Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On occasions it may be vital to produce controlled thrombosis of an abdominal aortic aneurysm when resection is not possible. A successful technique was evolved to achieve this in a 57-year-old man with malignant lymphoma. The tumor was found to infiltrate massively the retroperitoneum and the wall of a large abdominal aortic aneurysm. The large aneurysm was deemed to be technically unresectable at operation. An approach was devised to thrombose the aneurysm and to proceed safely with chemotherapy of the malignant lymphoma. An axillobifemoral bypass was made with the limbs anastomosed end to end to the common femoral arteries. The external iliac vessels were exteriorized through the abdominal wall. The aneurysmal sac outflow was occluded by balloon catheters introduced through the exteriorized iliac vessels. A right transaxillary catheter was inserted and placed at the level of the renal arteries to induce and to control the progress of thrombus formation in such a way as to ensure patency of the renal vessels. Thrombin was delivered into the sac via this transaxillary catheter. A high urinary output was maintained. Serial angiograms of the clotting process were obtained. Once the sac was thrombosed, the balloon catheters were removed and a final angiogram was obtained which demonstrated the obliteration of the aneurysmal sac and the patency of the renal vessels. The patient has been fully employed for 20 months.
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PMID:Induced thrombosis of inoperable abdominal aortic aneurysm. 68 31

In the A alpha-chain gene coding for an abnormal fibrinogen (fibrinogen Marburg) we identified a single base substitution (A-->T) that changes the codon A alpha 461 AAA (Lys) to TAA (Stop). The propositus was found to be homozygous for the mutation, whereas the father and five siblings were heterozygous, and three other siblings contained only the normal sequence. The stop codon at position 461 results in the deletion of the carboxyl-terminal segment A alpha 461-610. Purified fibrinogen Marburg contained an A alpha-chain with a relative molecular weight of approximately 47,000. The FpA release by thrombin was not affected by this deletion, whereas the fibrin polymerization was strongly decreased. The binding of endothelial cells to immobilized fibrinogen Marburg was almost completely abolished compared with normal fibrinogen. Fibrinogen Marburg contained a substantial amount of albumin linked to the fibrinogen molecule by disulfide bonds, and these fibrinogen-albumin complexes were also present in plasma. The plasma fibrinogen concentration of the propositus was measured by three different methods: a functional method (< 0.25 mg/mL), an immunologic method using polyclonal antibodies (0.6 mg/mL), and an immunologic method based on two monoclonal antibodies specific for the amino-terminus and carboxyl-terminus of the A alpha-chain (< 0.05 mg/mL). Using the two immunologic methods, it appeared that only 10% to 15% of the plasma fibrinogen of the heterozygous siblings was abnormal.
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PMID:Fibrinogen Marburg: a homozygous case of dysfibrinogenemia, lacking amino acids A alpha 461-610 (Lys 461 AAA-->stop TAA). 139 54

To determine the factors which influence perioperative coagulative and fibrinolytic function, we studied 41 patients who underwent surgical repair of unruptured abdominal aortic aneurysm (AAA) and 30 patients who underwent arterial reconstruction for arteriosclerosis obliterans (ASO). In patients with AAA, the levels of fibrin/fibrinogen degradation products (FDP) (11.4 +/- 20.1 micrograms/ml), thrombin-antithrombin III complex (TAT) (22.0 +/- 21.8 micrograms/l), plasmin-alpha 2 plasmin inhibitor complex (PIC) (2.6 +/- 2.9 micrograms/ml) and d-dimer of cross-linked fibrin degradation products (D-D) (8.4 +/- 10.8 micrograms/ml) were elevated, particularly when the AAAs had a large mural thrombus surface area or were accompanied by aneurysm of the iliac or femoral artery. In arterial aneurysms, blood coagulability and secondary fibrinolytic activity were believed to be enhanced. In patients with ASO, the level of TAT (17.2 +/- 24.8 micrograms/l) was so elevated that they were considered to show chronic hypercoagulability. Among the ASO patients with aorto-iliac lesions, those with concomitant graft occlusion or anastomotic aneurysm had significantly elevated levels of TAT. Proximal arterial occlusion or accompanying aneurysm in the ASO patients was associated with increased levels of PIC and D-D. Postoperative fluctuations in conventional hematological variables did not differ significantly among the surgical procedures. Conventional markers showed a transient decrease due to consumption during surgery, and a subsequent recovery or an actual increase within several days after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Perioperative changes in coagulative and fibrinolytic function during surgical treatment of abdominal aortic aneurysm and arteriosclerosis obliterans. 773 53

An inherited fibrinogen variant, fibrinogen Bern I, was isolated from plasma of an asymptomatic woman. Routine coagulation studies showed prolonged thrombin and reptilase clotting times. Fibrinogen concentration was diminished when determined by a functional assay, but was normal by the heat precipitation method. The release of fibrinopeptides A and B was not delayed. Two-dimensional gel electrophoresis of mercaptolyzed fragments D of fibrinogen, obtained by digestion with plasmin, showed an abnormal electrophoretic mobility in the gamma-chain remnants of fragments D1 and D2 from fibrinogen Bern I, whereas conversion of D2 to D3 by plasmin resulted in the loss of the abnormal charge, suggesting that the structural abnormality in this variant is located in the region gamma 303 through 356. The molecular defect in fibrinogen Bern I was identified by sequence analysis of genomic DNA amplified by polymerase chain reaction and cloned in M13mp19. The triplet AAC coding for asparagine at position gamma 337 was found to be substituted by AAA coding for lysine. We conclude that the substitution gamma 337 Asn-->Lys in fibrinogen Bern I is responsible for defective polymerization of fibrin monomers and for impaired protection by calcium against plasmic degradation.
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PMID:Fibrinogen Bern I: substitution gamma 337 Asn-->Lys is responsible for defective fibrin monomer polymerization. 840 Feb 60

We compared the efficacy of argatroban, a new synthetic thrombin-specific inhibitor, with that of heparin in pre-DIC state patients with abdominal aortic aneurysm (AAA). A pre-DIC state was diagnosed by a detection of soluble fibrin monomer complex (FM) and increased levels of thrombin-antithrombin III complex (TAT) of more than 20 ng/ml. Twelve patients showing a pre-DIC condition were treated with argatroban (40 mg/day, n = 6) or heparin (10,000 U/day, n = 6) for 5 days. Coagulation and fibrinolytic profiles were analyzed before and after drug administration. FM became negative in two (33%) patients after the argatroban treatment and in all (100%) of the heparin-treated patients. Plasma levels of TAT were significantly decreased after the heparin treatment, however, there was no significant alteration in this parameter after the argatroban treatment. In conclusion, the anticoagulant effects of heparin were superior to those of argatroban in controlling the pre-DIC state associated with AAA.
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PMID:Anticoagulant Effects of Argatroban on the Pre-DIC State in Patients with an Aortic Aneurysm: A Comparative Study of Heparin 958 57

BACKGROUND: Previous work has demonstrated that ruptured abdominal aortic aneurysm (AAA) is associated with systemic thrombin generation and inhibition of systemic fibrinolysis. The procoagulant and hypofibrinolytic state associated with ruptured AAA predisposes to microvascular and macrovascular thrombosis and subsequent myocardial injury. The aim of this study was to determine the relationship between haemostatic derangement and biochemical evidence of myocardial injury in patients operated on for ruptured AAA. METHODS: Ten patients undergoing repair of ruptured AAA were studied. Tissue plasminogen activator (tPA) activity, plasminogen activator inhibitor (PAI) activity, prothrombin fragment (PF) 1 + 2, D-dimer and fibrinogen levels were measured before operation, and immediately before and 5 min after aortic clamp release. Plasma levels of cardiac troponin (cTn) I were measured before operation, and 6 and 24 h after aortic clamp release. RESULTS: There was no relationship between tPA activity, PF 1 + 2, D-dimer or fibrinogen and cTn-I levels at any sampling point. There was, however, a significant positive correlation (Spearman rank test) between PAI activity immediately before (median 38.6 (range 13.0-39.4) units ml-1) and 5 min after (37.2 (10.6-39.4) units ml-1) aortic clamp release, and cTn-I at 6 h (median 3.17 (range less than 0.5 to 71.1) ng ml-1) and 24 h (5.55 (range less than 0.5 to 110) ng ml-1) after aortic clamp release. CONCLUSION: These data strongly support the hypothesis that the inhibition of systemic fibrinolysis which occurs in response to ischaemia and reperfusion during ruptured AAA repair contributes to the development of subsequent myocardial injury.
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PMID:Vascular surgical society of great britain and ireland: inhibition of systemic fibrinolysis is associated with myocardial injury in patients operated on for ruptured abdominal aortic aneurysm 1036 22

Endoleaks remain a significant challenge after endovascular abdominal aortic aneurysm repair (EVAR). Translumbar thrombin injection of the aneurysm sac has been used to treat endoleaks, with low reported morbidity. We present an unusual case of ischemic colitis following translumbar thrombin injection of an endoleak. A 67-year-old male with a 5.8-cm abdominal aortic aneurysm (AAA) was evaluated for endograft repair. The patient underwent preoperative embolization of the right hypogastric artery. The AAA was repaired using a unibody bifurcated graft (Ancure). Completion aortogram revealed no endoleak and a widely patent left hypogastric artery. Computed tomography (CT) at 2 months showed an endoleak appearing to originate from a lumbar artery near the proximal attachment site with outflow via the inferior mesenteric artery (IMA). The endoleak was successfully treated with CT-guided translumbar injection of 8000 units of thrombin into the aneurysm sac. The patient subsequently developed chronic abdominal pain, diarrhea, and a weight loss of 20 lbs. Colonoscopy revealed ischemic colitis of the rectosigmoid colon. Duplex evaluation indicated a patent superior mesenteric artery and IMA distal to its origin. Medical treatment failed and the patient underwent a low anterior resection 2 months later (4 months post-EVAR). Subsequently, the aneurysm has decreased to 5.4 cm, with no evidence of endoleak at 1 year. We conclude that ischemic colitis may occur following translumbar thrombin injection. Thrombin embolization into the rectosigmoid arcade via the IMA was most likely the cause in this case. This problem can potentially be avoided by treating the IMA endoleak outflow prior to translumbar thrombin injection of the aneurysm sac. Thorough arteriographic evaluation of endoleaks should be performed prior to any interventions.
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PMID:Ischemic colitis following translumbar thrombin injection for treatment of endoleak. 1471 80

This report describes the use of thrombin to treat a type II endoleak which was causing continued abdominal aortic aneurysm expansion in a patient who had undergone endovascular repair. A small quantity of thrombin was injected into the leak by a percutaneous approach directly into the aneurysm sac using color doppler ultrasound. The procedure was successful and required only a few minutes to perform. We believe this procedure is an alternative to some of the more complex and technically challenging means of treating this lesion.
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PMID:The use of direct thrombin injection to treat a type II endoleak following endovascular repair of abdominal aortic aneurysm. 1475 10

Perioperative hemorrhage is one of the principal causes of death in patients with ruptured abdominal aortic aneurysm (AAA). This study examines perioperative coagulation and fibrinolysis in patients undergoing ruptured AAA repair complicated by coagulopathy. Eight patients (8 men of median age 74, range 69-87, years) who developed clinical and laboratory evidence of coagulopathy during attempted repair of ruptured infrarenal AAA were prospectively studied. Platelet count, fibrinogen, clotting times, prothrombin fragment (PF) 1+2, and tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) activities were measured preoperatively, immediately before, and 5 min and 24 hr after aortic declamping. Six patients died, three intraoperatively, one within 24 hr, and two in the late postoperative period. All patients had thrombocytopenia and prolonged clotting times intraoperatively with evidence of increased thrombin generation (as demonstrated by elevated PF 1+2). Five patients had increased systemic fibrinolysis (as demonstrated by elevated t-PA activity) preoperatively and/or before aortic declamping and all of these patients died. Three patients had perioperative inhibition of systemic fibrinolysis (as demonstrated by elevated PAI activity) and two survived. These data demonstrate that coagulopathy in ruptured AAA repair may be associated with a hyperfibrinolytic state. Further research is required to determine if (a) a causal relationship exists between hyperfibrinolysis and coagulopathy and (b) whether antifibrinolytic agents can improve outcome if targeted at this group of patients.
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PMID:Coagulopathy and hyperfibrinolysis in ruptured abdominal aortic aneurysm repair. 1553 37

Elective surgery of abdominal aortic aneurysm (AAA) sometimes leads to excessive bleeding and disseminated intravascular coagulation (DIC), even in patients with normal preoperative coagulation parameters. Coagulation screen, performed routinely before surgery is of limited value in the assessment of compensated activation of the haemostatic system. In this study, we used a number of additional tests (D-dimer, prothrombin fragment 1+2, antithrombin, and activation of fibrinolysis in the platelet poor plasma) for the diagnosis of compensated activation of the haemostatic system in AAA-patients. D-dimer and marker of thrombin generation (prothrombin fragment 1+2) positively correlated with each other (r = 0.768, P < 0.001). Out of 71 AAA patients, 15 patients had normal global coagulation times, but those with a D- dimer concentration above 3000 ng/ml were selected for preoperative low molecular weight heparin (LMWH) treatment. Administration of LMWH diminished coagulation abnormalities (D-dimer and prothrombin fragment 1+2 decreased significantly) and resulted in the increase of platelet number and fibrinogen concentration, indicating their previous consumption. Despite differences in aneurysm diameters between the groups of 15 LMWH treated patients (mean 70.9 +/- 16 mm) and the reference group of 20 untreated AAA patients (mean 52.3 +/- 8.0 mm), intraoperative parameters (operation time, blood loss and transfusion demands) were similar.
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PMID:Compensated activation of coagulation in patients with abdominal aortic aneurysm: effects of heparin treatment prior to elective surgery. 1554 26


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