Premium
Hematocrit alters V erify N ow P 2 Y 12 assay results independently of intrinsic platelet reactivity and clopidogrel responsiveness
Author(s) -
Kakouros N.,
Kickler T. S.,
Laws K. M.,
Rade J. J.
Publication year - 2013
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/jth.12376
Subject(s) - clopidogrel , hematocrit , p2y12 , medicine , platelet , cardiology , platelet activation , thrombelastography , aspirin
Summary Background The V erify N ow P 2 Y 12 assay assesses the adequacy of clopidogrel therapy by measuring ADP ‐induced platelet activation in whole blood. Low hematocrit is associated with high clopidogrel on‐treatment platelet reactivity ( HTPR ) defined by this assay. Objectives To characterize the effect of hematocrit on V erify N ow values and determine if it is due to hematocrit‐dependent changes in intrinsic platelet reactivity or an in vitro assay phenomenon. Patients/Methods Adenosine diphosphate‐induced platelet activation was measured using the V erify N ow P 2 Y 12 assay, whole blood impedance and light transmission platelet aggregometry ( LTA ) before and after clopidogrel loading in 113 patients undergoing elective cardiac catheterization. Iso‐ TRAP ‐induced platelet activation was additionally measured using the V erify N ow device. Multivariate modeling employing clinical and laboratory variables was used to investigate the association between hematocrit and V erify N ow values. Results V erify N ow P 2 Y 12 reaction units ( PRU ) and iso‐ TRAP B ase units before and after clopidogrel loading, but not their relative change, exhibited strong negative correlation with hematocrit ( P ≤ 0.0005 for both). While hematocrit remained a strong predictor of post‐clopidogrel PRU ( P = 0.001) in multivariate modeling, it was independent of post‐clopidogrel ADP ‐induced platelet reactivity as measured by LTA ( P = 0.001). Correcting for the effects of hematocrit resulted in a 15–39% reduction in the prevalence of HTPR defined by thresholds of 208–236 PRU . Conclusions The effect of hematocrit on V erify N ow PRU values is an in vitro phenomenon that is independent of intrinsic change in ADP ‐induced platelet reactivity and clopidogrel responsiveness. Correcting for hematocrit when using this assay may more accurately identify patients with HTPR that may benefit from alternative antiplatelet therapy.