BACKGROUND: High on-treatment platelet reactivity (HTPR) after clopidogrel is associated with a higher risk of cardiovascular events after percutaneous coronary intervention (PCI). However, it remains unclear whether HTPR is of similar prognostic value for different clinical presentations. METHODS: We compared the prognostic impact of HTPR, measured by the VerifyNow P2Y12 assay (Accumetrics, San Diego, CA), on outcomes between 1,095 patients with acute coronary syndromes (ACS) and 1,329 patients with stable coronary artery disease (CAD) who were treated with PCI. Before PCI, patients received optimal clopidogrel treatment (75 mg daily for at least 5 days or if <5 days, 300-600 mg loading), and platelet reactivity was measured at 24 to 48 hours after PCI. The primary end point was a composite of death, myocardial infarction, stent thrombosis, or stroke. RESULTS: During follow-up (median, 22.0 months), HTPR was independently associated with higher risks of the primary end point (hazard ratio [HR] 2.03, 95% CI 1.30-3.18, P = .002) and mortality (HR 3.46, 95% CI 1.18-10.18, P = .02) in patients with ACS. By contrast, for patients with stable CAD, HTPR was not associated with adjusted risks of the primary end point (HR 1.00, 95% CI 0.71-1.39, P = .98) or mortality (HR 0.74, 95% CI 0.36-1.51, P = .41). Significant interactions were present between HTPR status and clinical presentations for the primary end point (P = .02) and mortality (P = .04). CONCLUSION: There was a substantial interaction between platelet reactivity on clopidogrel and clinical presentations on cardiovascular events after PCI. High on-treatment platelet reactivity was significantly associated with higher risks of cardiovascular events in ACS patients, whereas this association was absent in stable CAD patients.
BACKGROUND: High on-treatment platelet reactivity (HTPR) after clopidogrel is associated with a higher risk of cardiovascular events after percutaneous coronary intervention (PCI). However, it remains unclear whether HTPR is of similar prognostic value for different clinical presentations. METHODS: We compared the prognostic impact of HTPR, measured by the VerifyNow P2Y12 assay (Accumetrics, San Diego, CA), on outcomes between 1,095 patients with acute coronary syndromes (ACS) and 1,329 patients with stable coronary artery disease (CAD) who were treated with PCI. Before PCI, patients received optimal clopidogrel treatment (75 mg daily for at least 5 days or if <5 days, 300-600 mg loading), and platelet reactivity was measured at 24 to 48 hours after PCI. The primary end point was a composite of death, myocardial infarction, stent thrombosis, or stroke. RESULTS: During follow-up (median, 22.0 months), HTPR was independently associated with higher risks of the primary end point (hazard ratio [HR] 2.03, 95% CI 1.30-3.18, P = .002) and mortality (HR 3.46, 95% CI 1.18-10.18, P = .02) in patients with ACS. By contrast, for patients with stable CAD, HTPR was not associated with adjusted risks of the primary end point (HR 1.00, 95% CI 0.71-1.39, P = .98) or mortality (HR 0.74, 95% CI 0.36-1.51, P = .41). Significant interactions were present between HTPR status and clinical presentations for the primary end point (P = .02) and mortality (P = .04). CONCLUSION: There was a substantial interaction between platelet reactivity on clopidogrel and clinical presentations on cardiovascular events after PCI. High on-treatment platelet reactivity was significantly associated with higher risks of cardiovascular events in ACS patients, whereas this association was absent in stable CAD patients.
Authors: K Kukula; M Klopotowski; P K Kunicki; J Jamiolkowski; A Debski; P Bekta; M Polanska-Skrzypczyk; Z Chmielak; A Witkowski Journal: BMC Cardiovasc Disord Date: 2016-12-08 Impact factor: 2.298