Antiplatelet therapy in carotid revascularisation
on tailoring APT in carotid revascularization we performed a PubMed search for available prospective studies regarding ‘’platelet reactivity testing’’ and ‘’carotid revascularization’’ in humans. We wish to emphasize that this overview is intended as a topical summary of the available data and our assessment should not be considered as a systematic review or meta-analysis of all the literature available on the utility of platelet function testing. The articles we found have been divided by the performed intervention; carotid endarterectomy (table 2) and carotid artery stenting (table 3). A total of 16 relevant studies were found, of which three studies adjusted the antiplatelet therapy based on platelet reactivity test results; the largest study performed the VerifyNow-P2Y12 assay in 2014 patients with DAPT 1 hour before CAS14. Based on the results of this test, 99 patients with HCPR (PRU≥230) were randomly assigned to receive low dose clopidogrel (75 mg/d, n= 50) or to high dose clopidogrel (150 mg/d, n= 49). After 30 days, the second VerifyNow-P2Y12 assay was performed. The results of this study could not confirm a benefit for high dose clopidogrel in reducing platelet reactivity since the differences between median 30-day PRU (p=.483) and percentage of change of PRU (p=.442) were not significant. In a historical cohort analysis patients were measured with VerifyNow P2Y12 assay prior to neurovascular stent placement (51% CAS)15; initially 49 patients received 75 mg clopidogrel in the observational phase (2006-2008) and in the interventional phase (2008-2011) 47 patients were given tailored clopidogrel (maintenance dose 150-600 mg) with a goal inhibition of >20% . Overall 36.5% had HCPR (≤20% inhibition) and periprocedural thromboembolic complications were seen in 7 patients (7.3%). No significant decrease in thromboembolic complications were seen in the interventional group as compared to the observation group. In another historical cohort analysis with patients undergoing CAS, a benefit for tailoring APT was seen when adding cilostazol prior to intervention in patients with HCPR16; in period I (2010-2011) 28 patients, under which 12 with HCPR (PRU≥240 measured by VerifyNow P2Y12 assay) were all treated with DAPT and in period II (2011-2013) 36 patients all received DAPT including 13 patients with HCPR, who received extra cilostazol 200 mg daily prior to CAS. PRU was significantly lower (300 ± 36 and 240 ± 62; p=.006) and % inhibition was significantly higher (8.8 ± 8.7 and 28 ± 18; p=.005) in period II. Unfortunately no specified information about platelet reactivity in the 13 HCPR patients receiving extra cilostazol is reported. On diffusion-weighted imaging a significant decrease in new ischemic lesions was seen in period II compared to period I (p=.034). None of the patients had haemorrhagic or thromboembolic adverse events. Six other studies investigated the correlation of platelet reactivity levels and clinical outcome after CEA or CAS without adapting antiplatelet therapy based on the measured platelet reactivity; results showed higher platelet reactivity being linked to either more postoperative micro-embolic signals in CEA17, more new cerebral ischemic lesions after CAS18 or higher percentage of the composite endpoint ‘’ischemic events’’ (stroke, in-stent stenosis and neurologic deficit)15,19,20. This finding seems more evident in HCPR than in HAPR19.
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