Why the study?
Does aspirin treatment inhibit platelet activation during diagnostic and interventional coronary angiography?
Does aspirin treatment inhibit platelet activation during diagnostic and interventional coronary angiography?
Coronary angioplasty induces significant platelet activation that is not fully suppressed by aspirin, highlighting the potential need for more potent antiplatelet therapy during interventions.
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Angioplasty may drive platelet activation beyond aspirin's suppression; leaves open whether more potent regimens improve PCI safety.
In 30 patients we investigated the expression of activated GPIIb/IIIa-complex as an indicator of in vivo platelet activation before and after coronary angiography/angioplasty. Patients were divided into three groups according to aspirin treatment: group I: patients having a diagnostic coronary angiography without aspirin (n = 6); group II: patients having a diagnostic coronary angiography with low dose aspirin therapy (n = II); group III: patients having a coronary angioplasty with low dose aspirin therapy plus aspirin i.v. (n = 13). Platelets were identified in a flow cytometer by their characteristic light scatter profile and binding of anti-GP Ib, and activated platelets by an antibody to the activated GP IIb/IIIa. Cardiac catheterization lead to an increase of the mean anti-GP IIb/IIIa-fluorescence of the platelets and of the percentage of platelets with an anti-IIb/IIIa-FL exceeding a fixed threshold value (subpopulation). While aspirin substantially inhibited the increase induced by diagnostic angiography, the increase in the angioplasty group was the greatest of all groups despite aspirin.
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Scarlat et al. (1996) studied this question.
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