Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of several major trials of i.v. thrombolysis in patients with acute myocardial infarction have demonstrated the efficacy of the treatment in reducing mortality. Streptokinase and rt-PA have been shown to be effective (APSAC = anisoylated plasminogen streptokinase activator complex; GISSI = Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto miocardico, ASSET = Anglo Scandinavian study of early thrombolysis, rt-PA). This treatment is associated with the potential for cerebral and major bleeding, especially in elderly patients. The benefit of this treatment in patients with cardiogenic shock or hypotension (ISIS-2) is discussed. There is no convincing evidence that patients with ST-segment depression or those with an equivocal electrocardiogram had been benefited from i.v. thrombolysis. Further studies with i.v. thrombolysis and/or other strategies need to be explored. Overall the use of i.v. thrombolytic agents in combination with PTCA in patients with acute myocardial infarction have resulted in improvement in ventricular function and survival in patients eligible for this therapy. However, new techniques and therapeutic approaches to prevent reocclusion, to prevent reperfusion injury, to prevent restenosis after PTCA, to prevent atherosclerosis in the infarct and non-infarct related arteries, and to reduce the potential for ventricular arrhythmias and sudden death as well as the potential for mural thrombi and embolization after infarction are needed. The 1990's will see attempts to determine the optimum adjunctive therapy or "cocktail" of agents to be used with i.v. thrombolysis.
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PMID:Thrombolysis in acute myocardial infarction: need for a change in strategy and future directions. 212 41

The purpose of this study is to analyze the relationship between occurrence of hemorrhagic complications, kinetic of fibrinogen degradation-regeneration and the changes of prothrombin time (PT), partial thromboplastin time (PTT), after intravenous administration of Streptokinase (SK), 1.500.000 U., in acute myocardial infarction. 45 selected patients with acute myocardial infarction had pretreatment analysis and serial post-SK measurement of fibrinogen levels, PT, PTT (for 48 hours). Basal fibrinogen levels were 3.2 g/l and displayed significant depression for 18 hours (0.30-0.46 g/l) and normalization after 30 hours from SK infusion. Similar behaviour showed PT and PTT. Minor bleeding was identified in 25 patients. In bleeders mean fibrinogen levels, PT, PTT before and maximum changes after SK were not significantly different compared with non bleeders. We conclude that SK infusion produces important and prolonged changes of fibrinogen levels, PT, PTT; hemorrhagic risk is not related, however, to the extent of lytic state, but probably to pre-existent vascular derangement, predisposing to bleeding complications during fibrinolytic therapy. Therefore we believe to be prudent to delay the infusion of heparin for 12-18 hours after SK administration, when fibrinogen levels are beginning to increase.
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PMID:[Fibrinolysis and hemorrhage after streptokinase in acute myocardial infarct]. 367 11

The rabbits with CCl4-induced hepatic failure have revealed changes in hemostasis responses to streptokinase administration. The main distinction of hepatic dystrophy was the depression of plasma fibrinolytic activity accompanying the decrease in fibrinogen and antiplasmin concentrations. Streptokinase administration to rabbits with productive inflammatory liver disorders produced changes in hemostasis identical to those observed in intact rabbits, fibrinogen levels, however, remained unchanged. The common feature of all the toxic liver disorders is the increase of antithrombin III levels after streptokinase administration, whereas the antithrombin levels in the control animals were decreased.
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PMID:[Action of streptokinase on the hemostatic indices of rabbits with a toxic lesion of the liver due to carbon tetrachloride]. 381 94

To determine the effect of streptokinase on the ischemic myocardium independent of its effects on the occluding thrombus, the isolated rabbit heart, perfused with Krebs-Henseleit solution, was subjected to a 45-min period of ischemia--83% reduction in myocardial (perfusion) flow--plus anoxia (95% N2 and 5% CO2), followed by restoration of perfusion and reoxygenation. Streptokinase, 75 or 150 IU/min, was infused starting 15 min before reperfusion and continuing for 30 min after reperfusion. Compared with the control group, streptokinase was associated during reperfusion with a significant dose-dependent greater restoration or smaller depression of ventricular function, dP/dt, and developed pressure. To determine if streptokinase effects were mediated during the ischemic or reperfusion phase, the high streptokinase dose was administered in either the last 30 min of the ischemia or the first 30 min of reperfusion. The improvement in recovery of left ventricular function was primarily in the group having streptokinase administered only during the ischemic period. Thus, streptokinase affects the ischemic myocardium so that there is an acceleration in the recovery of ventricular function or a reduction of the impairment in ventricular function during myocardial reperfusion.
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PMID:Beneficial effects of streptokinase on left ventricular function after myocardial reoxygenation and reperfusion following global ischemia in the isolated rabbit heart. 620 68

In 37 consecutive patients with acute myocardial infarction undergoing Streptokinase infusion and acute coronary angiography, the electrocardiographic findings were compared with the findings during angiography. All 15 patients with an occluded right coronary artery demonstrated an electrocardiographic pattern of an acute inferior wall myocardial infarction, and 12 of 13 patients with an occluded left anterior descending coronary artery exhibited a pattern of an acute anteroseptal wall myocardial infarction. In six out of nine instances of an occluded circumflex artery, an inferior infarction pattern evolved, and in three cases, an anteroseptal wall myocardial infarction was demonstrated. precordial ST segment depression more than 1 mm in patients with acute inferior wall myocardial infarction did not correlate with disease of the left anterior descending coronary artery as suggested by others. The specificity of this finding was only 25 percent with a predictive value of 60 percent.
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PMID:The electrocardiogram in patients with acute myocardial infarctions treated with intracoronary Streptokinase infusion. 648 Dec 80

Streptokinase-streptodornase (SK-SD) skin tests and peripheral blood mononuclear stimulation to purified SK-SD delayed skin reactor (DSR) and phytohemagglutinin (PHA) was assessed in 41 patients with rheumatoid arthritis (RA) and 17 controls. Lymphocyte response to DSR correlated directly with the diameter of SK-SD-induced erythema, and PHA stimulation decreased with age. RA patients did not show significant depression by either test or did hyporesponsiveness predict rheumatoid disease activity or prognosis. Six patients without medication demonstrated increased PHA responsiveness and a direct rather than inverse correlation with age.
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PMID:In vitro lymphocyte response in early rheumatoid arthritis. 728 64

Thrombolytic treatment and aspirin will save about 50 in 1000 patients treated for acute myocardial infarction, but with a risk of cerebral or other serious bleeding in two to three in every 1000. Early treatment (< 4 h) about halves mortality; the benefits decline with time but are clearly proven up to 12 h from onset. Benefit is best and risk least when there is ST elevation and bundle branch (BB) block on the initial ECG. Hypotension is not a contraindication. There is no clear benefit from treatment of patients with ST depression, T wave change or a normal ECG. Streptokinase (SK), tissue plasminogen activator (tPA) or APSAC are equally effective with no mortality benefit for any of the drugs. SK is safer, particularly in older or more hypertensive patients. tPA is reserved for patients who have received SK during the previous year, when high antibody titres may neutralize its effect on a second myocardial infarction (MI). Heparin (either i.v. or high dose S/Q) added to aspirin may confer some small additional benefit, but at the cost of significantly increased risk of bleeding. It should be reserved for high risk patients. Routine angioplasty is unhelpful. Investigation should be reserved for patients with continuing symptoms or ECG evidence of ischaemia, at rest or after stress testing. The benefits of thrombolysis are seen at all ages, in both sexes, and whatever the site of the MI. Aspirin 75-100 mg daily should be continued long-term.
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PMID:Thrombolysis: state of the art. 828 68

This study assessed whether differences in the underlying mechanisms for various patterns of precordial ST-segment depression with inferior acute myocardial infarction (AMI) are associated with poorer prognoses. We studied 1,155 patients with inferior AMI who underwent thrombolysis in the Global Utilization of Streptokinase and TPA for Occluded arteries (GUSTO-I) angiographic substudy: those without precordial ST depression (n = 412; 35.7%), those with maximum ST depression in leads V1 to V3 (n = 547; 47.4%), and those with maximum ST depression in leads V4 to V6 (n = 196; 17.0%) on admission electrocardiogram. We compared the infarct-related artery, presence of left anterior descending or multivessel coronary artery disease, and left ventricular function among groups. Patients with maximum ST depression in leads V4 to V6 more often had 3-vessel disease (26.0%) than those without precordial ST depression (13.5%) or those with ST depression in leads V1 to V3 (15.7%; p = 0.002), and they had a lower ejection fraction (median 54% vs 60% and 55%, respectively; p <0.001). Patients with maximum ST depression in leads V1 to V3 less often had AMIs due to proximal right coronary artery obstruction (23.9%) than patients without precordial ST depression (35.2%) or those with ST depression in leads V4 to V6 (40.0%; p = 0.001) and had larger AMIs as estimated by peak creatine kinase. Different patterns of precordial ST depression are associated with distinctive coronary anatomy. ST depression in leads V4 to V6, but not V1 to V3, confers a greater likelihood of multivessel coronary artery disease.
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PMID:Correlation of angiographic findings and right (V1 to V3) versus left (V4 to V6) precordial ST-segment depression in inferior wall acute myocardial infarction. 1007 11