Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombotic thrombocytopenic purpura (TTP) is characterized by widespread occluding and persistent microthrombotic lesions. Evidence for both endothelial damage and primary platelet aggregation as possible pathogenetic mechanisms has been produced. Persistence of microthrombi has not been explained satisfactorily. In patients with TTP we studied plasma fibrinolysis and protein C. Tissue plasminogen activator (t-PA) activity levels, measured functionally, were low or unmeasurable in 11 of 12 patients; t-PA antigen levels, measured immunochemically, were normal in all six observed. The level of potent inhibitor of plasminogen activation directed against both t-PA and urokinase was elevated significantly in all 12, whereas the alpha 2-antiplasmin level was elevated in only two. Protein C antigen levels were low in three of six patients observed. Fibrinolysis levels in patients in remission did not differ from those in patients with acute disease. Plasma exchange resulted in temporary reversal of the abnormalities, but achievement of clinical remission was not associated with permanent normalization of fibrinolysis. Inasmuch as all 12 patients had severely depressed fibrinolytic mechanisms it is possible that a defect in the fibrin-clearing system permits thrombus formation to occur and proceed in an unchallenged fashion, thereby contributing to the complex events leading to arterial ischemia in vital organs.
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PMID:Fibrinolysis in health and disease: abnormal levels of plasminogen activator, plasminogen activator inhibitor, and protein C in thrombotic thrombocytopenic purpura. 243 36

Lupus-like anticoagulants (LLA), lupus anticoagulant and/or anticardiolipin antibody, are increasingly recognized in association with venous and arterial thrombotic events. We recently reviewed our experience with patients undergoing revascularization for lower-limb ischemia who were found to have LLA. Nine patients had LLA based on a prolongation of the partial thromboplastin time or by anticardiolipin assay by an enzyme-linked immunosorbent assay system. The ages of the patients ranged from 23 to 57 years. There were seven (78%) men, six (67%) blacks, two (22%) diabetic patients, and three (33%) hypertensive patients. One patient had systemic lupus erythematosus. All patients except one were cigarette smokers. Four patients had concurrent regulatory protein abnormalities: three protein C deficiencies, one protein S deficiency, and one plasminogen deficiency. The nine patients had 10 lower-extremity arterial reconstructions with two postoperative failures within 30 days. Patients were anticoagulated with heparin or aspirin after all but one operation. Patients at risk were identified on the basis of age (less than 51 years), unexplained early graft thrombosis, or history of venous or arterial thrombotic events. This group of patients is believed to be at risk for early postoperative thrombosis. Postoperative anticoagulation after revascularization for patients with LLA may be beneficial.
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PMID:Lupus-like anticoagulants and lower extremity arterial occlusive disease. 250 7

In this three year prospective study of 177 patients with acute peripheral arterial ischemia those subjects with acute iliofemoral emboli or ischemia with a neurosensory deficit had urgent operations. The remainder included patients less likely to have limb salvage after surgery and who therefore were treated with thrombolytic therapy. This was done in three open studies of intravenous, acylated, plasminogen-streptokinase activator complex, low dose intraarterial streptokinase and intraarterial tissue-plasminogen activator (t-PA). The overall outcome after 30 days of thrombolytic therapy was limb salvage (55%), amputation (15%), and death (30%). The severity of the presenting ischemia was the most important prognostic indicator. In patients with a neurosensory deficit, limb salvage after either embolectomy or surgical reconstruction (59%) was more likely than after thrombolysis (31%). In patients without a neurosensory deficit, limb salvage after thrombolysis (68%) was better, though not significantly, than after surgery (53%). Local intraarterial thrombolysis with either streptokinase or t-PA produced an encouraging 66% limb salvage in 59 cases. In management of acute peripheral arterial occlusions an approach based on the severity of ischemia is optimal, with urgent surgery for patients with a neurosensory deficit and intraarterial thrombolytic therapy reserved as an alternative in selected cases with stable ischemia.
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PMID:Acute peripheral arterial ischemia: a prospective evaluation of differential management with surgery or thrombolysis. 251 79

This study prospectively evaluates hypercoagulable states in patients under 51 years of age undergoing lower extremity revascularization for ischemia and assesses early outcome after operation. Twenty patients whose ages range from 23 to 50 years (mean 40.8 years) were identified prospectively who underwent lower extremity revascularization and evaluation of hypercoagulability. Fifteen patients were male (75%), 10 were black (50%), six had hypertension (30%), and four were diabetic (20%). All but two were cigarette smokers (90%). Seven aortoiliac procedures and 13 infrainguinal procedures were performed. Six patients had one or more abnormalities of regulatory proteins (protein S deficiency, four; protein C deficiency, three; presence of lupus-like anticoagulant, three; plasminogen deficiency, two). Eight of 17 patients in whom platelet aggregation profiles were obtained showed increased reactivity (47%). Only 4 of 17 patients (24%) were normal when tested for all parameters. Arterial or graft thrombosis developed in four of the 20 patients within 30 days after operation. Hypercoagulability was found in all four patients whose revascularizations failed. A high incidence of hypercoagulable states was found in patients under 51 years of age with lower limb ischemia requiring revascularization. Hypercoagulability may have contributed to early postoperative thrombosis of the vascular procedure.
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PMID:Hypercoagulable states and lower limb ischemia in young adults. 252 8

Pharmacologic intervention is critical to the management of myocardial ischemia. Four classes of drugs are now used in therapeutic regimens for ischemia. beta-Adrenergic blockers decrease ischemia by blocking beta 1-mediated inotropic and chronotropic effects, thereby decreasing myocardial oxygen consumption. Calcium channel blockers alter fast- and slow-response action potentials by decreasing transmembrane calcium flux, resulting in decreased conduction velocity and heart rate and prolonged effective refractory period. These effects positively influence ischemia and atrial dysrhythmias. Additionally, these agents decrease excitation-contraction coupling in vascular smooth muscle, resulting in coronary and peripheral vasodilation. Organic nitrates and nitrites decrease vascular smooth muscle contraction and preload, and afterload, precipitating a decrease in myocardial oxygen consumption and ischemia. They also improve blood flow to areas of compromised flow. Thrombolytic agents are administered in acute situations to dissolve the occluding thrombus, but they must be used within a few hours of the injury. These drugs activate the conversion of plasminogen to plasmin, which breaks down the clot into fibrin degradation products. The choice of agents is determined by the etiology of the patient's ischemia, his or her response to the drug, and the presence of concomitant disease processes.
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PMID:Pharmacologic management of myocardial ischemia. 257 Jan 35

Human arteries and veins contract with hypoxia and deprivation of substrate provoked by increasing calcium inflow into the cell and reduced energy. Such spasm may be eliminated by phosphoenolpyruvate which loads up the cell's energy, blocking glycogen reduction at the same time. Reperfusion will then guarantee a sufficient energy stroke. Therapy should pursue the following steps: 1. Phosphoenolpyruvate infusion (1 X 10(-6) up to 1 X 10(-3) gm/ml in tyrodes solution pH 7.3) into the arterial branch, proximal and distal to the injury. 2. Subsequent treatment with vasodilating drugs and rheologically active substances. 3. Failed therapy after more than three hours warm ischemia could be due to autolytic processes and requires resection of the affected vessel. 4. The imbalance of the thrombolytic system with the so-called no reflow phenomenon could be due to a plasminogen activator's inhibitor released during hypoxia. Such cases may reasonably be treated by urokinase or by streptokinase plasminogen complex.
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PMID:[Vascular spasms in microsurgery]. 362 68

Sixty-two patients hospitalized for recent angiographically documented arterial occlusion in the legs (46 femoropopliteal arteries and 16 grafts) benefited from local fibrinolytic therapy delivered at the site of the occlusion with a No. 4F or No. 5F catheter. This therapy combined a continuous urokinase (UK) infusion of 1000 U/kg/hr and a lysyl plasminogen (LYS-PLG) infusion of 15 mukat every 30 minutes. Angiographically confirmed lysis was obtained in 77% of the cases. Five percent of the patients had major and 8% had minor groin hematomas. Only two patients had concentrations of fibrinogen as low as 100 mg/dl. Intravascular infusion of UK and LYS-PLG is as effective as streptokinase but produces lower systemic fibrinolysis. However, local fibrinolysis remains a potentially hazardous procedure (10% suffered major complications) and must only be applied to patients with severe ischemia and little or no possibility of surgical intervention.
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PMID:Local thrombolysis in peripheral arteries and bypass grafts. 365 85

The paper presents an overview of the recent diagnostic and therapeutic feasibilities in acute coronary heart disease. In unstable angina the leading symptoms are new onset or increasing anginal pain or resting pain as well as ST-T-changes in the ecg without a rise in enzymes. Coronary arteriography shows double or triple vessel disease (70%), a left main stenosis (10 to 15%) or normal coronary arteries (10 to 15%). The treatment of unstable angina in the CCU consists of Nitroglycerin-infusion together with calcium channel blockers and/or betablockers. With this regimen, 80% of patients may be stabilized within 24 to 48 hours. Thereafter coronary arteriography is performed to settle the further therapeutic regimen (PTCA, CABG, medical therapy). Acute myocardial infarction is characterized by persisting (more than 30 min) pain, ST-T-changes in the ecg with or without development of Q-waves indicating irreversible myocardial damage. Angiographically, usually a subtotal or total occlusion of the corresponding artery is found. Aims of therapy in acute myocardial infarction is-besides treatment of complications like arrhythmias and left ventricular failure-reperfusion of the myocardium with reopening of the occluded vessels by intracoronary or systemic thrombolysis. Recently, also clot-specific streptokinase derivates and plasminogen activators are used with fewer bleeding complications. After recanalization of the vessel a persisting stenosis should be relieved either by PTCA or CABG to avoid reocclusion. However, these active forms of treatment can only be performed, if the patient reaches the hospital within 4 to 6 hours after the onset of ischemia.
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PMID:[Acute coronary heart disease. Current status of diagnostic and therapeutic possibilities in the intensive care station]. 372 2

Thirty-five patients hospitalized for recent angiographically documented arterial occlusion in the legs (27 femoropopliteal arteries and eight grafts) benefited from local fibrinolytic therapy delivered at the site of the occlusion with a 4- or 5-F catheter. This therapy combined a continuous urokinase (UK) infusion of 1,000 U/kg/hour and a lysyl plasminogen (LYS-PLG) infusion of 15 microkatals every 30 minutes. Angiographically confirmed lysis was obtained in 85% of the cases. Only 3% of the patients had major and 6% had minor groin hematomas. Only two patients had concentrations of fibrinogen as low as 100 mg/dl. Intravascular infusion of UK-LYS-PLG is as effective as streptokinase. Its excellent tolerance makes it a good alternative in the treatment of acute ischemia in the lower limbs.
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PMID:Acute peripheral arterial and graft occlusion: treatment with selective infusion of urokinase and lysyl plasminogen. 394 77

Low dose urokinase-lys plasminogen was used to treat 10 patients with acute ischemia of lower limbs. Preliminary results are reported and indications defined, the combination producing effective relief and being very well tolerated biologically and clinically. All patients presented clear signs of ischemia provoking a short term risk for the limb. Direct femoral puncture arteriography of the ischemic limb was an essential pretreatment investigation. A thin catheter left in contact with the thrombus allowed localized fibrinolysis to be performed. Follow up arteriography examinations assessed clinicopathologic results, while biologic surveillance of principal coagulation parameters showed a lack of significant alterations during treatment. Ischemic signs were totally relieved in 7 cases, with arterial repermeabilization allowing recuperation of one (3 cases) or both (2 cases) distal pulses. Persistence of a popliteal thrombus in one case required a fogarty after a direct approach and the limb was saved. Two patients had to be amputated because of delayed treatment. These encouraging results suggest that this procedure of local thrombolysis be reserved for popliteal or infra-popliteal occlusions accompanied by sensory-motor signs and of recent (less than 72 hours) onset. Follow up for 8 months is insufficient but has shown the absence of deterioration, but this is obviously a function of the natural course of the underlying atheromatous disease.
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PMID:[Indications and results of combined urokinase-lys plasminogen in acute ischemic pathology of the legs]. 409 20


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