| 61. |
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| 62. |
- Fransson, Sven-Göran, 1949-, et al.
(författare)
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Vascular injury following cardiac catheterization, coronary angiography, and coronary angioplasty
- 1994
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Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 15:2, s. 232-235
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Tidskriftsartikel (refereegranskat)abstract
- All vascular injuries occurring at this hospital department over a 5-year period (1987-91) as a result of cardiac catheterization, coronary angiography, or coronary angioplasty (PTCA) and requiring transfusion, surgical consultation, or repair, are reviewed. Such complications may occur late and, to detect cases not apparent from the protocol accompanying every examination, a questionnaire was sent to all surgical clinics in the region asking for details of vascular surgical intervention after angiography. The present review of 4879 examinations disclosed 18 patients with 19 vascular injuries (0.39%); four of them were detected by the questionnaire. The types of injury were: pseudoaneurysm (12), thrombembolic episode (4), and excessive bleeding (3). Of the patients with a vascular complication 11 (61%) were receiving anticoagulation treatment, compared to 10% in the whole series; two others suffered from a coagulopathic state. Catheterization was difficult or severe atherosclerosis was present in three, inadvertent mobilization occurred in one, and unintentional puncture distal to the common femoral artery occurred in two patients. With the increasing use of invasive diagnostic and interventional procedures in cardiovascular diseases, knowledge of the type and frequency of possible complications is important, especially of those that may occur late. In the present study anticoagulation, coagulation disorders, and cardiac catheterization combined with brachial puncture and angiography all predisposed to a vascular complication.
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| 63. |
- Friman, Styrbjörn, 1948, et al.
(författare)
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A possible role of ursodeoxycholic acid in liver transplantation.
- 1994
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Ingår i: Scandinavian journal of gastroenterology. Supplement. - 0085-5928. ; 204, s. 62-4
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Forskningsöversikt (refereegranskat)abstract
- There are many different causes of graft dysfunction and cholestasis after liver transplantation. These include non-primary function, preservation and reperfusion injury, acute rejection, artery thrombosis, drug toxicity, bile leakage, and bile duct stenosis. Medication with ursodeoxycholic acid (UDCA) has beneficial effects in different cholestatic conditions. The initial rationale for its use after liver transplantation was to alter the bile acid pool to a more atoxic composition, as liver transplantation can be associated with cholestasis and can stimulate the initial bile production. We have consecutively treated 41 patients with primary graft function with UDCA. During the first postoperative month, 17% of the UDCA treated patients had an episode of acute rejection compared with 75% of a historical control group of 8 patients. The results suggest that adjuvant treatment with UDCA reduces acute liver graft rejection. This has to be confirmed by controlled prospective trials; one is presently being carried out in the Nordic countries. Several studies have indicated an immunomodulating capacity of this bile acid and we have recently reported our results from a heart transplant model in the rat, where treatment with UDCA prolonged graft survival. Improvement in surgical technique and postoperative care as well as immunosuppressive treatment has improved the results of liver transplantation. Acute rejection is nowadays a dominating problem after liver transplantation and the inclusion of UDCA may reduce morbidity.
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| 64. |
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| 65. |
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| 66. |
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| 67. |
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| 68. |
- Lindén, Tomas, et al.
(författare)
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Serum triglycerides and HDL cholesterol--major predictors of long-term survival after coronary surgery.
- 1994
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Ingår i: European heart journal. - 0195-668X. ; 15:6, s. 747-52
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Tidskriftsartikel (refereegranskat)abstract
- The influence of pre-operative serum lipid levels on late clinical outcome after coronary artery bypass surgery was analysed in 83 patients undergoing coronary bypass surgery for stable angina pectoris. The mean follow-up period for surviving patients was 105 +/- 33 months (range 65-133). Twenty-two patients (27%) had died during follow-up, of whom 14 had sustained a fatal myocardial infarction and four had succumbed to other cardiovascular causes. Thirty-one patients sustained 35 cardiac events, defined as either fatal or non-fatal myocardial infarction, or reoperation, or PTCA during the follow-up period. With univariate analysis, pre-operative serum levels of total cholesterol and triglycerides were significantly related to cardiac events, P < 0.05 and P < 0.05, respectively. In a Cox proportional analysis, cardiac mortality and total mortality were related to serum triglycerides and HDL cholesterol (P < 0.05 and P < 0.01 respectively). Eighty-five percent of the patients with triglycerides < 2.0 mM.l-1 survived for 10 years, while only 48% of patients with triglycerides > 2.0 mM.l-1 remained alive for that period. Figures were similar for subjects with HDL cholesterol > 1.0 mM.l-1 or HDL cholesterol < 1.0 mM.l-1, at 89 and 38%, respectively. Only 28% of the patients with the combination triglycerides > 2.0 mM.l-1 and HDL cholesterol < 1.0 mM.l-1 were alive 10 years after surgery. These data suggest that dyslipidaemia, especially the combination of high serum triglycerides and low HDL cholesterol, is an important factor influencing long-term clinical outcome after coronary bypass surgery.
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| 69. |
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| 70. |
- Nilsson, Bengt E, 1949, et al.
(författare)
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VIP-antiserum inhibits fluid secretion by the inflamed gallbladder mucosa.
- 1994
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Ingår i: Regulatory peptides. - 0167-0115. ; 49:3, s. 179-84
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Tidskriftsartikel (refereegranskat)abstract
- The inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by an increased prostaglandin formation and is mediated by intramural nerves. In the present study the effect of VIP-antiserum on the inflammatory fluid secretion in the gallbladder was tested in a validated experimental model in cats. The animals were studied in acute experiments 6 weeks after a procedure when the cystic duct was tied and gallstones were implanted in the gallbladder. During basal conditions there was a continuous secretion of fluid into the lumen of the inflamed gallbladder averaging 0.43 +/- 0.18 ml/h. Injection of VIP antiserum, obtained from immunized rabbits and diluted with saline 1:10 in a bolus of 4 ml into the coeliac artery reversed this secretion into an absorption of 1.72 +/- 0.44 ml h-1 (P < 0.001). VIP-antiserum did not affect the fluid adsorption in control animals with an intact gallbladder and injection of control serum from rabbits not immunized to VIP did not affect fluid secretion in the inflamed gallbladders. The results support the idea that the inflammatory fluid secretion in the gallbladder mucosa is mediated by VIP-ergic nerve fibres.
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