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Titolo:
Incomplete thromboxane inhibition with 100 mg of intravenous acetylsalicylic acid in patients with acute ST elevation myocardial infarction - A placebo-controlled pilot trial
Autore:
Ziegler, BK; Kristensen, SD; Vissinger, H; Jensen, HK; Nielsen, HK; Husted, SE;
Indirizzi:
Aarhus Univ Hosp, Aarhus Kommune Hosp, Dept Med & Cardiol, DK-8000 Aarhus C, Denmark Aarhus Univ Hosp Aarhus Denmark C d & Cardiol, DK-8000 Aarhus C, Denmark Aarhus Univ, Dept Epidemiol & Social Med, DK-8000 Aarhus, Denmark Aarhus Univ Aarhus Denmark DK-8000 & Social Med, DK-8000 Aarhus, Denmark Aarhus Univ Hosp, Skejby Sygehus, Dept Cardiol, DK-8200 Aarhus N, Denmark Aarhus Univ Hosp Aarhus Denmark N ept Cardiol, DK-8200 Aarhus N, Denmark Braedstrup Sygehus, Dept Med, DK-8740 Braedstrup, Denmark Braedstrup Sygehus Braedstrup Denmark DK-8740 K-8740 Braedstrup, Denmark
Titolo Testata:
THROMBOSIS RESEARCH
fascicolo: 3, volume: 104, anno: 2001,
pagine: 175 - 180
SICI:
0049-3848(20011101)104:3<175:ITIW1M>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLATELET ACTIVATION; ARACHIDONIC-ACID; UNSTABLE ANGINA; ASPIRIN; STREPTOKINASE; THROMBOLYSIS; CYCLOOXYGENASE-2; SUPPRESSION; TIME;
Keywords:
blood platelets; clinical trial; drug therapy; myocardial infarction; streptokinase; thromboxane A(2);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Ziegler, BK Aarhus Univ Hosp, Aarhus Kommune Hosp, Dept Med & Cardiol, DK-8000 Aarhus C, Denmark Aarhus Univ Hosp Aarhus Denmark C DK-8000 Aarhus C, Denmark
Citazione:
B.K. Ziegler et al., "Incomplete thromboxane inhibition with 100 mg of intravenous acetylsalicylic acid in patients with acute ST elevation myocardial infarction - A placebo-controlled pilot trial", THROMB RES, 104(3), 2001, pp. 175-180

Abstract

Background: Acetylsalicylic acid (ASA) is now a standard treatment of acute myocardial infarction (AMI). ASA inhibits thromboxane A(2) (TXA(2)) production by blocking the constitutive cyclooxygenase (COX)-1 enzyme, but only to a small degree the inducible COX-2. COX-2 is induced by increased concentrations of cytokines, which is related to an enhanced inflammatory response. Previously, we have found a complete inhibition of TXA(2) synthesis in healthy volunteers after intravenous administration of 50 mg of ASA. We measured in a randomized, placebo-controlled pilot trial the effect of 100 mg of ASA injected intravenously on TXA(2) synthesis in AMI patients treated with streptokinase. Methods and results: Nineteen patients with AMI treated with streptokinase were randomized to 100 mg of ASA or placebo injected intravenously. Se-TXB2 and bleeding time were measured before and after drug administration. One hundred and eighty minutes after intravenous ASA administration, treatment with oral ASA was initiated. We found a significant decrease in serum concentrations of TXB2 after 30, 60 and 180 min following ASA injection compared to placebo, but in none of the patients was complete inhibition of TXA(2) production achieved. No significant change in bleeding time could be demonstrated. Conclusion: Intravenous ASA in a dosage of 100 mgdid not completely prevent TXA(2) production in AMI patients treated with streptokinase. This may be due to synthesis of TXA(2) by the inducible COX-2 enzyme and/or to a transcellular metabolism in platelets of prostanoids generated by endothelial cells. (C) 2001 Elsevier Science Ltd. All rights reserved.

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Documento generato il 18/02/20 alle ore 05:31:13