alpha angle value (ANOVA, P = 0.005)]. Fibrinogen levels were lower in the SC than in the IR group 5 (P = 0.013) and 60 min after unclamping (P = 0.02), but PT, PTT, and platelets did not differ between the groups at any time points. CONCLUSIONS: Thirty minutes of SC AXC does not result in fibrinolysis. There is increased clotting activity during SC clamping followed by decreased speed of clot formation and decreased fibrinogen levels after unclamping. These changes are consistent with clotting factor consumption.

Lymphoepithelial cyst in the pancreas: a case report and review of the literature.

BACKGROUND: Lymphoepithelial cysts of the pancreas constitute a rare clinicopathologic entity. CASE REPORT: We report a case of lymphoepithelial cyst of the pancreas and review the world literature. RESULTS: Lymphoepithelial cysts are true pancreatic cysts lined by squamous epithelium and surrounded by mature lymphoid tissue. The cyst arises typically in middle aged men, and is usually asymptomatic or causes nonspecific abdominal complaints. There is no specific serologic marker for this entity. None of its radiologic characteristics can help differentiate it from other cystic lesions of the pancreas. Fine-needle aspiration cytology may be able to suggest its benign nature and identify it as a true cyst of the pancreas. The outcome after surgical excision is uniformly good with good symptom control and no recurrences. RECOMMENDATIONS: In the symptomatic patient or the asymptomatic patient with acceptable surgical risk a simple cyst excision should be performed after verification of the diagnosis with frozen section. In the asymptomatic patient with a high surgical risk, in whom fine-needle aspiration suggests the diagnosis of a lymphoepithelial cyst, observation of the lesion is recommended. When simple cyst excision is technically not possible, extensive resections/reconstructions should be avoided and drainage/bypass procedures may be considered.

Phosphorus 31 nuclear magnetic resonance spectroscopy suggests a mitochondrial defect in claudicating skeletal muscle.

OBJECTIVE: Decreased oxygen supply is generally accepted as the primary cause of muscle dysfunction in patients with peripheral arterial occlusive disease (PAOD) and intermittent claudication, although reported morphologic changes in the mitochondria of claudicating muscle suggest that impaired energy utilization may also play a role. With the measurement of the phosphate-rich compounds of muscle energy metabolism (adenosinetriphosphate [ATP], adenosinediphosphate [ADP], and phosphocreatine [PCr]) and pH, phosphorus P 31 magnetic resonance spectroscopy ((31)P MRS) provides a unique, noninvasive method to investigate this hypothesis further. METHODS: Calf muscle bioenergetics were studied in 12 men with moderate claudication (ankle-brachial index >/=0.5 and .5, Pearson moment correlation). CONCLUSIONS: Phosphorus 31 MRS provides the first direct evidence of defective energy metabolism in the mitochondria of claudicating calf muscle. This defect appears to be independent of both arterial flow and the severity of occlusive disease in patients with mild to moderate claudication. Coupled with documented ultrastructural and DNA abnormalities in the mitochondria of claudicating skeletal muscle, these data provide evidence for a secondary cause of muscle dysfunction in intermittent claudication.