Impact of aspirin resistance on antiplatelet therapy management after coronary artery surgery

Dual antiplatelet therapy (APT) provides incremental platelet inhibition compared with either agent alone and more effective suppression of adverse ischaemic events [2]. This finding is confirmed by Awidi and coworkers who found that the combination of aspirin and clopidogrel had greater inhibitory effects on platelet aggregation than either agent alone in patients with coronary artery disease [3]. In our opinion, the addition of clopidogrel in the group of patients with AR inevitably affected both the observed clinical outcomes and the decrease in AR proportion. Following CAS, extensive evidence supports the use of aspirin, in doses of 100–325 mg/day, to be administered postoperatively and continued indefinitely [4]. A daily 100 mg dose of aspirin administered postoperatively in a study by Wang et al. [1], allows the possibility of different APT management strategies. For example, a stepwise increase in the aspirin dose with a subsequent platelet function assessment could probably bring a further decrease in the AR proportion and therefore, eliminate the need for dual APT. However, it still remains unclear, whether an aspirin dose increase would be superior to dual APT, in the context of a clinical outcome. Of note, a meta-analysis by Snoep et al. showed an overall prevalence of 21% of laboratory-defined clopidogrel low response [5]. We believe that these two different APT approaches should be evaluated in a large cohort randomized trial with an outcome evaluation of both ischaemic and bleeding events. The authors hypothesized that the Chinese population is more sensitive to aspirin therapy and presented no AR at a 6-month follow-up. It would be interesting if the authors analyzed the bleeding event occurrence at the 6-month follow-up in the group of patients on dual APT. APT management in cases of AR should be individually tailored, with aspirin dosage stepwise increased (up to 325 mg/day), and clopidogrel administration in cases of AR to high aspirin doses. Temporary AR requires temporary APT adjustment. The duration and intensity of the APT adjustment should be tailored according to drug specific platelet function tests in order to minimize both ischaemic and bleeding events. In conclusion, it is difficult to investigate by what amount the laboratory AR corresponds to the clinical AR. Prospective studies, with a large study sample necessitated by the infrequency of adverse ischaemic events, must determine the optimal threshold for AR, taking into consideration both the laboratory and clinical outcome findings.