Platelet activation plays a critical role in the development and perpetuation of coronary microvascular obstruction after PCI. By definition, the interven-tional devices used to treat an epicardial stenosis result in a break in the endothelial surface and release of debris into the coronary bloodstream. The exposed intraplaque contents stimulate platelet activation and aggregation at the site of PCI and probably in the downstream microvasculature. The platelet aggregates plugging the microcirculation cause mechanical obstruction and lead to biochemical responses due to their interaction with the injured endothe-lium, the neutrophils, and with more platelets. The release of vasoactive substances such as serotonin and endothelin-1 from the activated platelets and the injured endothelium lead to intense microvascu-lar vasoconstriction, which accentuates the ischemic injury and resultant myonecrosis.9,23
One study of aspirin resistance emphasized the role of platelet aggregation in the pathophysiology of PMI. Patients deemed to be resistant to aspirin therapy were found to have a significantly higher incidence of PMI, defined as any increase in the degree of CK-MB (51.7% versus 24.6%, P = .006).27 The odds of developing PMI in this cohort of 151 patients presenting for nonurgent PCI increase threefold if they are found to be aspirin-resistant before the procedure.27
Was this article helpful?