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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial infarction remains the leading cause of early and late death after abdominal aortic aneurysm (AAA) repair. Myocardial revascularization is staged either before or concomitant with AAA resection, but results are far from uniform. We retrospectively analyzed our experience with patients who underwent concomitant AAA resection and aortocoronary bypass (ACB) to examine the factors affecting early morbidity/mortality and early results. Forty-two patients (all men; mean age, 67.2 years) underwent simultaneous ACB grafting and AAA repair between 1975 and 1998. All were managed postoperatively in the cardiothoracic intensive care unit (mean stay, 6.1 days). The mean total hospital stay was 17.2 days. Two died in the early postoperative period (4.8%): 1 of sustained myocardial failure following a third ACB, and 1 of coagulopathy after concomitant ACB, aortic valve replacement, and AAA. One patient developed a nonfatal MI on postoperative day 3. The incidence of wound and bleeding complications was higher for patients undergoing both ACB and AAA repair than for patients undergoing AAA resection alone. On follow-up (mean, 10 years; range, 7 months to 15 years), only 2 of 10 late deaths were due to cardiovascular causes. We believe that concomitant myocardial revascularization is warranted in select patients requiring elective or urgent AAA resection in order to decrease perioperative risk and improve late survival. Cardiac failure or ischemia during aortic surgery can be prevented by proper perfusion with or without cardiopulmonary bypass. In patients undergoing simultaneous procedures, the increased risk is related to the severity of the vascular and coronary artery disease and not to the combined operations.
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PMID:Outcome after simultaneous abdominal aortic aneurysm repair and aortocoronary bypass. 1198 88

Although inhibiting interaction of beta(2) integrins with cognate immunoglobulin class adhesion receptor ligands is an effective neuroprotective strategy in small mammal models of stroke, the strategy has failed in human trials. A completely different antiadhesion receptor strategy was therefore rigorously tested in a model that may more closely approximate human reperfused stroke. Early leukoadhesive events in postischemic cerebral microvessels are mediated by upregulated selectin-class adhesion receptors on endothelial cells. Therefore, a blocking antibody prepared against common P- and E-selectin epitopes was humanized to suppress complement activation and tested in a reperfused hemispheric stroke model in Papio anubis (baboon). Histological examination of postischemic cerebral microvessels revealed a strong upregulation of E-and P-selectin expression. Placebo-blinded administration of the humanized anti-human E- and P-selectin monoclonal antibody (HuEP5C7, 20 mg/kg IV, n=9; placebo, n=9) immediately after the onset of 1 hour of temporary ischemia resulted in trends showing reduced polymorphonuclear leukocyte (PMN) infiltration into ischemic cortex, reduced infarct volumes (by 41%), improved neurological score (by 35%), and improved ability to self-care (by 39%). Importantly, there was no evidence of systemic complement activation, immune suppression, or pathological coagulopathy associated with this therapy. These data suggest that a humanized anti-E/P-selectin antibody approach is safe and may be effective as a clinical treatment for human stroke.
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PMID:HuEP5C7 as a humanized monoclonal anti-E/P-selectin neurovascular protective strategy in a blinded placebo-controlled trial of nonhuman primate stroke. 1243 35

Hepatic transplantation may result in coagulopathy caused by the release of mast-cell-derived heparin, and xanthine oxidase (XO) inhibition stabilizes mast cells. Thus, XO inactivation could decrease coagulopathy after hepatoenteric ischemia-reperfusion. Rabbits were fed a standard or XO-inactivating diet before hepatoenteric ischemia for 35 min and before 30 min of reperfusion. Hemostasis was assessed by thrombelastography. Heparin activity was quantified by anti-IIa. XO inactivation resulted in clot formation after reperfusion in all animals, whereas only 37.5% of animals with XO activity clotted (P<0.05). Anti-IIa activity was less in animals at baseline and after reperfusion with XO inactivation (45+/-5 and 65+/-5 mU/mL, respectively) compared to animals with XO activity (51+/-4 and 71+/-5 mU/mL, respectively) (P<0.05). Clot strength, which was mediated by coagulation proteins, was significantly greater at baseline and after reperfusion in animals with XO inactivation. XO inactivation enhances hemostasis by decreasing circulating heparin activity and increasing coagulation protein function before ischemia-reperfusion.
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PMID:Coagulopathy mediated by hepatoenteric ischemia-reperfusion in rabbits: role of xanthine oxidase. 1243 67

Human membrane cofactor protein (CD46) controls complement activation and when expressed sufficiently as a transgene protects xenografts against complement-mediated rejection, as shown here using non-immunosuppressed baboons and heterotopic CD46 transgenic pig kidney xenografts. This report is of a carefully engineered transgene that enables high-level CD46 expression. A novel CD46 minigene was validated by transfection and production of a transgenic pig line. Pig lymphocytes were tested for resistance to antibody and complement-mediated lysis, transgenic tissues were characterized for CD46 expression, and kidneys were transplanted to baboons without immunosuppression. Absorption of anti-Galalpha(1,3)Gal epitope (anti-GAL) serum antibodies was measured. Transgenic pigs expressed high levels of CD46 in all tissues, especially vascular endothelium, with stable expression through three generations that was readily monitored by flow cytometry of transgenic peripheral blood mononuclear cells (PBMC). Transgenic PBMC pre-sensitized with antibody were highly resistant to human complement-mediated lysis which readily lysed normal pig PBMC. Normal pig kidneys transplanted without cold ischemia into non-immunosuppressed adult baboons survived a median of 3.5 h (n = 7) whereas transgenic grafts (n = 9), harvested at approximately 24-h intervals, were either macroscopically normal (at 29, 48 and 68 h) or showed limited macroscopic damage (median > 50 h). Microscopic assessment of transplanted transgenic kidneys showed only focal tubular infarcts with viable renal tissue elsewhere, no endothelial swelling or polymorph adherence and infiltration by lymphocytes beginning at 3 days. Coagulopathy was not a feature of the histology in four kidneys not rejected and assessed at 48 h or later after transplantation. Baboon anti-GAL serum antibody titers were high before transplantation and, in one extensively analyzed recipient, reduced approximately 8-fold within 5.5 h. The data demonstrate that a single CD46 transgene controls hyperacute kidney graft rejection in untreated baboons despite the presence of antibody and complement deposition. The expression levels, tissue distribution and in vitro functional tests indicate highly efficient CD46 function, controlling both classical and alternative pathway complement activation, which suggests it might be the complement regulator of choice to protect xenografts.
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PMID:Characterization of a CD46 transgenic pig and protection of transgenic kidneys against hyperacute rejection in non-immunosuppressed baboons. 1496 79

The incidence of iatrogenic femoral false aneurysms has risen dramatically in recent years and is estimated at 0,5% for diagnostic procedures and may rise to 9% or more for therapeutic procedures. This increased incidence is related to the increased number of arterial punctures performed for diagnostic or therapeutic purposes and their major complexity and duration. Risk factors for the development of iatrogenic false aneurysms include operator inexperience, age greater than 60, female gender, catheter size greater than 8F and concurrent anticoagulation. Prevention of false aneurysms is based upon an atraumatic arterial puncture, good compression therapy after sheath removal and use of percutaneous arterial closure devices. Contrarily to the arterial lesions following severe injuries, the natural course of false aneurysms is quite benign with spontaneous occlusion in the majority of cases. Therefore, a mandatory surgical approach is no longer advocated and alternative therapeutic options have been proposed. These include sonographic surveillance, compression ultrasonography, percutaneous thrombin or coil embolization. Surgery is still clearly indicated in presence of local nervous or venous compression, associated homolateral lower limb ischemia, great size of the aneurysm, and unsuccessful non-invasive treatment. Sonographic surveillance has shown to be safe in hospitalized or ambulatory patients. However, fear of aneurysm rupture and cost of repeated ultrasonographic exams preclude widespread utilisation. Compression ultrasonography is safe and effectiveness varies between 70 and 100%, according to studies. Compression ultrasonography may be painful, has often to be associated with mild analgesia, is time consuming and less effective in presence of concurrent anticoagulation. Thrombin injection seems particularly effective, is painless and has a limited rate of complications in expert hands. Severe anaphylactic reactions and severe coagulopathy in reexposed patients have been described and represent clear contra-indications to thrombin injection. Coil embolization of the false aneurysm is as effective as thrombin injection and is reported in a limited number of patients. There is no formal consensus about treatment of the vast majority of non-surgical false aneurysms. In an absence of stringent indication to surgical approach, compression ultrasonography may be used first as it is widely available, and does not require highly specialized skills. Compression therapy should be done after a transient interruption of anticoagulant treatment, if allowed by clinical context. If compression therapy fails, percutaneous injection of thrombin or coil embolization are effective and associated with a low complication rate. However, these techniques are less widely available and necessitate an experienced operator. As recurrences have been described with each of these techniques, every non-surgically-treated false aneurysm should be monitored for 24 hour with ultrasonography control to ensure effective thrombosis.
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PMID:[Treatment of postcatheterization femoral false aneurysms]. 1522 1

A patient with a partially thrombosed fusiform giant basilar trunk aneurysm presented with devastating headache and symptoms of progressive brain stem compression. Having an aneurysm inaccessible for endovascular treatment, and after failing a vertebral artery balloon occlusion test, he was offered bypass surgery in order to exclude the aneurysm from the cerebral circulation and relieve his symptoms. A connection between the intracranial internal carotid artery and the superior cerebellar artery was created whereupon the basilar artery was ligated just distally to the aneurysm. The proximal anastomosis on the internal carotid artery was made using the excimer laser-assisted non-occlusive anastomosis (ELANA) technique, while a conventional end-to-side anastomosis was used for the distal anastomosis on the superior cerebellar artery. Intra-operative flowmetry showed a flow through the bypass of 40 ml/min after ligation of the basilar artery. An angiogram 24 hours later showed normal filling of the bypass and the vessels supplied by it, but also disclosed a subtotal occlusion of the proximal ipsilateral middle cerebral artery with delayed filling distally. The patient, who had a known thrombogenic coagulopathy, died the following day. Autopsy showed no signs of ischemia in the territories supplied by the bypass, but a thrombus in the proximal middle cerebral artery and massive acute hemorrhagic infarction with swelling in its territory and uncal herniation. Multiple fresh thrombi were found in the lungs. The ELANA anastomosis showed re-endothelialisation without thrombus formation on the inside.
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PMID:The ELANA technique: constructing a high flow bypass using a non-occlusive anastomosis on the ICA and a conventional anastomosis on the SCA in the treatment of a fusiform giant basilar trunk aneurysm. 1534 Aug 13

Activation of the coagulation cascade during invasive infection can result in purpura fulminans, with rapid progression of tissue ischemia, or may manifest as abnormal clotting indices alone. Although severe derangements in coagulation are associated with organ dysfunction and increased mortality, the contribution of coagulopathy to the pathophysiology of sepsis remains incompletely understood. Over the past decade, investigators have evaluated several therapeutic anticoagulant strategies in sepsis, and manipulation of the coagulation system has emerged as a key concept in the current management of this disease. Clinical observations during treatment of septic patients with the endogenous anticoagulant activated protein C have stimulated additional study of interactions between endothelial injury, coagulation, and inflammation. This review describes clotting abnormalities during sepsis and discusses the clinical experience with therapeutic strategies intended to oppose excessive coagulation.
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PMID:Coagulation in sepsis. 1548 34

Nonocclusive mesenteric ischemia (NOMI) is a rare abdominal pathology caused by mucosal hypoperfusion without actual obstruction to the mesenteric arteries. We present a case of NOMI after a cardiopulmonary bypass operation. The patient was a 79-year-old woman with a history of hypertension and diabetes mellitus. A coronary bypass operation was performed with stable hemodynamic conditions, and continuous venovenous hemodialysis was performed on the second postoperative day because of renal insufficiency. After 24 h of hemodialysis, the hematocrit level increased from 29.1% to 36.1%. The patient had some vague abdominal pain on the third postoperative day with abnormal laboratory values: leukocytes 17.10 x 10(3)/microl, creatine kinase 1085 U/l, glutamic-oxyloacetic transaminase 6188 U/l, and lactate dehydrogenase 8695 U/l. Selective angiography showed diffuse stenosis of the superior mesenteric artery (SMA) without any occlusive findings on the major branches; the patient was therefore diagnosed with NOMI. An infusion of urokinase and prostaglandin E1 was started; however, disseminated intravascular coagulopathy had developed and the patient died on the 21st postoperative day as a result of multiple organ failure. The autopsy demonstrated extensive necrosis and hemorrhage in the small intestine without any occlusive findings on the major branches of the SMA.
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PMID:Nonocclusive mesenteric ischemia after cardiopulmonary bypass. 1555 39

Malfunctions of central hemostasis chains, activation of blood coagulation systems and decreased antithrombogenic potentials of vascular walls are typical of craniocerebral trauma at exacerbation. It provokes the onset of the DIC-syndrome in 98.8% of examinees; the below signs are observed in such condition: decreased platelet resistance of vascular walls, increased aggregation activity of platelets, activated coagulation chain of hemostasis and increased blood viscosity. The prognostically unfavorable criteria of coagulopathy in acute craniocerebral trauma are as follows: pathological response of the vascular wall to transitory ischemia observed concurrently with a reduced dynamic FW activity; a persistently low and/or decreased dynamic AT-III activity; decreased fibrinolytic activities of plasma and platelet counts; and persistently higher concentrations and/or higher dynamic concentrations of fibrinogen and soluble fibrin mono-measured complexes (according to coagulation tests). Hemostasis should be corrected with respect to the above hemostasiologic syndromes.
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PMID:[Lesions of the vascular endothelium and impairments of haemostatic coagulation in patients with severe craniocerebral trauma]. 1571 16

Repair of thoracoabdominal aortic aneurysms (TAAA) is associated with major blood loss, often exceeding the patient's intravascular volume, and complex intraoperative and postoperative coagulopathies necessitating large-volume transfusion of blood products. Abnormalities sufficient to cause thrombocytopenia or clinically important prolongation of clotting parameters are rarely present before surgery in elective aneurysms but are more common with ruptured aneurysms. The finding of intraoperative and postoperative deficiencies of clotting factors, along with thrombin generation and activation of the thrombolytic system, is reflective of massive blood losses, visceral ischemia, and massive transfusions. An aggressive strategy of transfusion of blood products is critical to the prevention of clinically significant coagulopathy during surgery. Adjuncts to reduce blood losses and blood product use include low-dose aprotinin or epsilon -aminocaproic acid, intraoperative blood salvaging, and acute normovolemic hemodilution. In TAAA repair, an average blood loss of 5000 to 6000 mL and average transfusion of allogeneic blood products of 50 to 60 U are to be anticipated.
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PMID:Coagulation disorders and blood product use in patients undergoing thoracoabdominal aortic aneurysm repair. 1585 42


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