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Jpn J Thorac Cardiovasc Surg. 2002 May;50(5):220-3.
Successful surgical management of patients with infective endocarditis associated with acute neurologic deficits.
Sawamura Y, Fukuju T, Kikuchi S, Kitahara M, Ito T, Tabayashi K.
Department of Cardiovascular Surgery, Ishinomaki Red Cross Hospital, Miyagi, Japan.
Subjects were 2 patients with neurologic deficits due to infective endocarditis. The first, a 30-year-old woman with acute ischemic stroke, was found to have vegetation from infective endocarditis as the embolic source. Two weeks after she experienced an acute ischemic stroke, we conducted elective cardiac surgery. The second, a 16-year-old girl with infective endocarditis, suffered a ruptured mycotic aneurysm in the left carotid system complicated by intracranial hemorrhage. We conducted a successful staged mitral valve replacement following craniotomy.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12048917&dopt=Abstract hemorrhage
Pacing Clin Electrophysiol. 2002 May;25(5):860-2.
Can radiofrequency current isthmus ablation damage the right coronary artery? Histopathological findings following the use of a long (8 mm) tip electrode.
Weiss C, Becker J, Hoffmann M, Willems S.
Department of Cardiology, University Hospital Eppendorf, Hamburg, Germany. Weiske.uni-hamburg.de
This report describes the histopathological findings following successful RF isthmus ablation for common atrial flutter in a 68-years-old man using a long 8-mm tip ablation catheter. No acute complication was observed. The patient died 3 weeks after ablation due to severe heart failure and consecutive pneumonia. Lesion width (1.0 and 2.4 cm) and depth (0.4 and 0.8 cm) was measured. The right coronary artery showed an intramural hemorrhage adjacent to the side of the lesion. However, despite this finding no apparent injury of other layers of the coronary artery was detectable.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12049382&dopt=Abstract hemorrhage
Development. 2002 Jun;129(12):2891-903.
beta8 integrins are required for vascular morphogenesis in mouse embryos.
Zhu J, Motejlek K, Wang D, Zang K, Schmidt A, Reichardt LF.
Howard Hughes Medical Institute and Department of Physiology, University of California, San Francisco, San Francisco, CA 94143, USA.
In order to assess the in vivo function of integrins containing the beta8 subunit, we have generated integrin beta8-deficient mice. Ablation of beta8 results in embryonic or perinatal lethality with profound defects in vascular development. Sixty-five percent of integrin beta8-deficient embryos die at midgestation, with evidence of insufficient vascularization of the placenta and yolk sac. The remaining 35% die shortly after birth with extensive intracerebral hemorrhage. Examination of brain tissue from integrin beta8-deficient embryos reveals abnormal vascular morphogenesis resulting in distended and leaky capillary vessels, as well as aberrant brain capillary patterning. In addition, endothelial cell hyperplasia is found in these mutant brains. Expression studies show that integrin beta8 transcripts are localized in endodermal cells surrounding endothelium in the yolk sac and in periventricular cells of the neuroepithelium in the brain. We propose that integrin beta8 is required for vascular morphogenesis by providing proper cues for capillary growth in both yolk sac and embryonic brain. This study thus identifies a molecule crucial for vascular patterning in embryonic yolk sac and brain.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12050137&dopt=Abstract hemorrhage
Development. 2002 Jun;129(12):3009-19.
Disruption of acvrl1 increases endothelial cell number in zebrafish cranial vessels.
Roman BL, Pham VN, Lawson ND, Kulik M, Childs S, Lekven AC, Garrity DM, Moon RT, Fishman MC, Lechleider RJ, Weinstein BM.
Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
The zebrafish mutant violet beauregarde (vbg) can be identified at two days post-fertilization by an abnormal circulation pattern in which most blood cells flow through a limited number of dilated cranial vessels and fail to perfuse the trunk and tail. This phenotype cannot be explained by caudal vessel abnormalities or by a defect in cranial vessel patterning, but instead stems from an increase in endothelial cell number in specific cranial vessels. We show that vbg encodes activin receptor-like kinase 1 (Acvrl1; also known as Alk1), a TGFbeta type I receptor that is expressed predominantly in the endothelium of the vessels that become dilated in vbg mutants. Thus, vbg provides a model for the human autosomal dominant disorder, hereditary hemorrhagic telangiectasia type 2, in which disruption of ACVRL1 causes vessel malformations that may result in hemorrhage or stroke. Movies available on-line
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12050147&dopt=Abstract hemorrhage
J Vasc Interv Radiol. 2002 Jun;13(6):577-80.
Catheter-directed thrombolysis in deep venous thrombosis with use of reteplase: immediate results and complications from a pilot study.
Castaneda F, Li R, Young K, Swischuk JL, Smouse B, Brady T.
Department of Radiology, University of Illinois College of Medicine at Peoria, 1 Illini Drive, Box 1649, Peoria, Illinois 61656, USA. flaviiit.com
PURPOSE: To prospectively determine the thrombolytic success and complication rates of catheter-directed thrombolytic infusions in deep vein thrombosis (DVT) with use of reteplase. MATERIALS AND METHODS: After approval by the institutional review board, prospective, detailed data were obtained for 25 consecutive patients with acute and chronic DVT of the upper or lower extremity (seven upper extremity; 14 lower extremity; four vena cava). Infusion rates were 1.0 U/h in five patients and 0.5 U/h in the remaining 20. Subtherapeutic heparin doses of 300-400 U/h were administered. Thrombolytic success was defined as 95% thrombolysis with return of antegrade flow. Data, including complications such as bleeding, need for transfusions, and laboratory values (fibrinogen, platelets, hematocrit, hemoglobin, and prothrombin time) were obtained throughout the infusions. RESULTS: The total dose of reteplase administered ranged from 2.5 to 42 U (median, 16.5 U). The total infusion time ranged from 0.3 to 84 hours (median, 29 h). Thrombolytic success was achieved in 92% of patients. Endovascular stent placement and/or percutaneous transluminal angioplasty were required in 52% of patients to ensure maintenance of patency. Pre- and postprocedural average fibrinogen levels were 340 mg/dL and 315.3 mg/dL, respectively. The lowest mean fibrinogen levels for the two dose groups were 265.86 mg/dL for the 0.5 U/h group and 314.18 mg/dL for the 1.0 U/h group. The lowest fibrinogen level during the procedure was 252.3 mg/dL (range, 35 to >700). There were only two instances of fibrinogen levels that decreased to below 90 mg/dL: 35 mg/dL and 43 mg/dL. Thrombolytic failures occurred in two patients: one with acquired immune deficiency syndrome in a hypercoagulable state and one with a major bleeding complication. This was the only patient with a bleeding complication (4%). Hemorrhage occurred from the site of a previous mediastinal biopsy-which should have rendered her ineligible for the study-performed 18 hours before the thrombolysis. If thrombolysis had not been attempted in this patient, the complication rate would have been 0%. CONCLUSION: Although there are reports of thrombolytic therapy in peripheral vascular occlusive disease, this study is one of the first to evaluate thrombolytic drugs in the deep venous system exclusively. Reteplase was found to be effective in the thrombolytic treatment of acute and chronic DVT.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12050297&dopt=Abstract hemorrhage
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