Syphilitic aneurysm.

Syphilis was once the most common cause of aortic aneurysm. For the last 60 years syphilis has been well controlled in the UK population. However, we present the recent case of a 52-year-old female black South African immigrant who was found to have a syphilitic aneurysm.

Norwood-type operation with adjustable systemic-pulmonary shunt using hemostatic clip.

The postoperative course of a patient with hypoplastic left heart syndrome after a first-stage Norwood operation is governed to a large extent by the balance between the systemic and pulmonary circulations. Here we describe a simple and convenient technique for establishing an optimally sized systemic-pulmonary shunt by the application of a hemostatic clip. The method has been used in 6 patients.

A three year experience with the toronto stentless porcine valve.

In the three year period from March 1994, 112 Toronto Stentless Porcine Valves (SPV TM) were implanted in the Western Infirmary, Glasgow. There were 55 males and 57 females aged between 45 and 86 years (mean 70.9 +/- 7.2 yrs). The mean preoperative aortic gradient was 89 +/- 27 mmHg. Fifty-three patients (47%) had an isolated first time aortic valve replacement. Myocardial revascularisation was carried out in 51 patients (46%) with a mean of 1.7 +/- 0.9 coronary bypass grafts per patient. Six patients (5.3%) had associated mitral valve procedures and six patients (5.3%) had previous open heart surgery. Four patients (3.6%) had a minimally invasive procedure. There was one perioperative death (0.9%) which was not valve related. Of the 111 survivors there were three late deaths (cerebrovascular accident at two months and congestive cardiac failure at two months and four months). Two patients developed prosthetic valve endocarditis at three and five months respectively, one requiring a repair of a periprosthetic leak. To compare the effects of stented and stentless prostheses on early haemodynamic function and late left ventricular mass regression, a prospective randomized clinical trial was conducted. Following valve sizing, 20 patients were randomized to receive a Carpentier-Edwards SAV stented bioprosthesis (mean annular size-25.3 mm, mean valve size-23 mm) of which eight also had bypass grafts. Twenty patients were randomized to receive a Toronto SPV (mean annular size-25.5 mm, mean valve size-26 mm) of which nine had bypass grafts. The stentless valve group had a longer ischaemic time (77.9 +/- 20.9 min v 60.9 +/- 21.9 min) and bypass time (101.7 +/- 27.1 min v 82.9 +/- 20.2 min). Using continuous cardiac output monitoring, no statistically significant differences were found in early haemodynamic indices although the stentless group required less inotropes and had a shorter ventilation time (16.1 +/- 4.2 hrs v 55.2 +/- 104.9 hrs) and intensive care stay (1.1 +/- 0.2 days v 4.6 +/- 8.3 days). Mean and peak aortic gradients one week postoperatively were lower in the stentless group (5.6 +/- 3 mmHg v 8.9 +/- 2.3 mmHg and 12.5 +/- 7.8 mmHg v 24.4 +/- 8.8 mmHg respectively). Magnetic resonance imaging at six months showed a 15% reduction in the end systolic muscle mass index in the stented group but a greater reduction of 29% in the stentless group. This study shows that despite requiring a more demanding technique of insertion, aortic valve replacement with the Toronto stentless porcine valve can produce satisfactory early clinical results.

Management of nasopharyngeal and oropharyngeal stenosis in children.

Nasopharyngeal stenosis and oropharyngeal stenosis are rare and challenging problems in the pediatric population. The most common etiology is currently the surgical trauma associated with adenotonsillectomy. Stenosis can vary from a thin band to a complete obstructing cicatrix. Presenting symptoms range from mild hyponasal speech to severe airway obstruction. We present a series of eight children with varying degrees of stenosis and associated symptoms. Choice of treatment varied with the severity of disease. In our series, successful interventions included triamcinolone acetonide injection, lysis of adhesions, rotational and advancement mucosal flaps, and jejunal free flap. Preoperative evaluation and individualized surgical repair are essential for successful treatment.

Hepatocyte growth factor levels in liver and serum increase during chemical hepatocarcinogenesis.

Hepatocyte growth factor (HGF) is mitogenic for hepatocytes and some tumor cell lines. Elevations in plasma HGF levels have been detected in patients with hepatocellular carcinoma (HCC), and it is possible that HGF is involved in the promotion and/or progression of tumor growth. We measured serum and liver tissue HGF levels during chemically induced hepatocarcinogenesis. Wistar rats were given diethylnitrosamine (DEN) in drinking water for 10 weeks with controls receiving drinking water only. Animals were killed at 10, 16, and 19 weeks. Liver HGF levels were determined from immunoblotted protein by scanning densitometry, and serum HGF levels were measured by sandwich enzyme-linked immunosorbent assay (ELISA). HGF was also immunolocalized in fixed liver tissue sections. In DEN-treated animals, at 10 weeks, there was necroinflammation but no dysplasia. Serum HGF was elevated compared with controls (P < .001) but there was no increase in liver HGF. At 16 weeks, there was liver cell dysplasia with minimal necroinflammation; serum and tissue HGF levels were both significantly elevated above controls. At 19 weeks, hepatocellular carcinomas (HCC) were present in five of six DEN-treated animals; liver HGF (P < .05) and serum HGF (P < .001) were both elevated compared with controls. HGF was localized in basement membranes around bile ducts and vessels and some perisinusoidal cells. Increased HGF immunolabeling was observed at 16 and 19 weeks, but dysplastic hepatocytes and tumor cells were HGF-negative. HGF may serve as a growth promoter at early stages during liver tumor development acting through possibly endocrine and paracrine pathways. Recent observations have described HGF as being mitoinhibitory for HCC cell lines; it is possible therefore that the continued up-regulation of HGF in the latter stages of our DEN model may inhibit tumor cell growth, and thus represent a form of antitumor host response.