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The aim of this study was to audit the management of hyperlipidaemia in a cohort of 206 consecutive patients, with known or suspected coronary artery disease, referred for diagnostic coronary angiography. The association of lipid subfraction values with the presence and extent of coronary artery disease was explored to identify the indices of greatest potential value to the hospital cardiologist, in the management of secondary prevention. Patients were questioned about previous lipid tests performed, advice received and treatment prescribed. Referral letters and hospital notes were reviewed to identify documentation of lipid results and treatment strategies. De novo fasting lipid estimations were obtained on 205 subjects at the time of catheterization. In only 46/206 (22%) cases was some form of lipid result recorded in the existing hospital notes or referral documentation. No patient was aware of the levels of the high or low density lipoprotein cholesterol subfractions (HDL, LDL) nor were these specifically recorded, or the subject of clinical comment, in any of the referral documentation. Patients who knew their total cholesterol (in mmol.1-1) result either as a value or as a "high' or "normal' categorization proved accurate witnesses. In keeping with other angiographic studies, we found that low values of HDL and high TC/HDL ratios were significantly associated with both disease presence and extent. Total cholesterol, calculated LDL and triglyceride levels had no such association. In the group as a whole and despite current therapy, 169/206 (82%) patients had a total cholesterol > 5.2 and 163/206 (79%) a TC/HDL ratio > 5. Only 22 (11%) patients were on drug therapy with a further 43 (21%) practising dietary modification. In the vast majority of subjects receiving some form of lipid intervention, target lipid levels had not been achieved. This study identifies the need for more intensive management of hyperlipidaemia in patients with coronary artery disease. Knowledge of HDL levels may be of value in guiding lipid secondary prevention management in the patient population evaluated at an angiographic centre.

Background: Restenosis of arteries or bypass grafts after vascular reconstruction is a common clinical entity that significantly limits long-term patency. This process, termed intimal hyperplasia (IH), is characterized by smooth muscle cell proliferation in the intima and subsequent accumulation of intercellular matrix. This study was designed to test the hypothesis that endothelial cell (EC) seeding of acutely injured arteries accelerates reendothelialization of the flow surface and limits the development of IH., Methods: ECs were harvested from jugular veins of New Zealand white rabbits (n = 13) and were amplified in tissue culture. Each animal subsequently underwent bilateral balloon catheter injury of the iliofemoral arteries; one side was immediately seeded with cultured autologous ECs at supraconfluent density, whereas the contralateral vessel served as a nonseeded control. Animals were killed 33 +/- 5 days after balloon injury. Intimal thickening was quantitated on histologic sections of vessels (three sections per vessel, total of 60 sections) and percent endothelialization was assessed by SEM; measurements were obtained by use of computer-aided morphometry performed by a blinded observer. Data were analyzed by use of a paired t test for comparison between seeded and control vessels., Results: Seeded vessels exhibited a greater degree of reendothelialization (93.9% +/- 7.6% of the surface) than their unseeded counterparts (65.1% +/- 22.5%, p < 0.01). Intimal cross-sectional area and the ratio of intimal area to medial area were not significantly different between seeded and control vessels (intima: 0.32 +/- 0.19 vs 0.37 +/- 0.11 mm2, p = 0.28; intimal area to medial area ratio: 0.84 +/- 0.35 vs 1.02 +/- 0.2, p = 0.24)., Conclusions: We conclude that seeding with autologous venous ECs accelerated restoration of the endothelial monolayer but failed to attenuate IH in balloon-injured rabbit arteries. Further studies are necessary to determine the functional properties of seeded endothelium and to examine the effect of EC seeding on intimal thickening in other clinically relevant models.

A 12-question survey designed to examine venepuncture techniques and instruction and uptake of hepatitis B vaccination was completed by 172 of the 275 medical students to whom it was distributed (a response rate of 62.5%). Seventy-five injuries were reported, at an average of 0.3 per student per year. Of the respondents, 63% resheathed needles after use, a practice frequently cited as a cause of needlestick injury. However, in this sample resheathing was not significantly associated with a higher or lower injury rate (chi 2 = 2.07, P > 0.1). Of the respondents from the most recent intake, only 20 out of 57 had completed a course of hepatitis B vaccinations prior to the commencement of venepuncture duties. There was almost universal ignorance concerning the correct course of action following 'sharps' injury. Recommendations are made concerning hepatitis B vaccination and teaching strategies for medical students.

During ureterolysis in a patient with "idiopathic retroperitoneal fibrosis", fresh samples of peri-ureteric and peri-aortic tissue were obtained. An abdominal CT scan confirmed the peri-aortic distribution of the inflammation associated with advanced abdominal aortic atherosclerosis. Histology confirmed the presence of fibrosis and a variable chronic inflammatory cell infiltrate. Monoclonal antibodies were used to identify the inflammatory cells. B and T lymphocytes were present with the majority of T lymphocytes of the T helper phenotype. The majority of lymphocytes and macrophages and most vascular endothelial cells were HLA-DR positive. Ki67 and BerH2 staining was found in B cells and T helper cells, indicating that these cells were proliferating and activated. These findings compare with the characterisation of inflammatory cells associated with "inflammatory aneurysms" and with the inflammatory cells present in the spectrum of inflammation seen as a complication of advanced atherosclerosis--conditions known as "chronic peri-aortitis". It is suggested that our findings support the view that idiopathic retroperitoneal fibrosis represents clinical chronic peri-aortitis seen in an undilated aorta.