Impact and Diagnosis of Antiplatelet Therapy Resistance in Patients Undergoing Cardiac Surgery

Abstract

Coronary artery bypass grafting (CABG) is highly effective in the treatment of severe coronary artery disease. Antiplatelet therapy is a critical component of the medical management of patients following CABG. Patient idiosyncrasies in responsiveness to antiplatelet agents, however, lead to variable suppression of platelet aggregation. This problem is underscored by inconsistent findings from the different laboratory instruments used to document antiplatelet drug responsiveness and its uncertain clinical impact. The laboratory results reveal a spectrum of platelet inhibition effects. The cutoff values discriminating between "resistance" and "response" to antiplatelet therapy often rely solely on definition. It is therefore not surprising that regular testing for antiplatelet therapy response has neither been routinely instituted in a wider clinical arena nor is there unequivocal evidence to support it. The purpose of this review is to offer insight into the incidence and clinical impact of antiplatelet therapy resistance in patients undergoing surgical myocardial revascularization. Drug Dev Res 74 : 492-504, 2013.

Impact of aspirin resistance on outcomes among patients following coronary artery bypass grafting: exploratory analysis from randomized controlled trial (NCT01159639)

“…Extensive evidece describing the phenomenon of AR in patients undergoing cardiac surgery is available in literature 11,24,25 . Based on underlying mechanisms, we can assume that there are three types of aspirin resistance: 1) Pharmacokinetic AR where inadequate in vivo efficacy exists despite sufficient in vitro performance 24,25 .…”

“…Based on underlying mechanisms, we can assume that there are three types of aspirin resistance: 1) Pharmacokinetic AR where inadequate in vivo efficacy exists despite sufficient in vitro performance 24,25 . In such a cases, patient non-compliance, inadequate absorption and drug to drug interactions should be considered 24,25 .…”

“…Early postoperative increased platelet turnover and reactivity 12 as well as COX-1 polymorphism may be underlying cause for such a phenomenon 24,25 .…”

“…3) Pseudoresistance implies that adequate COX-1 inhibition is achieved, however platelet express activation via thromboxane independent pathways 24,25 . This type of AR underlines the importance of comprehensive approach in management of AR.…”

“…Moreover, platelet ADP receptor inhibitory response to thienopyridines should be quantified, as there is evidence that up to 30% of patients on clopidogrel may be considered as clopidogrel resistant 24,26 .…”