Background: Large-scale clinical trials have shown that routine monitoring of the platelet function in patients after percutanous coronary intervention (PCI) is not necessary. However, it is still unclear whether patients received high-risk PCI would benefit from a therapy which is guided by a selective platelet function monitoring. This explanatory study sought to assess the benefit of a therapy guided by platelet function monitoring for these patients.
Methods: Acute coronary syndrome (ACS) patients (n = 384) who received high-risk, complex PCI were randomized into two groups. PCI in the two types of lesions described below was defined as high-risk, complex PCI: lesions that could result in severe clinical outcomes if stent thrombosis occurred or lesions at high risk for stent thrombosis. The patients in the conventionally treated group received standard dual antiplatelet therapy. The patients in the platelet function monitoring guided group received an antiplated therapy guided by a modified thromboelastography (TEG) platelet mapping: If inhibition of platelet aggregation (IPA) induced by arachidonic acid (AA) was less than 50% the aspirin dosage was raised to 200 mg/d; if IPA induced by adenosine diphosphate (ADP) was less than 30% the clopidogrel dosage was raised to 150 mg/d, for three months. The primary efficacy endpoint was a composite of myocardial infarction, emergency target vessel revascularization (eTVR), stent thrombosis, and death in six months.
Results: This study included 384 patients; 191 and 193 in the conventionally treated group and platelet function monitoring guided group, respectively. No significant differences were observed in the baseline clinical characteristics and interventional data between the two groups. In the platelet function monitoring guided group, the mean IPA induced by AA and ADP were (69.2 ± 24.5)% (range, 4.8% to 100.0%) and (51.4 ± 29.8)% (range, 0.2% to 100.0%), respectively. The AA-induced IPA of forty-three (22.2%) patients was less than 50% and the ADP-induced IPA of fifty-seven (29.5%) patients was less than 30%; therefore, their drug dosages were adjusted. The TEG was rechecked one to four weeks after PCI, and the results indicated that the IPAs had significantly improved (P < 0.01). However, no significant differences were found in the rates of the primary efficacy endpoint. Rates in the conventionally treated group and platelet function monitoring guided group were 4.7% and 5.2%, respectively (hazard ratio: 1.13; P = 0.79).
Conclusion: An antiplatelet therapy guided by TEG monitored platelet function could not improve clinical efficacy even in ACS patients treated with high-risk complex PCI.