fibrinopeptide-a has been researched along with Aortic-Aneurysm* in 3 studies
2 trial(s) available for fibrinopeptide-a and Aortic-Aneurysm
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Thrombogenicity of a new injectable biocompatible elastomer for aneurysm exclusion, compared to expanded polytetrafluoroethylene in a human ex vivo model.
Customized aortic repair (CAR) is a new concept for endovascular aortic aneurysm repair in which a non-polymerised elastomer is injected to fill the aneurysm sac around a balloon catheter. Amongst other variables, the thrombogenicity of the elastomer should be tested, before further clinical experiments can take place. The aim of this human ex vivo study was to measure the thrombogenicity of the elastomer and to compare it to expanded polytetrafluoroethylene (ePTFE).. In a validated ex vivo model, non-anticoagulated blood was drawn from the antecubital veins of 10 healthy donors with a 19-gauge needle. It was drawn through elastomer tubes and through ePTFE Gore-Tex vascular grafts, both 60 cm long and with an inner diameter of 3 mm.. Fibrinopeptide A (FPA) and P-selectin expression was measured in blood samples, collected at the end of the grafts. After the experiments, the deposition of platelets and fibrin onto the grafts was visualised by scanning electron microscopy.. For these graft types, a progressive increase in FPA production was observed in time. No significant difference was observed between the elastomer and ePTFE grafts (p > 0.05). No increase in P-selectin expression, and thereby no platelet activation, was observed in the perfusate of either grafts (p > 0.05). By scanning electron microscopy, numerous platelet aggregates were observed on the ePTFE grafts, whereas just a few adhered platelets and no aggregates were observed in the elastomer grafts.. The elastomer in its current formulation has a low thrombogenicity, comparable to ePTFE, making it an ideal substance for endovascular aneurysm sac filling. Further research should clarify the feasibility of CAR in vivo. Topics: Adult; Aortic Aneurysm; Blood Vessel Prosthesis; Blood Vessel Prosthesis Implantation; Dimethylpolysiloxanes; Endovascular Procedures; Fibrin; Fibrinopeptide A; Humans; Injections; Male; Microscopy, Electron, Scanning; P-Selectin; Platelet Adhesiveness; Polytetrafluoroethylene; Prosthesis Design; Silicone Elastomers; Thrombosis; Time Factors; Young Adult | 2012 |
Systemic effects of collagen-impregnated aortoiliac Dacron vascular prostheses on platelet activation and fibrin formation.
To minimize intraoperative blood loss a watertight knitted Dacron aortoiliac prosthesis has been developed by impregnation with bovine collagen. A potential disadvantage is that collagen may be associated with an increase in thrombus formation. We conducted a prospective randomized trial to study the systemic effects of collagen-impregnated prostheses and of aortoiliac operation as such on the coagulation mechanism during the first 10 days after operation. Forty-one patients randomly received either a collagen-impregnated (n = 20) or a nonimpregnated prosthesis (n = 21). Twelve patients who underwent cholecystectomies served as controls. Three markers of the coagulation mechanism were monitored: beta-thromboglobulin, fibrinopeptide A, and fibrin/fibrinogen degradation products. We found no significant differences in median beta-thromboglobulin, fibrinopeptide A, and fibrin/fibrinogen degradation product levels between patients in the collagen-impregnated prosthesis group and patients in the nonimpregnated prosthesis group. This indicates that collagen does not stimulate the coagulation cascade any more than conventional Dacron protheses do. In a comparison of patients who underwent aortoiliac reconstruction and patients who underwent cholecystectomies, the results indicated a significant increased platelet activation and fibrin metabolism in aortoiliac reconstruction group compared with the control group. Finally, we observed a significantly higher preoperative fibrin metabolism in patients with vascular disease than in control subjects. This difference is attributable to the high preoperative fibrin/fibrinogen degradation product values in patients with aortic aneurysms. Topics: Adult; Aged; Aged, 80 and over; Aorta; Aortic Aneurysm; Arterial Occlusive Diseases; beta-Thromboglobulin; Blood Vessel Prosthesis; Collagen; Female; Femoral Artery; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Graft Occlusion, Vascular; Humans; Iliac Artery; Male; Middle Aged; Platelet Activation; Polyethylene Terephthalates | 1991 |
1 other study(ies) available for fibrinopeptide-a and Aortic-Aneurysm
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Fibrinopeptide A excretion in urine in patients with atherosclerotic artery disease.
Urinary fpA excretion and fpA in plasma were studied in patients with peripheral artery disease, aortic aneurysm, severe coronary artery disease, acute myocardial infarction and in normal controls. Mean urinary fpA was significantly higher in all groups of patients than in normal controls whose excretion was 1.9 +/- 1.2 micrograms/24 hours (mean +/- SD). We found a good correlation between urinary fpA excretion and plasma fpA (r = 0.68, p less than 0.01, n = 81). The highest levels of urinary fpA were found in 9 patients with aortic aneurysm (11.9 +/- 6.1 micrograms/24 hours). The 10 patients with acute myocardial infarction had also abnormally elevated values (4.3 +/- 1.8 micrograms/24 hours) which were only slightly higher than the levels found in another 10 patients with myocardial infarction receiving subcutaneous heparin in a dosage of 2 X 5000 IU daily (2.9 +/- 1.7 micrograms/24 hours). The 13 patients with peripheral artery disease showed an increase in urinary fpA excretion from 4.0 +/- 1.7 to 10.5 +/- 2.3 micrograms/24 hours after percutaneous angioplasty (p less than 0.001). These data demonstrate that urinary fpA excretion may represent a valid means to detect the cumulative effect of thrombin action on fibrinogen in patients with atherosclerotic vascular disease and after therapeutic intervention. Topics: Aortic Aneurysm; Arteriosclerosis; Fibrinogen; Fibrinopeptide A; Humans; Myocardial Infarction; Radioimmunoassay | 1985 |