Circulation, Vol 80, 1718-1725, Copyright © 1989 by American Heart Association
DM Kerins, L Roy, GA FitzGerald and DJ Fitzgerald
Platelet activation may limit the response to tissue-type plasminogen
activator (t-PA) during coronary thrombolysis in humans. As an index of
platelet activation, we assessed thromboxane A2 biosynthesis during
coronary thrombolysis with intravenous t-PA in patients with acute
myocardial infarction. Urinary 2,3-dinor-thromboxane B2, a metabolite of
thromboxane A2, was increased to a peak of 3,327 +/- 511 pg/mg creatinine
(n = 12) following administration of intravenous t-PA and remained elevated
for 48 hours. This increase was abolished by pretreatment with aspirin 325
mg orally (n = 6), indicating de novo biosynthesis of thromboxane A2 rather
than washout of preformed metabolites during reperfusion. Prostacyclin
(PGI2) biosynthesis, determined by excretion of 2,3-dinor-6-keto-PGF1
alpha, also increased after t-PA administration. However, this increase was
less pronounced in patients who reperfused (28 +/- 3.3 ng.hr/mg creatinine)
than in patients who failed to reperfuse (118 +/- 30 ng.hr/mg creatinine, p
less than 0.05). These data provide evidence of platelet activation during
coronary thrombolysis with t-PA. In patients who reperfuse, the reduction
in PGI2 biosynthesis may be a marker of reperfusion injury to the
vasculature and may further amplify platelet activation.
ARTICLES
Platelet and vascular function during coronary thrombolysis with tissue- type plasminogen activator
Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37232.
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