Circulation, Vol 72, 1336-1345, Copyright © 1985 by American Heart Association
HS Mueller, PS Rao, MA Greenberg, PM Buttrick, II Sussman, HA Levite, RM Grose, V Perez-Davila, JE Strain and TH Spaet
There is increasing evidence that platelets play an important role in the
pathogenesis of acute ischemic heart disease. Therefore an understanding of
factors that influence platelet performance is important. This study was
undertaken (1) to characterize during evolving myocardial infarction
platelet activity in the peripheral circulation and across the
ischemic/infarcting myocardial compartment, the locus of presumed platelet
hyperactivity, and (2) to evaluate the effects of prostacyclin (PGI2), a
most potent antiplatelet agent and vasodilator. A total of 59 patients with
evolving myocardial infarction were studied. Twenty-two patients were
instrumented with arterial and coronary sinus catheters and received
intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90
min. In 15 patients with anterior myocardial infarction, transcardiac
platelet function and response to PGI2 were studied. Plasma levels of
beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo
measures of platelet activity, were elevated three- and 10-fold.
6-Keto-prostaglandin F 1 alpha, the stable end product of PGI2, was less
than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio.
Platelets circulating during evolving myocardial infarction ("ischemic
platelets") were hyperaggregable in response to ADP and relatively
resistant to PGI2, both in vivo and in vitro. Concentrations of platelet
cyclic AMP and the cyclic AMP response to PGI2 were diminished. The
platelet hyperreactivity, expressed by plasma beta-TG, platelet
aggregation, and PGI2-induced inhibition of aggregation, was most intense
early during infarct evolution and decreased with time. The increased
platelet performance resulted in "platelet fatigue," indicated by decreased
contents of beta-TG of the ischemic platelet and decreased TxA2 production
in response to collagen. However, the ischemic platelet produced twice
normal TxA2 in response to arachidonic acid (stimulus and substrate),
demonstrating a heightened metabolic capacity. TxA2 was produced across the
ischemic/infarcting compartment in 10 of 15 patients with anterior
myocardial infarction. The antiplatelet effect of PGI2 was greatly
diminished. In summary, the data define an abnormal pattern of platelet
behavior during evolving myocardial infarction, characterized by a
proaggregatory environment, heightened platelet reactivity in both the
peripheral and coronary circulation, and relative resistance to PGI2. The
clinical consequences of the data are that the patient in the acute phase
of myocardial infarction may benefit from suppression of platelet function
and requires significantly greater doses of PGI2 than normal
subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
ARTICLES
Systemic and transcardiac platelet activity in acute myocardial infarction in man: resistance to prostacyclin
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