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)

A thirty-one-year-old woman with long-standing mixed connective tissue disease and severe obliterative vasculopathy of the digits developed digital thrombosis of the first three digits of the left hand after using an electric blow dryer. The digits remained cool, cyanotic, and painful for thirty-six hours before medical evaluation. She was given 100 mg recombinant tissue plasminogen activator (TPA) intravenously. Within one hour the blood flow to the digits returned, accompanied by severe intermittent vasospasm of the digits. The thumb did not necrose; however, the second and third digits required amputation. No improvement was noted in the patient's baseline Raynaud's phenomenon or digital pressures of the uninvolved digits after TPA treatment. This case documents the usefulness of TPA for digital thrombosis in the setting of vasculopathy of connective tissue disease. However, it does not support the utility of a single dose of TPA for severe Raynaud's phenomenon and recurrent digital ischemia in patients with connective tissue disease.
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PMID:Tissue plasminogen activator treatment of digital thrombosis in severe Raynaud's phenomenon--a case report. 832 85

The purpose of this study was to investigate the effects of beraprost sodium, a stable prostacyclin analog, on the parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. Thirty-one patients with exertional angina who had significant organic coronary artery stenosis in at least one of the three major coronary arteries were selected. All patients underwent quantitative exercise thallium-201 emission computed tomography before and 1 month after 120 micrograms per day of beraprost sodium administration. Before exercise, blood samples were collected from 8:30 a.m. to 9:30 a.m. after the patients had been lying in bed undisturbed for at least 10 minutes. Plasma platelet factor 4 (PF4), fibrinopeptide A (FPA), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 activity (PAI-1) were measured. There were no significant differences in exercise parameters on both exercise tests. However, both the extent and severity scores of ischemia were significantly aggravated (p < 0.05 for both) during beraprost sodium administration. Plasma FPA levels decreased significantly during beraprost sodium administration (p < 0.01). Likewise, plasma PF4 levels decreased significantly during beraprost sodium administration (p < 0.05). As for plasma t-PA antigen levels, there was no significant difference before versus during beraprost sodium administration. Plasma PAI-1 activity levels decreased significantly during beraprost sodium administration (p < 0.05). The results indicate that beraprost sodium has strong antithrombogenic properties. However, its aggravation of myocardial ischemia may limit clinical usage.
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PMID:Effects of beraprost sodium, a new prostaglandin I2 analog, on parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. 854 11

Although coronary thrombosis is thought to play a pivotal role in the pathogenesis of unstable angina and non-Q wave myocardial infarction and antithrombotic therapy is a mainstay in the early management of these patients, the relation between measures of systemic anticoagulation and clinical events has not been defined clearly. In the Thrombolysis in Myocardial Ischemia III trial, 1473 patients with ischemic chest pain at rest evaluated within 24 hours of symptom onset were randomized to (1) tissue plasminogen activator (TPA) or placebo and (2) an early invasive or an early conservative strategy. All patients received a full complement of anti-ischemic medication, aspirin, and continuous intravenous heparin titrated to an activated partial thromboplastin time (aPTT) of 1.5 to 2.0 times control for 72 to 96 hours. The median aPTT in all study groups exceeded the minimum threshold (45 seconds) by 24 hours and remained within the designated range during the protocol-directed heparin infusion. No differences in median aPTT values for the 72- to 96-hour study period were observed between groups (p=not significant). Median 12-hour heparin concentrations were >0.2 U/ml in all groups; however, values <0.2 U/ml were common thereafter, particularly in TPA-treated patients. Time-dependent covariate analyses failed to identify statistically significant differences in either aPTT or heparin levels between patients with in-hospital clinical events (spontaneous ischemia, myocardial infarction, or death) and those without events (p=0.27). Furthermore, early clinical events occurred in a similar percentage of patients with optimal anticoagulation (all aPTTs >60 seconds, all heparin levels>0.2 U/ml), and those with aPTTs or heparin levels below these thresholds. Aggressive (high-intensity) anticoagulation with heparin to achieve aPTTs >2.0 times control does not appear to offer additional clinical benefit to lower levels (1.5 to 2.0 times control) among patients with unstable angina and non-Q wave myocardial infarction receiving intravenous heparin and oral aspirin. Therefore, the optimal level of anticoagulation in this common clinical setting is between 45 and 60 seconds when heparin is included in the treatment strategy. Direct plasma heparin measurement does not offer an advantage to routine aPTT monitoring. The occurrence of spontaneous ischemia, myocardial infarction, and death in spite of antischemic therapy and optimal anticoagulation (as it is currently defined) with heparin supports ongoing efforts to develop more effective antithrombotic agents.
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PMID:Relation between systemic anticoagulation as determined by activated partial thromboplastin time and heparin measurements and in-hospital clinical events in unstable angina and non-Q wave myocardiaL infarction. Thrombolysis in Myocardial Ischemia III B Investigators. 860 20

A previously healthy woman presented with ischemic cardiac pain and ST elevation suggestive of acute myocardial infarction following a 45 min argument. Despite receiving tissue plasminogen activator, she developed cardiogenic shock and objective evidence of recurrent ischemia, with only a small creatine kinase rise. Angiography revealed the unexpected findings of normal coronary anatomy and akinesis of the distal two-thirds of the left ventricle. Apart from an iliac vein thrombosis, the remainder of her course was characterized by dramatic recovery of cardiac function. The differential diagnosis of myocardial infarction with angiographically normal coronary arteries is discussed, with emphasis on aspects relevant to this case. The presence of high titre anticentromere antibodies, anticardiolipin antibodies, protein S deficiency and supportive physical findings, suggested the diagnosis of concurrent antiphospholipid antibody syndrome (with secondary acquired protein S deficiency) and CREST syndrome. The pathogenesis likely involved an interaction between stress, vasospasm, and thrombosis.
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PMID:Reversible cardiogenic shock in an angry woman--case report and review of the literature. 868 41

In the Primary Angioplasty in Myocardial Infarction trial, 395 patients with acute myocardial infarction (AMI) were prospectively randomized to tissue plasminogen activator (tPA) or primary percutaneous transluminal coronary angioplasty (PTCA). In 138 patients with anterior wall AMI, in-hospital mortality was significantly reduced by treatment with PTCA compared with tPA (1.4% vs 11.9%, p = 0.01). PTCA also resulted in lower rates of death or reinfarction (1.4% vs 18.0%, p = 0.0009), recurrent myocardial ischemia (11.3% vs 28.4%, p = 0.01), and stroke (0.0% vs 6.0%, p = 0.037) in anterior wall AMI. The independent beneficial effect of treatment with primary PTCA rather than tPA in anterior wall AMI was confirmed by multivariate analysis and interaction testing. The in-hospital mortality of 257 patients with nonanterior wall AMI was similar after PTCA and tPA (3.2% vs 3.8%, p = 0.82). Compared with tPA, however, primary PTCA resulted in a markedly lower rate of recurrent myocardial ischemia (9.7% vs 27.8%, p = 0.0002), fewer unscheduled catheterization and revascularization procedures, and a shorter hospital stay (7.0 vs 8.6 days, p = 0.01) in nonanterior wall AMI. Thus, compared with tPA, primary PTCA in patients with anterior wall AMI results in significantly improved survival, with lower rates of stroke, reinfarction, and recurrent myocardial ischemia. In nonanterior wall AMI, treatment with PTCA and tPA results in similar early mortality, although PTCA-treated patients have a more stable hospital course characterized by reduced recurrent ischemia, fewer subsequent invasive procedures, and earlier discharge.
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PMID:Influence of acute myocardial infarction location on in-hospital and late outcome after primary percutaneous transluminal coronary angioplasty versus tissue plasminogen activator therapy. 871 12

The use of fibrinolytic agents in acute ischemic stroke has received increasing attention due to the completion of several prospective studies examining the efficacy and safety of these drugs in this clinical setting. Experience with plasminogen activators indicates that recanalization of carotid and vertebrobasilar territory occlusion is feasible within 4-6 hours of symptom onset. The optimal plasminogen activator, its dose-rate and delivery system, however, is not known. The phase III trial of the European Cooperative Acute Stroke Study (ECASS) suggests potential modest benefit in outcome, although recombinant tissue plasminogen activator (rt-PA) had an increased risk of hemorrhage attributable to those patients with early CT-scan signs of ischemia. Complete cervical internal carotid artery occlusions by in situ thrombosis appear more resistant to thrombolysis than occlusions of the stem and major branches of the middle cerebral artery. The issue of hemorrhagic transformation is unsettled. It seams to be increased by delayed intervention on the one hand, but it is not different from that observed in placebo patients in phase I/II series.
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PMID:Thrombolysis in acute stroke. 871 49

Therapy for stroke is undergoing major changes. Many of the changes parallel the advances made in the therapy for myocardial infarction. Acute intervention with cytoprotective and thrombolytic agents is undergoing active investigation. Cytoprotective therapy includes drugs that act to prevent cell death during ischemia and reperfusion. These agents include calpain inhibitors, voltage-sensitive calcium- and sodium-channel antagonists, receptor-mediated calcium-channel antagonists [including N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) antagonists], glutamate-synthesis inhibitors, glutamate-release antagonists, gamma-aminobenzoic acid (GABA) antagonists, 5-HT (serotonin) receptor agonists, gangliosides, antioxidants, growth factors, antiapoptotic agents, and antiadhesion molecules. Thrombolysis is effective in myocardial infarction. Thrombolysis is undergoing evaluation in stroke with streptokinase, anisoylated plasminogen streptokinase activator complex (APSAC), tissue plasminogen activator (t-PA; including recombinant t-PA), urokinase, and single-chain urokinase (scu-PA). Both systemic and selective administration are being evaluated. Preventive therapy with both antiplatelet and anticoagulant drugs sheds new light on how best to stratify patients in terms of a risk-benefit ratio. Continuing public education will be essential as stroke therapy advances.
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PMID:Medical therapy for ischemic stroke. 877 66

To characterize the vasospastic angina patients with exercise-induced ischemia, we measured hemostasis (platelet factor 4; PF4, fibrinopeptide A; FPA) and fibrinolytic parameters (tissue plasminogen activator antigen; t-PA, free plasminogen activator inhibitor-1 antigen; free PAI-1) in 15 normal subjects and 33 vasospastic angina patients without significant coronary artery stenosis (less than 50% stenosis). All of the vasospastic angina patients began to feel chest pain within 3 months before diagnostic coronary angiography. Blood samples were obtained from all of the study patients at 8:30-9:30 am before exercise 201Tl emission computed tomography. Vasospastic angina patients were divided into 2 groups; 15 patients with exercise-induced ischemia (group 1) and 18 patients without exercise-induced ischemia (group 2). On coronary angiography, the severity of coronary artery stenosis at the site of spasm in group 1 (34 +/- 5%) was greater than that in group 2 (18 +/- 3%). Plasma FPA and PF 4 levels in group 1 were also significantly higher than those in normal subjects and group 2. Plasma t-PA and free PAI-1 levels in group 1 were significantly higher than those in normal subjects and group 2. Plasma levels of free PAI-1 group 2 were also significantly higher than those in normal subjects. The present study demonstrated that all of the patients with vasospastic angina had impaired fibrinolysis, and these patients with exercise-induced ischemia showed enhanced platelet activation, an enhanced coagulation system, and advanced atherosclerotic lesions. These results suggest that vasospastic angina with exercise-induced ischemia puts patients at increased risk for thrombus formation.
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PMID:Characteristics of vasospastic angina with exercised-induced ischemia--analysis of parameters of hemostasis and fibrinolysis. 880 21

We analyzed the 395 patients randomized into the Primary Angioplasty in Myocardial Infarction (PAMI) trial to receive tissue plasminogen activator (tPA) or to undergo primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI). Of these, 168 were current smokers and 128 had never smoked. Univariate analyses of baseline characteristics and outcome, including death, recurrent AMI, and recurrent ischemia, were done by chi-square analysis. Multivariate stratified analysis was then performed controlling for age and gender, which were found to be confounders of outcome. The combined in-hospital outcomes of death, recurrent AMI, and recurrent ischemia were similar for smokers and nonsmokers (p = 0.12). When stratified according to treatment modality, non-smokers treated with PTCA had a lower frequency of death and nonfatal recurrent AMI (7% vs 18%; p = 0.05), in-hospital ischemia (11% vs 33%; p = 0.004), or the combined event (13% vs 40%; p = 0.001). At 6 months, nonsmokers treated with PTCA continued to have a lower incidence of death or nonfatal recurrent AMI (11% vs 24%; p = 0.07) compared with tPA. Conversely, in smokers, the treatment strategy did not significantly affect hospital outcomes: recurrent ischemia (12% vs 23%; p = 0.07), death and recurrent AMI (6% vs 8%; p = 0.55), or the combined event (15% vs 25%; p = 0.12). The statistical significance of these associations was maintained when multivariate analysis controlling for age and gender was used. Thus, nonsmokers presenting with AMI had a significantly better outcome when treated with primary angioplasty; these differences were not seen in smokers.
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PMID:Effect of reperfusion modality on outcome in nonsmokers and smokers with acute myocardial infarction (a Primary Angioplasty in Myocardial Infarction [PAMI] substudy). PAMI Investigators. 880 33

The causes of perioperative ischemia and myocardial infarction (MI) in coronary artery bypass graft (CABG) patients are almost certainly multifactorial, although not well understood. Ultimately, outcome after CABG is dependent on myocardial preservation and prevention of further myocardial ischemia. The largest number of ST-T-wave events come immediately after protamine is given, suggesting that re-establishment of coagulation function after cardiopulmonary bypass (CPB) may be an important event. CPB induces an inflammatory state that involves platelet-endothelial-cell interactions and vasospastic responses that result in low flow states in the coronary vasculature. The fibrinolytic system is activated during CPB, with raised tissue plasminogen activator (tPA) levels and related falls in plasminogen activator inhibitor (PAI-1). PAI-1 levels rise during the postoperative period. There is a huge variability in human response. However, the patients with the highest tPA surge are not the same patients who have the highest PAI surge. It could be postulated that patients with high PAI-1 levels are at highest risk for early ischemia. New data just being evaluated from the Multicenter Study of Perioperative Ischemia (McSPI) Research Groups' database in San Francisco may support the hypothesis that coagulation influences perioperative ischemia. The study of approximately 2,400 patients undergoing CABG surgery at 24 major institutions in the United States revealed that intensive care unit (ICU) entry hematocrit was significantly related to the risk for postoperative MI. Patients entering the ICU with hematocrits below 24% had the lowest MI rate (3.7%), whereas those with hematocrits greater than 34% had the highest rate (8.1%). Patients with ICU entry hematocrits below 18% had a zero incidence of perioperative MI. One possible explanation for these findings is that platelets are involved. As red cells stream down vessels, they marginate the smaller formed elements of the blood. As hematocrit is increased, the number of platelets moved to the outer sides of the vessels increases. Therefore, the number of endothelial-platelet interactions would increase over time with higher hematocrits.
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PMID:Ischemia--a coagulation problem? 893 82


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