Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ridogrel, a compound with the dual property of inhibiting the synthesis of thromboxane and blocking the receptors of thromboxane/prostaglandin/endoperoxides, has been shown to accelerate the speed of recanalization and to delay or prevent reocclusion during systemic thrombolysis with tissue plasminogen activator in experimental animals. Ninety patients who had not taken any antiplatelet drugs within the last 10 days were randomized to either intravenous ASA 250 mg immediately before the thrombolytic treatment and 100 mg once a day orally thereafter or ridogrel 300 mg i.v. before thrombolytic treatment and 300 mg b.i.d. orally thereafter. All patients were given intravenous heparin concomitantly with alteplase. The patency of the infarct-related artery was determined by coronary angiography before the administration of the thrombolytic agent and by repeated coronary angiography every 15 min until the end of the administration of alteplase. A final angiogram was obtained 48 to 72 h later. At 90 min, the recanalization and patency rates were the same in the two treatment groups with no intergroup difference in the speed of recanalization.
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PMID:Ridogrel does not increase the speed and rate of coronary recanalization in patients with myocardial infarction treated with alteplase and heparin. 805 7

An open pilot study was performed to assess the safety and preliminary efficacy of ridogrel, a selective thromboxane-A2 synthetase inhibitor and thromboxane-A2/prostaglandin endoperoxide receptor blocker, as adjunct to thrombolysis, with alteplase and heparin. In 50 patients with acute myocardial infarction, 300 mg ridogrel was injected intravenously in addition to alteplase and heparin. Ridogrel was continued orally (300 mg) twice daily for 5 days. Patency rate at initial (90 min) angiography, defined as thrombolysis in myocardial infarction perfusion grades 2 or 3, was 86%. Rescue percutaneous transluminal coronary angioplasty was performed in 10 patients; immediate results were good in nine, while a large dissection occurred in one patient. New ischemia occurred in 10 patients within 24 h, and after the second angiogram in seven cases. Three underwent coronary artery bypass grafting and seven percutaneous transluminal coronary angioplasty without further complication. Patency rate at second angiography (between 6 and 24 h) was 94%. New Q-waves appeared in 56% of the patients; 36% had a non-Q-wave infarction and 8% had no enzyme rise. Enzymatic infarct size, estimated by the cumulative quantity of alpha-hydroxybutyrate dehydrogenase released in 72 h, was substantially smaller than in comparable studies with rt-PA and heparin. One patient died due to a cerebrovascular hemorrhage. No other deaths occurred. Bleeding complications were seen in 18 patients (36%), necessitating blood transfusion in three. Reinfarction did not occur. Eventually 49 patients were discharged in good condition. Safety with regard to bleeding complications of ridogrel in conjunction with alteplase is about the same as that of aspirin. Immediate and late patency rates were high. Rescue percutaneous transluminal coronary angioplasty could be performed with relative safety and early reocclusion could be successfully dealt with by repeat percutaneous transluminal coronary angioplasty. Further studies with this or similar compounds seem warranted.
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PMID:Ridogrel as an adjunct to thrombolysis in acute myocardial infarction. 874 72