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)

Coronary thrombolysis with streptokinase or tissue plasminogen activator is useful for the treatment of acute myocardial infarction in selected patients. This treatment is associated with local hemorrhagic complications and age-related cerebral hemorrhage. Coronary thrombolysis is contraindicated in patients with transient cerebral ischemia and stroke, arterial hypertension, cerebral trauma, cerebral aneurysms, and arteriovenous malformations, because of the risk of cerebral hemorrhage. We report the occurrence of a cerebral hemorrhage related to cerebral amyloid angiopathy in a patient who underwent thrombolysis and treatment with heparin for acute myocardial infarction. Despite normal coagulation parameters, the cerebral hematoma enlarged over 36 hours, as documented by sequential computed tomographic scans, to produce significant mass effect, which prompted surgical evacuation. Histological examination of the resected specimen demonstrated the strong affinity for Congo red and yellow-green birefringence that are characteristic of cerebral amyloid angiopathy. Hemostasis was difficult to achieve, as the divided or disrupted amyloid-laden cortical vessels failed to vasoconstrict, their contractile elements replaced by amyloid beta protein. The patient died of recurrent myocardial ischemia 3 days postoperatively. The incidence of cerebral amyloid angiopathy increases with advancing age. It must be considered as a potential source of cerebral hemorrhage in elderly patients undergoing thrombolysis for cardiac ischemia. Such an occurrence presents a difficult challenge because cardiac function is compromised, the coagulation profile may be altered, the cerebral hematoma is life threatening, and intracranial hemostasis is difficult to achieve.
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PMID:Cerebral hemorrhage from amyloid angiopathy and coronary thrombolysis. 140 40

The treatment of digital ischemia in systemic sclerosis remains inadequate. We report a double blind, placebo controlled trial of recombinant tissue plasminogen activator (rtPA), a potent thrombolytic agent. Ten patients received rtPA. A potent, acute fibrinolytic effect was observed. During the infusion of rtPA, improvements in skin blood flow were seen. These improvements were shortlived.
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PMID:A double blind placebo controlled trial of recombinant tissue plasminogen activator in the treatment of digital ischemia in systemic sclerosis. 161

An open angiography-based, dose rate escalation study on the effect of intravenous infusion of recombinant tissue plasminogen activator (rt-PA) on cerebral arterial recanalization in patients with acute focal cerebral ischemia was performed at 16 centers. Arterial occlusions consistent with acute ischemia in the carotid or vertebrobasilar territory in the absence of detectable intracerebral hemorrhage were prerequisites for treatment. After the 60-minute rt-PA infusion, arterial perfusion was assessed by repeat angiography and computed tomography scans were performed at 24 hours to assess hemorrhagic transformation. Of 139 patients with symptoms of focal ischemia, 80.6% (112) had complete occlusion of the primary vessel at a mean of 5.4 +/- 1.7 hours after symptom onset. No dose rate response of cerebral arterial recanalization was observed in 93 patients who completed the rt-PA infusion. Middle cerebral artery division (M2) and branch (M3) occlusions were more likely to undergo recanalization by 60 minutes than were internal carotid artery occlusions. Hemorrhagic infarction occurred in 20.2% and parenchymatous hematoma in 10.6% of patients over all dose rates, while neurological worsening accompanied hemorrhagic transformation (hemorrhagic infarction and parenchymatous hematoma) in 9.6% of patients. All findings were within prospective safety guidelines. No dose rate correlation with hemorrhagic infarction, parenchymatous hematoma, or both was seen. Hemorrhagic transformation occurred significantly more frequently in patients receiving treatment at least 6 hours after symptom onset. No relationship between hemorrhagic transformation and recanalization was observed. This study indicates that site of occlusion, time to recanalization, and time to treatment are important variables in acute stroke intervention with this agent.
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PMID:Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke. 164 75

We studied the effects of transforming growth factor-beta (TGF-beta), tissue plasminogen activator (tPA), and their combination in cats subjected to splanchnic artery occlusion (SAO) with reperfusion. Untreated anesthetized cats subjected to total occlusion of the celiac, superior, and inferior mesenteric arteries for 120 min, followed by reperfusion, uniformly died within 120 min after reperfusion. The mean survival time was 75 +/- 8 min. Plasma amino-nitrogen concentrations and cathepsin D and myocardial depressant factor (MDF) activities were markedly elevated following reperfusion. Superior mesenteric artery (SMA) rings isolated from cats subjected to SAO with reperfusion exhibited a significant loss of vasorelaxation to the endothelium-dependent dilators acetylcholine and A-23187. Administration of tPA (1 mg/kg) intravenously just before reperfusion did not prolong survival time (81 +/- 10 min) nor did it influence any biochemical or cardiovascular responses following reperfusion or ameliorate the depressed endothelium-dependent relaxation of SMA rings. In contrast, TGF-beta (50 micrograms/cat) ameliorated the SAO postreperfusion state in terms of survival rate and plasma MDF activity, and protected against depressed endothelium-dependent relaxation of SMA rings. TGF-beta alone slightly increased the survival time to 102 +/- 11 min. However, combined treatment with tPA (1 mg/kg) and TGF-beta (50 micrograms/cat) preserved endothelium-dependent relaxation and prevented increases in plasma amino-nitrogen more prominently than TGF-beta given alone and significantly increased the survival time to 118 +/- 3 min (p less than 0.01). These results indicate that TGF-beta exerts beneficial effects in SAO followed by reperfusion in cats, and tPA has an augmenting action on some of the beneficial effects of TGF-beta. These findings suggest that TGF-beta alone or in combination with tPA may be potentially useful therapeutic regimens in splanchnic ischemia shock by preserving splanchnic parenchymal and endothelial cells.
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PMID:Beneficial effects of transforming growth factor-beta and tissue plasminogen activator in splanchnic artery occlusion and reperfusion in cats. 171 97

This investigation was designed to determine if acute ischemic cardiac injury causes the release of the 98 amino acid (aa) N-terminus of the 126 aa atrial natriuretic factor prohormone (pro ANF). Seventeen patients with acute myocardial infarction, but without clinical evidence of congestive heart failure, had their circulating concentrations of the whole N-terminus (ie, pro ANF 1-98), the midportion of the N-terminus of the ANF prohormone (consisting of aa 31-67; pro ANF 31-67) and creatine phosphokinase (CPK) monitored daily for 14 days. All seventeen patients had elevated plasma pro ANF 1-98 and pro ANF 31-67 concentrations at the time of presentation. Maximal increase on day three post-infarction correlated with the size of infarction estimated by the maximal CPK (r = 0.675; p less than 0.05) but did not correlate with the amount of left ventricular dysfunction. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured pro ANF 1-98 and pro ANF 31-67 levels in these patients were within our normal range and significantly lower (p less than 0.001) than seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina, likewise, had normal circulating pro ANFs 1-98 and 31-67 concentrations during prolonged episodes of chest pain. These data suggest that myocardial necrosis but not ischemia triggers the release of the entire 126 aa prohormone.
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PMID:Acute and sustained release of the atrial natriuretic factor prohormone N-terminus with acute myocardial infarction. 182 42

The effects of exercise training on myocardial perfusion during the first 3 months after acute myocardial infarction (AMI) were assessed by exercise myocardial scintigraphy and fibrinolytic examinations. Symptom-limited treadmill exercise with thallium-201 myocardial single photon emission CT (SPECT) and fibrinolytic examinations (tissue plasminogen activator antigen: tPA, plasminogen activator inhibitor-1 antigen : PAI-1) were performed 2 and 14 weeks after AMI in 13 patients with exercise training and in 12 patients without exercise training. For quantitative analysis, counts of region of interest in the infarct area and normal reference area were calculated on a polar map obtained from myocardial SPECT. Severity of the hypoperfused myocardium was determined as an initial percent uptake (%IU) and a delayed percent uptake (%DU). The difference (%DU-%IU) was defined as a parameter of residual ischemia in the infarct area (%redistribution : %RD). Total treadmill exercise duration according to the Bruce protocol increased significantly in the training group (351 +/- 89 to 431 +/- 118 sec, p < 0.01); whereas, there was no significant change in the non-training group (340 +/- 95 to 356 +/- 123 sec). In the training group the pressure-rate product and %DU increased significantly (225 +/- 55 to 259 +/- 58 mmHg.beats/min x 100, 59 +/- 19 to 65 +/- 20%, p < 0.01, respectively), and %RD decreased significantly (8.8 +/- 6.7 to 4.8 +/- 4.5%, p < 0.01), but there was no significant change in the non-training group (231 +/- 89 to 240 +/- 86 mmHg.beats/min x 100, 56 +/- 17 to 57 +/- 12% and 7.4 +/- 5.5 to 6.2 +/- 6.5%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac rehabilitation in patients with acute myocardial infarction: assessments with T1-201 myocardial scintigraphy]. 184 44

This paper reports the immediate effects of thrombolysis and their subsequent influence on revascularisation procedures and clinical outcome over the subsequent twelve months. Coronary arteriography was performed at 21 days on 131 of 145 patients who received recombinant tissue plasminogen activator (n = 68) or placebo (n = 63) within 2.5 hours of symptom onset after primary coronary occlusion. Patency rates (TIMI grades 2 and 3) of the infarct-related artery were 81% with plasminogen activator and 63% with placebo (P = 0.02). Early (within 21 days) angiography for recurrent ischaemia was necessary in 31 (21%) patients (20 plasminogen activator, 11 placebo NS) and definite reinfarction occurred in 8 (5%) patients (4 plasminogen activator, 4 placebo). During one year follow-up without planned secondary intervention, coronary artery bypass grafting was more frequent in patients who had received thrombolytic therapy (23% plasminogen activator, 4% placebo P = 0.001); coronary angioplasty procedures were similar in both groups (12% plasminogen activator, 11% placebo NS). Mortality at 21 days was 5% (4 plasminogen activator, 4 placebo) and at one year was 7% (5 plasminogen activator, 5 placebo). Logistic regression analysis identified models comprising characteristics predictive of subsequent bypass grafting (plasminogen activator, multivessel disease, occluded infarct-related artery) and coronary angioplasty (non-q wave infarction, severe (91-99%) residual stenosis, left anterior descending infarct-related artery). Initial non-q wave infarction was the only predictor of early recurrent ischemia (odds ratio 4, P = 0.02) irrespective of residual stenosis severity.
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PMID:Determinants of recurrent ischaemia and revascularisation procedures after thrombolysis with recombinant tissue plasminogen activator in primary coronary occlusion. 189 9

The effect of an intravenous infusion of recombinant tissue plasminogen activator on hemorrhagic transformation early after middle cerebral artery territory ischemia was studied in an established awake nonhuman primate (baboon) model. Following 3 hours' occlusion of the middle cerebral artery and 30 minutes' reperfusion in each of 30 baboons, a 60-minute infusion of recombinant tissue plasminogen activator (at three doses: Group A, 0.3 mg/kg, n = 6; Group B, 1.5 mg/kg, n = 6; Group C, 10 mg/kg, n = 6) or normal saline (n = 12) was undertaken. The frequency and volume of intracerebral hemorrhage, the volume of infarction, and clinical alterations were determined by computed tomography at 24 hours and 10 days, neuropathology at 14 days, and serial daily neurologic evaluations, respectively. Peripheral (nonintracranial) hemorrhage (Group A, p = 0.46; Group B, p = 0.015; Group C, p = 0.002) and peak plasma tissue plasminogen activator levels varied directly with the dose of recombinant tissue plasminogen activator. Petechial hemorrhagic infarction was a common finding among the 30 baboons. No significant differences in the incidences or volumes of infarction-related hemorrhage were apparent in any group compared with the respective saline-treated baboons. In pooled data, no significant relation between the volume of hemorrhage and the volume of infarction could be established. We conclude that the incidence and severity of hemorrhagic transformation are not related to infarction size and that recombinant tissue plasminogen activator does not increase the incidence or severity (volume) of hemorrhage when given early (less than or equal to 3.5 hours) after the onset of focal cerebral ischemia in this model.
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PMID:Hemorrhagic transformation following tissue plasminogen activator in experimental cerebral infarction. 210 75

Reported is the case of a patient with vertebrobasilar artery ischemia who received tissue plasminogen activator with resulting hemorrhage into the tongue and nearly exsanguinating hemorrhage from a branch of the lingual artery. Suggestions for immediate management of the hemorrhage as well as prevention are presented. As the use of thrombolytic agents increases and the list of their indications expands, unusual life-threatening hemorrhagic problems other than gastrointestinal or intracranial bleeding will be seen, and management decisions may be life saving.
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PMID:Tissue plasminogen activator-associated lingual artery hemorrhage. 212 Oct 76

A prospective randomized study was undertaken in 50 patients treated with intravenous thrombolysis (streptokinase, tissue plasminogen activator, association of the two thrombolytics) for acute myocardial infarction to determine the best time to perform percutaneous transluminal coronary angioplasty (PTCA). Coronary angiography was carried out 24 to 72 hours after thrombolysis. This investigation allowed identification of the patients in whom PTCA was technically feasible. These patients were then divided into two groups: Group A: early PTCA (24-72 hours) and Group B: delayed PTCA (8-10 days). During the hospital period, the patients were prescribed heparin therapy and aspirin. Recurrent ischemia (RI) was investigated and treated by PTCA. The criteria of success of strategies A and B were a primary success of PTCA and no RI during the hospital period. Coronary angiography was performed in 108 successive patients of whom 50 were included for the comparative trial, 25 in Group A and 25 in Group B. In group A, PTCA was successful in 24 cases and there were 2 incidents of RI (6 hours and 12 days). In Group B, 4 episodes of RI were observed in the 24 hours following coronary angiography: after 10 days, 15 of the 20 patients with uncomplicated courses underwent PTCA; 1 patient refused consent, 2 regressions of stenosis and 3 asymptomatic reocclusions were observed. A primary success of PTCA was obtained in 13 of the 15 patients. There was no statistically significant difference between the results of the strategies adopted in Groups A and B. A therapeutic success was obtained in 22 of the 25 patients in Group A, and 19 of the 25 patients in Group B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immediate delayed coronary angioplasty after intravenous thrombolysis in myocardial infarction. Prospective study]. 212 55


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