Determinants of agreement between proposed therapeutic windows of platelet function tests in vulnerable patients.
Therapeutic windows for residual platelet reactivity in patients with coronary artery disease on P2Y12 inhibitors were proposed in a consensus document. We aimed to explore the level of agreement between windows for different platelet function tests (PFTs) used to classify patients in low, optimal, and high on-treatment platelet reactivity categories, and to identify variables contributing to the level of agreement.



In this explorative clinical study, the VerifyNow P2Y12, Multiplate adenosine diphosphate (ADP), and light transmission aggregometry (LTA) 20 μmol/L ADP were performed simultaneously in 145 consecutive vulnerable patients. Measurements were performed within 6 months of percutaneous intervention. Patients were considered vulnerable if they had ≥2 risk factors for bleeding or ischaemic events. Window-agreement between PFT pairs was slight to moderate. Multiplate-VerifyNow agreed in 72 patients (50%), κ = 0.41; VerifyNow-LTA agreed in 76 patients (52%), κ = 0.36; and LTA-Multiplate agreed in 64 patients (44%), κ = 0.20. Several variables including the type of P2Y12 inhibitor, aspirin, haemoglobin level, platelet count, age, and previous stroke significantly influenced agreement between PFTs.



Our results suggest that the PFTs, with accompanying therapeutic windows, are not interchangeable when determining the response to antiplatelet therapy in vulnerable coronary artery disease patients on P2Y12 inhibitors. Hence, the type of PFT can directly affect the treatment strategy, which may be especially relevant for patients with multiple factors influencing individual PFTs and thereby test agreement.
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands m.vries@maastrichtuniversity.nl.
Minka J A
MJ
Vries
Department of Internal Medicine, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Heleen J
HJ
Bouman
Department of Internal Medicine, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.|Thrombosis Expertise Centre, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Renske H
RH
Olie
Department of Cardiology, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Leo F
LF
Veenstra
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.
Suzanne
S
Zwaveling
Central Diagnostic Laboratory, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Paul W M
PW
Verhezen
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.|Thrombosis Expertise Centre, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Arina J
AJ
Ten Cate-Hoek
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.|Department of Internal Medicine, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.|Thrombosis Expertise Centre, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Hugo
H
Ten Cate
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.|Central Diagnostic Laboratory, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Yvonne M C
YM
Henskens
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.|Thrombosis Expertise Centre, Maastricht University Medical Centre + (MUMC+), Maastricht, The Netherlands.
Paola E J
PE
van der Meijden
D000368:Aged; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy* / Q000601:surgery; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D062645:Percutaneous Coronary Intervention; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010976:Platelet Count; D010979:Platelet Function Tests / Q000379:methods; D000068799:Prasugrel Hydrochloride / Q000627:therapeutic use; D058921:Purinergic P2Y Receptor Antagonists / Q000627:therapeutic use*; D012372:ROC Curve; D012189:Retrospective Studies; D012307:Risk Factors; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use*; D016896:Treatment Outcome; D035862:Vulnerable Populations
D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine
Concordance; Coronary artery disease; Influencing factors; P2Y12 inhibitors; Platelet reactivity test