The effect of antiplatelet drugs, heparin, and preanalytical variables on platelet function detected by the platelet function analyzer (PFA-100).
The platelet function analyzer (PFA)-100 is a newly developed instrument that provides a rapid, in vitro, quantitative measurement of platelet adhesion and aggregation in whole blood flowing through a small aperture under high shear conditions. Thirty patients undergoing percutaneous transluminal coronary angioplasty (PTCA) and ten normal individuals were included in this study. In vitro and in vivo studies were conducted to discern the effect of combinations of antiplatelet drugs (aspirin, ticlopidine, abciximab) and heparin on the performance of the device as well as the effects of preanalytical variables, such as method of sample collection and ex vivo anticoagulants. Studies were also conducted examining the effect of aperture size (standard 150 microns vs. smaller 120 microns) on the ability of the device to detect the effect of antiplatelet drugs. There was no difference in mean PFA-100 closure time with citrate versus PPACK anticoagulants or with venipuncture vs. sheath sampling. Closure times did not vary with heparin administration. Closure times were slightly longer for patients taking aspirin plus ticlopidine compared to aspirin alone (p = NS). In contrast adenosine disphosphate (ADP) induced platelet aggregation was significantly less in patients that took aspirin plus ticlopidine vs. aspirin alone (p = .0005). In vitro, there was a dose-dependent increase in closure time for both aperture sizes with increasing abciximab concentration. Although both cartridges showed infinite closure times at an abciximab concentration of 2.25 micrograms/mL, there was a slight benefit to using the 120 microns aperture cartridges at abciximab concentrations of 1.75 to 2.0 micrograms/mL. In ten patients who were followed during abciximab therapy to assess the effect of aperture size, the PFA-100 was able to detect in vivo platelet inhibition by abciximab, but detection of recovery from abciximab-induced platelet dysfunction was slightly better for the PFA-100 with the 120 microns aperture compared to the standard 150 microns aperture collagen/ADP cartridge.
Kottke-Marchant
K
K
Department of Clinical Pathology, Cleveland Clinic Foundation, Ohio. 44195, USA.
Powers
J B
JB
Brooks
L
L
Kundu
S
S
Christie
D J
DJ
D000077284:Abciximab; D000244:Adenosine Diphosphate / Q000494:pharmacology; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D001800:Blood Specimen Collection; D002118:Calcium / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D003201:Computers; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D004867:Equipment Design; D006493:Heparin / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage / Q000494:pharmacology; D015539:Platelet Activation; D010973:Platelet Adhesiveness / Q000187:drug effects*; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D010979:Platelet Function Tests / Q000295:instrumentation* / Q000379:methods; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D013988:Ticlopidine / Q000008:administration & dosage / Q000494:pharmacology
D000911:Antibodies, Monoclonal; D002614:Chelating Agents; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000244:Adenosine Diphosphate; D006493:Heparin; D013988:Ticlopidine; D001241:Aspirin; D002118:Calcium; D000077284:Abciximab