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      Depressed plasma platelet-activating factor acetylhydrolase in patients presenting with acute myocardial infarction.


      1-Alkyl-2-acetylglycerophosphocholine Esterase, Adult, Biological Markers, blood, Electrocardiography, Female, Fibrinolytic Agents, therapeutic use, Humans, Male, Middle Aged, Myocardial Infarction, drug therapy, enzymology, physiopathology, Phospholipases A, Platelet Activating Factor, metabolism, Severity of Illness Index, Thrombolytic Therapy

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          Cell membrane phospholipids, including platelet-activating factor (PAF), participate in the pathogenesis of acute myocardial infarction (AMI). The plasma level of PAF acetylhydrolase (AH) was determined in 18 patients at presentation with AMI before thrombolysis, and the administration of adjunctive therapy, and compared with 13 healthy controls. Plasma levels of PAF-AH were significantly lower in the AMI patients (23.15 +/- 1.75 nmol/min/ml) than in the controls (30.43 +/- 2.13 nmol/min/ml; p = 0.027). Considering normal plasma levels of PAF and lyso-PAF, and lack of evidence that anti-PAF antibodies are really beneficial in myocardial ischemia-reperfusion, it is reasonable to speculate that an inability of systemic PAF to 'turn on' PAF-AH enzymatic activity could contribute substantially to the observed events. Decreased PAF-AH activity in AMI patients may represent not a consequence, but rather, a risk factor for the development of acute coronary syndromes.

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          A comparison of reteplase with alteplase for acute myocardial infarction. The Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO III) Investigators.

          Reteplase (recombinant plasminogen activator), a mutant of alteplase tissue plasminogen activator, has a longer half-life than its parent molecule and produced superior angiographic results in pilot studies of acute myocardial infarction. In this large clinical trial, we compared the efficacy and safety of these two thrombolytic agents. A total of 15,059 patients from 807 hospitals in 20 countries who presented within 6 hours after the onset of symptoms with ST-segment elevation or bundle-branch block were randomly assigned in a 2:1 ratio to receive reteplase, in two bolus doses or 10 MU each given 30 minutes apart, or an accelerated infusion of alteplase, up to 100 mg infused over a period of 90 minutes. The primary hypothesis was that mortality at 30 days would be significantly lower with reteplase. The mortality rate at 30 days was 7.47 percent for reteplase and 7.24 percent for alteplase (adjusted P=0.54; odds ratio, 1.03; 95 percent confidence interval, 0.91 to 1.18). The 95 percent confidence interval for the absolute difference in mortality rates was -1.1 to 0.66 percent. Stroke occurred in 1.64 percent of patients treated with reteplase and in 1.79 percent of those treated with alteplase (P= 0.50). The respective rates of the combined end point of death or nonfatal, disabling stroke were 7.89 percent and 7.91 percent (P=0.97; odds ratio, 1.0; 95 percent confidence interval, 0.88 to 1.13). As compared with an accelerated infusion of alteplase, reteplase, although easier to administer, did not provide any additional survival benefit in the treatment of acute myocardial infarction. Other results, particularly for the combined end point of death or nonfatal, disabling stroke, were remarkably similar for the two plasminogen activators.

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