TY - JOUR
T1 - Impact of atorvastatin or rosuvastatin co-administration on platelet reactivity in patients treated with dual antiplatelet therapy
AU - the Novara Atherosclerosis Study Group (NAS)
AU - Verdoia, Monica
AU - Nardin, Matteo
AU - Sartori, Chiara
AU - Pergolini, Patrizia
AU - Rolla, Roberta
AU - Barbieri, Lucia
AU - Marino, Paolo
AU - Bellomo, Giorgio
AU - Suryapranata, Harry
AU - De Luca, Giuseppe
N1 - Publisher Copyright:
© 2015 Elsevier Ireland Ltd.
PY - 2015/12/1
Y1 - 2015/12/1
N2 - Background: Residual high-on treatment platelet reactivity (HRPR) still represents a challenging matter in patients with coronary artery disease. Drug-to-drug interaction has been suggested between some statin and antiplatelet agents, despite their co-administration is mandatory in patients after an acute cardiovascular event or coronary stenting. Therefore, the aim of the current study was to investigate any impact of rosuvastatin or atorvastatin co-administration on platelet reactivity in patients receiving dual antiplatelet therapy (DAPT). Methods: Our population is represented by patients on DAPT (ASA and either clopidogrel 75 mg or ticagrelor 90 mg b.i.d) after an ACS or percutaneous revascularization, and receiving rosuvastatin or atorvastatin. Platelet function was assessed by Multiplate Impedance Aggregometry (Roche Diagnostics AG). Results: We included a total of 374 patients, 240 (64.2%) receiving atorvastatin, 134 (35.8%) rosuvastatin. Rosuvastatin treated patients were more often using beta-blockers (p = 0.05), diuretics (p = 0.04) and displayed higher HDL (p < 0.001) and lower LDL cholesterol (p < 0.001). The prevalence of HRPR for ASA was low, with no difference according to statin type (0.8% vs 1.5%, p = 0.62, adjusted OR[95%CI] = 2[0.23-16.6], p = 0.52). Concerning ADP-antagonists, in the 163 patients treated with clopidogrel, rosuvastatin co-administration was associated with a significantly increased rate of HRPR (55.6%vs 32%, p = 0.01, adjusted OR[95%CI] = 2.69[1.22-5.96], p = 0.015) with higher ADP-mediated platelet reactivity (p = 0.01) and TRAP-test results (p = 0.04). On the contrary, in the 211 ticagrelor treated patients, statin type did not affect mean platelet reactivity or the prevalence of HRPR with ticagrelor (10.5% vs 11.2%, p = 0.99, adjusted OR[95%CI] = 0.86[0.34-2.22], p = 0.76). Conclusions: Among patients receiving DAPT, rosuvastatin but not atorvastatin is associated with an increased rate of HRPR for clopidogrel, without any influence on the antiplatelet effect of ASA or ticagrelor. Therefore, cautiousness should be exerted for clopidogrel and rosuvastatin therapeutic association.
AB - Background: Residual high-on treatment platelet reactivity (HRPR) still represents a challenging matter in patients with coronary artery disease. Drug-to-drug interaction has been suggested between some statin and antiplatelet agents, despite their co-administration is mandatory in patients after an acute cardiovascular event or coronary stenting. Therefore, the aim of the current study was to investigate any impact of rosuvastatin or atorvastatin co-administration on platelet reactivity in patients receiving dual antiplatelet therapy (DAPT). Methods: Our population is represented by patients on DAPT (ASA and either clopidogrel 75 mg or ticagrelor 90 mg b.i.d) after an ACS or percutaneous revascularization, and receiving rosuvastatin or atorvastatin. Platelet function was assessed by Multiplate Impedance Aggregometry (Roche Diagnostics AG). Results: We included a total of 374 patients, 240 (64.2%) receiving atorvastatin, 134 (35.8%) rosuvastatin. Rosuvastatin treated patients were more often using beta-blockers (p = 0.05), diuretics (p = 0.04) and displayed higher HDL (p < 0.001) and lower LDL cholesterol (p < 0.001). The prevalence of HRPR for ASA was low, with no difference according to statin type (0.8% vs 1.5%, p = 0.62, adjusted OR[95%CI] = 2[0.23-16.6], p = 0.52). Concerning ADP-antagonists, in the 163 patients treated with clopidogrel, rosuvastatin co-administration was associated with a significantly increased rate of HRPR (55.6%vs 32%, p = 0.01, adjusted OR[95%CI] = 2.69[1.22-5.96], p = 0.015) with higher ADP-mediated platelet reactivity (p = 0.01) and TRAP-test results (p = 0.04). On the contrary, in the 211 ticagrelor treated patients, statin type did not affect mean platelet reactivity or the prevalence of HRPR with ticagrelor (10.5% vs 11.2%, p = 0.99, adjusted OR[95%CI] = 0.86[0.34-2.22], p = 0.76). Conclusions: Among patients receiving DAPT, rosuvastatin but not atorvastatin is associated with an increased rate of HRPR for clopidogrel, without any influence on the antiplatelet effect of ASA or ticagrelor. Therefore, cautiousness should be exerted for clopidogrel and rosuvastatin therapeutic association.
KW - Clopidogrel
KW - Cythocromes
KW - Rosuvastatin
KW - Ticagrelor
UR - http://www.scopus.com/inward/record.url?scp=84946215360&partnerID=8YFLogxK
U2 - 10.1016/j.atherosclerosis.2015.10.005
DO - 10.1016/j.atherosclerosis.2015.10.005
M3 - Article
SN - 0021-9150
VL - 243
SP - 389
EP - 394
JO - Atherosclerosis
JF - Atherosclerosis
IS - 2
ER -