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There have been significant advances in the technique and application of endovascular repair of thoracic aortic pathology over the past 20 years. The Stanford type A and the complicated type B dissection patients require urgent/emergent intervention. In the last decade, earlier intervention has been pursued for uncomplicated type B dissections. The INvestigation of STent-grafts in Aortic Dissection (INSTEAD) Long term (XL) study showed that there was significant crossover from medical management to Thoracic EndoVascular Aortic Repair (TEVAR) at year 3, suggesting TEVAR might benefit this population long term. Today, the application of TEVAR, which was initially designed to address aneurysmal disease, has become a standard and Food and Drug Administrative (FDA) approved management option in dissections. Currently there are four FDA approved TEVAR devices in the United States for the treatment of the thoracic dissections, namely Gore, Medtronic, Cook, and Terumo. With each iteration, there are increased opportunities for customization and widespread use in individualized patient’s pathology. As the technology improves and the feasibility of the grafts expands, the complication rates continue to decline cementing the safety and efficacy of these thoracic aortic grafts. Two rare but catastrophic complications in spinal ischemia and retrograde Stanford type A aortic dissection are further discussed. With the success of the TEVAR, a new frontier of hybrid aortic surgery has developed. The debranching of the aortic arch vessels in order to advance the TEVAR proximal landing zones has been aggressively pursued. With the widespread growth of TEVAR technology it is apparent that complex aortic pathology can be safely repaired endovascularly. Article Details

Objectives Patients infected with HIV have an increased propensity for developing thoracic empyemas secondary to their susceptibility to polymicrobial pulmonary infections. We performed an assessment of the clinical outcomes of HIV patients undergoing surgical treatment of thoracic empyemas and reviewed the microbiology of these infections. Methods We completed a retrospective analysis of the patients who had been referred for surgical treatment of thoracic empyemas over an 11-year period, ending in 2002. The patients were treated at a major metropolitan medical teaching facility that cares for a substantial number of HIV-positive patients. Results Twenty-one HIV-infected patients underwent surgical treatment of thoracic empyemas. There were no immediate deaths. Sixty-two percent of the patients had CD4 counts of Conclusions Surgeons can obtain satisfactory operative outcomes when treating thoracic empyemas in HIV patients; however, the treatment strategy should be individualized. Patients with CD4 counts of

Purulent pericarditis with esophagopericardial fistula secondary to metastatic colon disease is uncommon. Current reports in the literature describe successful palliation via endoluminal esophageal stent insertion. We present our management strategy for a difficult case in which (complete) esophageal occlusion by tumor burden precluded endoscopic passage of the guide wire required to successfully perform such a procedure. Simple tube pericardiostomy is presented as an alternative procedure that produced a satisfactory outcome. This surgical procedure is an appropriate palliative alternative when an endoscopic procedure is not feasible, and is much less invasive than the surgical palliative procedures reported in the literature.

We investigated the potential of dietary saturated fatty acids to decrease endotoxemia and suppress expression of cyclooxygenase 2 (Cox-2) and tumor necrosis factor alpha (TNF-alpha) in established alcohol-induced liver injury. Six groups (five rats/group) of male Wistar rats were studied. Rats in group 1 were fed a fish oil-ethanol diet for 6 weeks. Rats in groups 2, 3, and 4 were fed fish oil and ethanol for 6 weeks. Ethanol administration was stopped at this time, and the rats were switched to isocaloric diets containing dextrose with fish oil (group 2), palm oil (group 3), or medium-chain triglycerides (group 4) as the source of fat for an additional 2 weeks. Rats in groups 5 and 6 were fed fish oil-ethanol and fish oil-dextrose, respectively, for 8 weeks. Liver samples were analyzed for histopathology, lipid peroxidation, and levels of messenger RNA (mRNA) for Cox-2 and TNF-alpha. Concentrations of endotoxin were determined in plasma. The most severe inflammation and fibrosis were detected in groups 1 and 5, as were the highest levels of endotoxin, lipid peroxidation, and mRNA for Cox-2 and TNF-alpha. After ethanol was discontinued, there was minimal histological improvement in group 2 but near normalization of the histology, including regression of fibrosis, in groups 3 and 4. Histological improvement was associated with decreased levels of endotoxin, lipid peroxidation, and reduced expression of Cox-2 and TNF-alpha. The data indicate that a diet enriched in saturated fatty acids (groups 3 and 4) effectively reverses alcohol-induced liver injury, including fibrosis. The therapeutic effects of saturated fatty acids may be explained, at least in part, by reduced endotoxemia and lipid peroxidation, which in turn result in decreased levels of TNF-alpha and Cox-2.

BACKGROUND & AIMS: Thromboxane levels correlate with severity of liver injury in rats given alcohol. The aim of this study was to evaluate the effect of thromboxane inhibitors on pathological changes in experimental alcoholic liver disease. METHODS: Male Wistar rats were given a liquid diet and ethanol intragastrically for 1 month. The thromboxane inhibitors tested were a thromboxane receptor antagonist (TXRA) and a thromboxane synthase inhibitor (TXSI). Pathological changes, liver and plasma thromboxane levels, 6-ketoprostaglandin F1 alpha levels, lipid peroxidation, and messenger RNA levels for tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF) beta were evaluated. RESULTS: Treatment with thromboxane inhibitors prevented necrosis and inflammation. In the TXSI-treated group, fatty liver was also decreased. Ethanol administration led to a 3-4-fold increase in liver thromboxane levels; a reduction in thromboxane levels and lipid peroxidation was seen in the TXSI group. In all treatment groups, TNF-alpha and TGF-beta messenger RNA levels were decreased. CONCLUSIONS: The prevention of necroinflammatory changes in thromboxane- treated groups is related to a decrease in TNF-alpha levels. Inhibition of TGF-beta expression may also prevent fibrosis in ethanol-treated rats. (Gastroenterology 1997 Jan;112(1):200-7)

We used the intragastric feeding rat model for alcoholic liver disease to evaluate the relationship between morphologic and functional indicators of endothelial cell dysfunction.Twelve groups of rats (4-5 rats/group) were fed the following diets: saturated fat and dextrose (SD), saturated fat and ethanol (SE), corn oil and dextrose (CD), corn oil and ethanol (CE). Four of the 12 groups were sacrificed at 2 weeks, four groups at 4 weeks and remaining four groups at 8 weeks. The following were evaluated at sacrifice: pathologic changes in the liver, endothelial cell proliferation using a monoclonal antibody to proliferating cell nuclear antigen, factor VIII-related antigen staining of endothelial cells in liver, plasma endotoxin, hyaluronan and prostaglandin F2 alpha.Only CE rats at 4 and 8 weeks showed pathologic changes. The plasma levels of HA were significantly higher in the CE groups compared to the other groups at all time intervals studied. In the CE rats, a significant correlation was obtained between plasma endotoxin and hyaluronan (r = 0.84, p0.01). Endotoxin levels also correlated significantly with the number of G1/S arrested hepatic sinusoidal endothelial cell (r = 0.61, p0.05). A role for prostaglandin F2 alpha, in causing endothelial dysfunction, was suggested by a significant correlation between plasma hyaluronan and prostaglandin F2 alpha levels (r = 0.95, p0.01). Positive factor VIII related antigen staining of hepatic endothelial cells was seen in rats with high plasma hyaluronan levels.We propose that endotoxin, mediating part of its effect through prostaglandin F2 alpha, plays a role in hepatic sinusoidal endothelial cell G1/S arrest. This morphologic change, associated with increased plasma hyaluronan levels, precedes capillarization in this model of alcoholic liver injury.

We investigated the association between vitamin E, lipid peroxidation and eicosanoid production in experimental alcoholic liver injury. We used the intragastric feeding rat model in which animals were fed corn oil and ethanol (CO+E) and corn oil and dextrose (CO+D) for 2 and 4 week periods. At sacrifice, we measured plasma levels of alpha-tocopherol, 8-isoprostane, thromboxane B2 (TXB2) and 6-ketoprostaglandin F1 alpha (6-KetoPGF1 alpha). Animals fed CO+E had significantly lower concentrations of alpha-tocopherol and higher concentrations of 8 isoprostane at both 2 and 4 weeks. a significant inverse correlation was seen between alpha-tocopherol concentrations and the TXB2: PGF1 alpha ratio (r = 0.72, p0.01). A positive correlation was seen between the TXB2: PGF1 alpha ratio and 8 isoprostane levels (r = 0.84, p0.001). These results suggest that vitamin E depletion and enhanced lipid peroxidation may affect eicosanoid metabolism in experimental alcoholic liver disease in such a way so as to increase the thromboxane to prostacyclin ration.

We used the intragastric feeding rat model for alcohol liver disease to investigate the relationship between endothelin and pathologic liver injury. Rats were fed the following diets for periods of 1, 2 and 4 weeks: corn oil plus ethanol (CE), corn oil plus dextrose (CD) and saturated fat plus ethanol (SE). Plasma endothelin levels were significantly higher in the CE group compared to the other groups at all time periods studied. The CE animals, also, developed pathologic liver injury which is in contrast to the SE and CD animals which showed no pathologic changes. We propose that endothelin, because of its powerful vasoconstrictive effects, leads to a reduction in hepatic blood flow which is important in the pathogenesis of alcoholic liver disease.

Autoimmune serological testing is a useful aid for identifying a paraneoplastic basis for sporadic motor neuron disease. A 67-year-old woman with ovarian carcinoma presented with progressive weakness. Neurological examination was suggestive of motor neuron disease with signs of upper motor neuron disorder. Electromyography revealed severe motor neuronopathy of the upper extremities. Characteristic type 1 Purkinje cell antibodies (anti-Yo antibody) was detected in the serum diluted at 1:61,400.

Patients infected with HIV have an increased propensity for developing thoracic empyemas secondary to their susceptibility to polymicrobial pulmonary infections. We performed an assessment of the clinical outcomes of HIV patients undergoing surgical treatment of thoracic empyemas and reviewed the microbiology of these infections.We completed a retrospective analysis of the patients who had been referred for surgical treatment of thoracic empyemas over an 11-year period, ending in 2002. The patients were treated at a major metropolitan medical teaching facility that cares for a substantial number of HIV-positive patients.Twenty-one HIV-infected patients underwent surgical treatment of thoracic empyemas. There were no immediate deaths. Sixty-two percent of the patients had CD4 counts of200 cells/microL. Eight patients had postoperative complications. Six of the patients with complications had CD4 counts of200 cells/microL. Patients with lower CD4 counts were at risk for mycobacterial and fungal infections. Additionally, they often had complex empyemas that were not favorable for treatment by video-assisted thoracic surgery. Therefore, these patients often required surgery with lung resection, which necessitated longer periods of postoperative chest tube drainage.Surgeons can obtain satisfactory operative outcomes when treating thoracic empyemas in HIV patients; however, the treatment strategy should be individualized. Patients with CD4 counts of200 cells/microL more commonly have complex empyemas that require surgery with open decortication and drainage. Although these patients have a higher incidence of postoperative complications, we think that HIV patients with thoracic empyemas can be safely and effectively treated with surgical techniques.

The Ross procedure is an ideal aortic valve replacement for the teenage patient because the pulmonary autograft is durable, is nonthrombogenic, has excellent hemodynamics, and grows. Since 1992, our center has performed 194 Ross procedures, and 53 of these were in teenagers (10 to 21 years of age). In this group, there have been no perioperative deaths, hospital length of stay was 4 days, and re-operation for autograft failure was only 2% at mean follow-up of 69 months. All patients are in NYHA heart failure class I. Because of its proven efficacy, the Ross operation is our preferred aortic valve replacement for the teenage patient.

Gastrointestinal stromal tumor (GIST) is a rare, but potentially aggressive tumor. We present an asymptomatic 64-year-old man with an incidental 9-cm GIST that arose in the posterior mediastinum. Wide surgical excision was performed with rotation of an intercostal muscle flap to buttress a surgically created esophageal wall defect. The patient is now free of disease 26 months postoperative. This tumor is defined by the carcinogenic over-expression of KIT-protein, a tyrosine kinase receptor. Accurate diagnosis of gastrointestinal stromal tumor is imperative, as specific medical therapy is now available for potential control of recurrent or metastatic disease.

Based on studies that show a role for the low-density lipoprotein (LDL)-receptor in arachidonic acid delivery and eicosanoid synthesis in macrophages, the present study investigated the effect of cholesterol supplementation on pathological changes and thromboxane (TX) synthesis in alcoholic liver injury. Male Wistar rats were intragastrically fed ethanol with either corn oil or fish oil for 1 month. Control rats received isocaloric amounts of dextrose instead of ethanol. An additional group of rats fed either ethanol or dextrose with fish oil or corn oil were supplemented with 1% cholesterol. At the time of killing, all rats had the following evaluated: liver histopathology, lipid peroxidation, liver and plasma thromboxane levels, plasma endotoxin and messenger RNA (mRNA) levels of LDL-receptor, tumor necrosis factor alpha (TNF-alpha), cyclooxygenase (Cox)-1 and -2, and transforming growth factor beta (TGF-beta). Rats fed ethanol with either fish oil or corn oil developed fatty liver, necrosis, inflammation, and central vein collagen deposition. Cholesterol supplementation enhanced the degree of fibrosis but prevented necrosis and inflammation. These alterations in pathological changes by cholesterol were accompanied by absent TNF-alpha and Cox-2 mRNAs, decreased thromboxane levels, decreased lipid peroxidation, and increased TGF-beta mRNA. Cholesterol enrichment of the diet thus decreases proinflammatory components, but enhances fibrosis in ethanol-fed rats. (Hepatology 1997 Jul;26(1):90-7)

measurements of lipid peroxidation, tumor necrosis factor (TNF)-a, COX-1 and COX-2 messenger RNA that stimulate expression of COX-2, we hypothesized (mRNA), endotoxin, and liver and plasma thromboxane that COX-2 would be induced in experimental ALD. In were performed. Results: Increased expression of COX- the rat intragastric feeding model of ALD, we and others 2 mRNA was detected in the livers of rats showing have shown that an inverse relationship exists between necroinflammatory changes. The Kupffer cell was the the state of saturation of lipids in diet and the severity cell primarily responsible for the increase in COX-2 of alcohol-induced liver injury. 13-17 Thus, rats fed etha- mRNA level. Increased expression of COX-2 was associ- nol and diets enriched in saturated fatty acids 14 are pro- ated with increased levels of endotoxin, TNF-a mRNA, tected from liver injury, whereas diets enriched in poly- lipid peroxidation, and synthesis of thromboxane. COX- unsaturated fatty acids 15-17 promote alcoholic liver 1 mRNA was decreased in Kupffer cells in rats with the injury. Thus, the rat intragastric feeding model is useful most severe liver injury. Conclusions: Up-regulation of to elucidate the pathogenesis of ALD. In the current COX-2 in alcoholic liver injury occurred in the presence study, we used this model of liver injury to study the of proinflammatory stimuli and resulted in increased synthesis of inflammatory and vasoactive eicosanoids. relationship between liver pathology and COX expres- Down-regulation of COX-1 may result in decreased syn- sion and to attempt to identify the factors responsible thesis of cytoprotective eicosanoids and additionally for induction of COX-2 in ALD. exacerbate liver injury. Our results show that necrosis and inflammation in ALD are associated with increased expression of COX- 2 and higher levels of plasma endotoxin, liver TNF-a

We used the intragastric feeding rat model for alcoholic liver disease to investigate the relationship between prostacyclin and liver injury. Rats were fed the following diets for periods ranging from 1 to 8 weeks: corn oil plus ethanol (CO+E), corn oil plus dextrose (CO+D), saturated fat plus ethanol (SF+E) and saturated fat plus dextrose (SF+D). Prostacyclin production (assessed by 6-ketoprostaglandin F1 alpha) by liver non-parenchymal cells decreased steadily over the 8 week period in animals fed CO+E (liver injury present) whereas in animals fed SF+E (no liver injury) there was no change in prostacyclin production. Plasma levels of 6-ketoprostaglandin F1 alpha were also significantly lower in the CO+E group compared to the other groups studied. We propose that decreased prostacyclin production by liver non-parenchymal cells may contribute to the hepatotoxic effect of ethanol.