Determination of platelet aggregation inhibition during percutaneous coronary intervention with the platelet function analyzer PFA-100

被引:27
作者
Madan, M
Berkowitz, SD
Christie, DJ
Smit, AC
Sigmon, KN
Tcheng, JE
机构
[1] Duke Clin Res Inst, Durham, NC USA
[2] Dade Behring Inc, Deerfield, IL USA
关键词
D O I
10.1067/mhj.2002.123581
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background A simple device to rapidly evaluate platelet function may aid in optimizing glycoprotein IIb/IIIa inhibition during percutaneous coronary intervention (PCI). We prospectively studied platelet function in 250 patients receiving abciximab or eptifibatide during PCI. Methods and Results The platelet function analyzer PFA-100 (Dade-Behring, Deerfield, 111) measures platelet function by determining the time to occlusion of an aperture in a biochemically active membrane as whole blood flows under high shear conditions. Platelet aggregation causes aperture occlusion, and results are reported as a closure time (CT). All patients received either abciximab or eptifibaticle, along with aspirin and heparin; patients undergoing stent implantation received aspirin and a thienopyricline postprocedure. The CT was measured at baseline and 10 minutes, 4 hours, 12 hours (abciximab-on(y), and 24 hours after the bolus. Profound inhibition was exhibited in most patients shortly after the platelet inhibitor bolus and during the course of therapy. We observed recovery of platelet function 12 hours after discontinuation of abciximab, with a high degree of interpatient variability, and ongoing profound platelet inhibition 4 to 6 hours after the discontinuation of eptifibaticle. Among patients treated with abciximab, patients who were obese recovered from platelet inhibition sooner than patients who were not obese, whereas patients who were elderly had delayed recovery compared with patients who were not elderly. Failure to achieve maximal platelet inhibition (nonclosure) at 10 minutes indicated a possible association with adverse clinical events at the 6-month follow-up examination (60% vs 20%). Conclusions PFA-100 is a rapid simple assay used as a means of assessing inhibition of platelet aggregation during PCI performed with glycoprotein IIb/IIIa inhibition. Failure to achieve nonclosure early after the initiation of abciximab therapy warrants further investigation because there may be an association with adverse cardiac events at 6-month follow-up.
引用
收藏
页码:151 / 158
页数:8
相关论文
共 26 条
[1]   BLEEDING COMPLICATIONS WITH THE CHIMERIC ANTIBODY TO PLATELET GLYCOPROTEIN IIB/IIIA INTEGRIN IN PATIENTS UNDERGOING PERCUTANEOUS CORONARY INTERVENTION [J].
AGUIRRE, FV ;
TOPOL, EJ ;
FERGUSON, JJ ;
ANDERSON, K ;
BLANKENSHIP, JC ;
HEUSER, RR ;
SIGMON, K ;
TAYLOR, M ;
GOTTLIEB, R ;
HANOVICH, G ;
ROSENBERG, M ;
DONOHUE, TJ ;
WEISMAN, HF ;
CALIFF, RM .
CIRCULATION, 1995, 91 (12) :2882-2890
[2]   Progress in point-of-care laboratory testing for assessing platelet function [J].
Berkowitz, SD ;
Frelinger, AL ;
Hillman, RS .
AMERICAN HEART JOURNAL, 1998, 136 (04) :S51-S65
[3]   Vascular access site complications after percutaneous coronary intervention with abciximab in the evaluation of c7E3 for the prevention of ischemic complications (EPIC) trial [J].
Blankenship, JC ;
Hellkamp, AS ;
Aguirre, FV ;
Demko, SL ;
Topol, EJ ;
Califf, RM .
AMERICAN JOURNAL OF CARDIOLOGY, 1998, 81 (01) :36-40
[4]   USE OF A MONOCLONAL-ANTIBODY DIRECTED AGAINST THE PLATELET GLYCOPROTEIN IIB/IIIA RECEPTOR IN HIGH-RISK CORONARY ANGIOPLASTY [J].
CALIFF, RM ;
SHADOFF, N ;
VALETT, N ;
BATES, E ;
GALEANA, A ;
KNOPF, W ;
SHAFTEL, J ;
BENDER, MJ ;
AVERSANO, T ;
RAQUENO, J ;
GURBEL, P ;
COWFER, J ;
COHEN, M ;
CROSS, P ;
BITTL, J ;
EDDINGS, K ;
TAYLOR, M ;
DEROSA, K ;
HATTEL, L ;
COOPER, L ;
ESHELMAN, B ;
FINTEL, D ;
NIEMYSKI, P ;
KLEIN, L ;
KENNEDY, H ;
THORNTON, T ;
KEREIAKES, D ;
MARTIN, L ;
ANDERSON, L ;
HIGBY, N ;
ELLIS, S ;
BREZINA, K ;
GEORGE, B ;
CHAPEKIS, A ;
SMITH, D ;
ANWAR, A ;
GERBER, TL ;
PRITCHARD, GL ;
MYLER, R ;
SHAW, R ;
MURPHY, M ;
WARD, K ;
MADIGAN, NP ;
BLANKENSHIP, J ;
HALBERT, M ;
FLANAGAN, C ;
TANNENBAUM, M ;
POLICH, M ;
STEVENSON, C ;
TCHENG, J .
NEW ENGLAND JOURNAL OF MEDICINE, 1994, 330 (14) :956-961
[5]  
Coller BS, 1997, CIRCULATION, V96, P3828
[6]   Screening for von Willebrand disease with a new analyzer using high shear stress: A study of 60 cases [J].
Fressinaud, E ;
Veyradier, A ;
Truchaud, F ;
Martin, I ;
Boyer-Neumann, C ;
Trossaert, M ;
Meyer, D .
BLOOD, 1998, 91 (04) :1325-1331
[7]   Clopidogrel inhibition of stent, graft, and vascular thrombogenesis with antithrombotic enhancement by aspirin in nonhuman primates [J].
Harker, LA ;
Marzec, UM ;
Kelly, AB ;
Chronos, NRF ;
Sundell, IB ;
Hanson, SR ;
Herbert, JM .
CIRCULATION, 1998, 98 (22) :2461-2469
[8]   Time course, magnitude, and consistency of platelet inhibition by abciximab, tirofiban, or eptifibatide in patients with unstable angina pectoris undergoing percutaneous coronary intervention [J].
Kereiakes, DJ ;
Broderick, TM ;
Roth, EM ;
Whang, D ;
Shimshak, T ;
Runyon, JP ;
Hattemer, C ;
Schneider, J ;
Lacock, P ;
Mueller, M ;
Abbottsmith, CW .
AMERICAN JOURNAL OF CARDIOLOGY, 1999, 84 (04) :391-395
[9]   Clinical outcomes of therapeutic agents that block the platelet glycoprotein IIb/IIIa integrin in ischemic heart disease [J].
Kong, DF ;
Califf, RM ;
Miller, DP ;
Moliterno, DJ ;
White, HD ;
Harrington, RA ;
Tcheng, JE ;
Lincoff, AM ;
Hasselblad, V ;
Topol, EJ .
CIRCULATION, 1998, 98 (25) :2829-2835
[10]   The effect of antiplatelet drugs, heparin, and preanalytical variables on platelet function detected by the platelet function analyzer (PFA-100®) [J].
Kottke-Marchant, K ;
Powers, JB ;
Brooks, L ;
Kundu, S ;
Christie, DJ .
CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS, 1999, 5 (02) :122-130