Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two hundred five men, 40 to 70 years of age, admitted to the coronary care unit with unstable coronary artery disease (unstable angina or non-Q wave myocardial infarction), were randomized to double-blind placebo-controlled treatment with an intravenous infusion of recombinant tissue-type plasminogen activator (rTPA), 1 mg/kg body weight (maximum 100 mg) during 4 hours, in addition to aspirin, heparin, and beta-blockade. No severe complications occurred. Myocardial ischemia, defined as myocardial infarction, incapacitating angina despite medication, or signs of ischemia at the exercise test, was reduced by treatment with rTPA compared with placebo both at discharge, 53% compared with 70% (p = 0.02), and at 1 month, 61% compared with 80% (p = 0.005). Signs of myocardial ischemia during the exercise test were reduced at discharge 51.0% compared with 68% (p = 0.03) and at 1 month 48% compared with 62% (p = 0.09). Coronary angiography after 1 month showed no difference in major coronary lesions between the groups, nor was there any reduction in the number of performed coronary revascularization procedures. In conclusion, treatment with rTPA in unstable coronary artery disease in men reduced myocardial ischemia but did not significantly reduce the need for revascularization in long-term follow-up.
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PMID:Thrombolysis with recombinant human tissue-type plasminogen activator during instability in coronary artery disease: effect on myocardial ischemia and need for coronary revascularization. TRIC Study Group. 146 94

We measured levels of tissue plasminogen activator (t-PA) antigen in 100 patients within six hours of the onset of acute myocardial infarction, in 34 patients with chronic angina but no recent infarction, and in 36 normal subjects. We also assayed von Willebrand factor in the acute patients and in the normal subjects. Measurements were repeated in 40 acute patients at three weeks after myocardial infarction. Although resting levels of t-PA antigen were not significantly different from normal during myocardial infarction, the capacity of the vascular endothelium to release t-PA after five minutes of venous occlusion was impaired (p less than 0.01). The acute phase vessel wall release of von Willebrand factor was increased during acute infarction (p less than 0.01). We conclude that impairment of t-PA production is associated with acute coronary thrombosis, although it is not possible to differentiate between a causative role or a secondary response due to exhaustion of the t-PA producing mechanism.
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PMID:Reduced synthesis of tissue plasminogen activator by vascular endothelium during acute myocardial infarction. 149 53

Eighty-nine consecutive Chinese patients (69 males, 20 females) with acute myocardial infarction treated by 100 mg recombinant tissue-plasminogen activator (rt-PA) (7 intracoronarily, 82 intravenously) at 3.7 +/- 1.0 hours after onset, and intravenous heparin or dipyridamole therapy started at 3 hours, were studied prospectively. Their mean age was 59.6 +/- 10.6 years. Forty-six patients (51.7%) had anterior and 39 patients (43.8%) had inferior infarcts. Clinical evidence of reperfusion was seen in 63 patients (72.8%), while new complications included hypotension (5.6%), heart failure (6.7%), cardiac arrhythmias (76.4%), hematoma around vascular access sites (23.6%), melena (2.2%) and cerebral infarction (2.2%). Maximal changes in coagulation profiles were seen at 3 hours, including a decrease in fibrinogen (by 64.2%), an increase in FDP by 11.7 times and D-dimers by 4.4 times. Nine patients (10.1%) had recurrence of angina and 6 patients (6.9%) died due to pump failure (5) and reinfarction (1). Angiogram at 14 days confirmed TIMI (2 or 3) patency of infarct related arteries in 62/81 (76.5%) patients, with a mean global ejection fraction of 52.5 +/- 12.4%. Nearly all survivors could maintain class I-II functional status after discharge. The safety and promises of rt-PA for acute myocardial infarction in the Chinese were confirmed.
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PMID:Recombinant tissue-plasminogen activator (rt-PA) in acute myocardial infarction in the Chinese in Hong Kong. 149 66

With intravenous thrombolysis mortality of acute myocardial infarction can be significantly reduced, not only in the first hours after the onset of symptoms, but also up to 24 hours. The open infarct related coronary artery is important concerning long-term clinical outcome. If thrombolysis can be administered within the first three to six hours, limitation of infarct size and preservation of left ventricular function contribute to an impressive reduction in mortality. Long-term assessments of clinical outcome have surprisingly shown that the prognosis is much more dependent upon patency of the infarct related artery than from the time to treatment. Since a correlation is suspected between the degree of residual stenosis and the clinical course, recurrence of ischemia, reinfarction, hemodynamic instability and death, and the fact that mortality is highest within the first three days after thrombolysis the emphasis of numerous investigations has been on possibilities of PTCA in the acute stage of myocardial infarction. The application of interventional techniques was tested at different times within the progression of myocardial infarction. PTCA can be applied as primary, direct therapy without thrombolysis, immediately and during intravenous thrombolysis, following successful pharmacological recanalisation, as rescue-PTCA for failed thrombolytic therapy, delayed and as a prophylactic measure up to until days after the infarction or later when accompanied by careful observation of the patient, when limited to few indications with spontaneous or stress-related angina pectoris, hemodynamic instability or predetermined angiographic criteria. Important results have been gathered by the larger studies of the last few years, TAMI, ECSG, and TIMI as well as by numerous smaller investigations, about the pathophysiology and treatment of myocardial infarction. Despite different study design, the three larger trials have come to the same conclusion regarding PTCA and rt-PA thrombolysis, early PTCA is without advantage compared to a deferred treatment; the acute results are usually worse and the clinical course more complicated. It must be mentioned however, that major problems still remain unresolved: primary or direct angioplasty, PTCA in combination with non-fibrin specific plasminogen activators, as well as rescue-PTCA after failed thrombolysis. Specially, 90 minutes after thrombolysis 23 to 44% of the coronaries are still occluded, depending on the plasminogen activator, and there is no non-invasive procedure to detect this patient-group and to advise further treatment. Due to the high mortality rate within the first three days attempts of treatment are concentrated on this time-span.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[PTCA in acute myocardial infarct: primary, immediate, delayed or elective?]. 154 50

The significance of antecedent angina in predicting clinical outcome was assessed in 8,329 patients with acute myocardial infarction who received thrombolytic therapy with either recombinant tissue-type plasminogen activator or streptokinase. There were 2,370 patients with antecedent angina for greater than 1 month, 1,512 patients with antecedent angina for less than or equal to 1 month and 4,447 patients with no antecedent angina. The longer the duration of angina, the worse the baseline characteristics in the three groups: the mean patient age was 65 versus 62 versus 61 years, respectively (p less than 0.0001); the rate of previous myocardial infarction was 37% versus 18% versus 10% (p less than 0.0001); and the rate of hypertension was 40% versus 31% versus 27% (p less than 0.0001). Antecedent angina was associated with a longer hospital stay (11.3 and 11.7 days vs. 10.8 days, p less than 0.0001), a higher incidence of bypass surgery (2.2% vs. 1.2% vs. 0.7%, p = 0.0001), a worse Killip class at discharge (10.6% of patients in class greater than 1 vs. 8.7% vs. 6.4%, p = 0.0001), and a higher hospital and 6-month mortality (12.1% and 18% vs. 8.9% and 11.6% vs. 6.6% and 9.2%, respectively, p less than 0.0001). A multivariate analysis taking into account all baseline characteristics confirmed the independent association of antecedent angina with mortality, with a relative risk of 1.4 to 1.47 (p less than 0.001). Antecedent angina predicts a worse clinical outcome and a more intense use of medical resources in patients with acute myocardial infarction receiving thrombolytic therapy.
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PMID:Antecedent angina pectoris predicts worse outcome after myocardial infarction in patients receiving thrombolytic therapy: experience gleaned from the International Tissue Plasminogen Activator/Streptokinase Mortality Trial. 160 36

The authors examined the activities of plasminogen activator, its inhibitor, the levels of C protein, antithrombin III, alpha 2-antiplasmin, plasminogen, fibrinogen, fibrinogen/fibrin degradation products in 22 patients with unstable angina by using the vein occlusive test. No significant differences were found in the examined parameters while comparing the group of stable angina patients and healthy subjects. It was concluded that thrombogenesis disturbances in unstable angina were regional and the recording of peripheral blood fibrinolytic parameters failed to detect any changes characteristic of unstable angina.
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PMID:[Unstable angina: tissue plasminogen activator, tissue plasminogen activator inhibitors, protein C and other factors of the blood fibrinolytic system]. 167 68

The clinical effect of a low-dose rapid-infusion intravenous regimen was assessed using human recombinant tissue-type plasminogen activator (rt-PA) in unstable angina. Fifty patients with unstable angina pectoris were randomly assigned to blinded treatment with either placebo (24 patients) or low-dose (20 mg bolus, 30 mg infusion over 1 hour) intravenous rt-PA (26 patients). Before randomization, all patients were treated with aspirin, twice-daily subcutaneous heparin, and maximally tolerated antianginal therapy. Of the 50 patients assigned, 26 received rt-PA and the outcome was successful in 15 (58%) (angina settled, no myocardial infarction or urgent intervention) compared with 9 (38%) successful outcomes in the 24 who received placebo (0.5 greater than p greater than 0.1). Angina remained refractory in 8 (31%) of the rt-PA group and in 13 (54%) of the placebo group (0.1 greater than p greater than 0.05). Urgent interventions were required in 6 patients (23%) who received rt-PA and in 11 patients (46%) who received placebo. Three patients in each group sustained a myocardial infarction within 72 hours of entering the trial and there were 3 deaths (1 in the active treatment group, 2 in placebo group) within 2 weeks of the trial (p = not significant). Administration of intravenous rt-PA was not associated with any complications. Low-dose rt-PA administration in patients with unstable angina was associated with a tendency to stabilization of anginal symptoms and a reduction in the need for urgent intervention. However, these trends did not achieve statistical significance.
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PMID:Tissue plasminogen activator using a rapid-infusion low-dose regimen for unstable angina. 173 54

To assess the role of fibrinolytic system, 19 patients with rest angina and insignificant coronary artery stenosis and 23 controls performed symptom-limited multistage exercise. Vasospasm was angiographically demonstrated in 12 patients. Pre- and peak exercise blood samples from each patient were assayed to determine the fibrinolytic components. The patients displayed significantly increased PAI activity both under the basal conditions (p less than 0.01) and at peak exercise (p less than 0.01) as compared with the controls. However, the values of other fibrinolytic components, such as t-PA antigen, t-PA/PAI-1 complex and free PAI-1 antigen, in the controls and patients were similar. Nineteen patients were divided into two groups according to PAI activity levels under basal conditions. Nine patients displayed high PAI activity (more than the mean + 1 SD of the control value) under the basal conditions. When compared to the remaining 10 patients, the high PAI activity group had both a significantly short time interval from the last attack to the time of getting the blood sample (p less than 0.05), and a worse short-term prognosis (p less than 0.05). Thus, the level of PAI activity under basal conditions reflected the extent of disease activity, suggesting that PAI activity may be a useful clinical indicator of the severity of rest angina in patients without significant coronary stenosis.
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PMID:Plasminogen activator inhibitor activity as a possible indicator of disease activity in rest angina with angiographically insignificant coronary artery stenosis. 175 2

To evaluate the effect of recombinant tissue plasminogen activator (alteplase) on the clinical course, angiographic changes and the outcome of subsequent coronary angioplasty, 36 patients with angina at rest, despite bedrest and medical treatment including heparin, and with concomitant ECG changes, were studied. After diagnostic angiography, patients were randomized to receive either alteplase 100 mg in 3 h (19 patients), or placebo (17 patients). The mean interval between qualifying anginal episode and initial angiography was 10 and 9 h for the alteplase and placebo group, respectively. Angiography was repeated and angioplasty was performed within 24 hours. Between the first and the second angiogram, five patients in the alteplase and seven in the placebo group had recurrent ischaemic episodes, while four alteplase and three placebo patients showed signs of myocardial necrosis (creatine kinase (CK) rise greater than or equal to twice the upper limit for normal). Intracoronary clots were recognized in three alteplase patients and one placebo patient at the first angiogram, while two alteplase patients and one placebo patient showed total occlusion of the ischaemic-related vessel. After infusion, thrombi were present in four alteplase patients and one placebo patient, and total occlusion in three alteplase patients and one placebo patient. Quantitative coronary angiography showed no change in the percentage diameter stenosis of the ischaemia-related segment after drug infusion, (alteplase 67 +/- 16 to 69 +/- 16%; placebo 65 +/- 11 to 63 +/- 12%). Angioplasty was successful in 14 of 19 alteplase and 14 of 16 placebo patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue plasminogen activator in refractory unstable angina. A randomized double-blind placebo-controlled trial in patients with refractory unstable angina and subsequent angioplasty. 178 51

Fibrinolysis and lipid disturbances have been considered as independent risk factors for coronary artery disease. Besides this, lipoprotein(a), which is characterized by its homology with plasminogen may interfere with the fibrinolytic function. To evaluate the eventual correlation between fibrinolytic parameters, lipoprotein (a) and other risk factors, 46 patients with coronary artery disease (34 with chronic angina pectoris and 12 with myocardial infarction) were studied. Increased basal values of t-PA antigen (8.2 and 6.6 vs. 4.2 ng/ml) but decreased response after stimulus (2.2 and 1.8 vs. 3.8 ng/ml) and increased levels of lipoprotein(a) (24.7 and 35.9 vs. 10.5 mg/dl) were the most relevant differences between coronary artery disease patients and controls. No correlation between lipoprotein(a) and fibrinolytic parameters was found. Therefore plasma concentration of the main plasma fibrinolytic parameters and lipoprotein(a) seem to be unrelated though the relevance of this interaction at a local level needs to be studied.
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PMID:Fibrinolytic parameters and lipoprotein (a) levels in plasma of patients with coronary artery disease. 183 82


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