Semin Thromb Hemost 2005; 31(4): 416-419
DOI: 10.1055/s-2005-916676
Copyright © 2005 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Influence of Systemic Inflammation on the Interpretation of Response to Antiplatelet Therapy, Monitored by PFA-100

Sophie Ziegler1 , 4 , Elisabeth Alt1 , Martin Brunner2 , Wolfgang Speiser3 , Erich Minar1
  • 1Clinical Department of Angiology, Medical University of Vienna, Vienna, Austria
  • 2Clinical Department of Pharmacology, Medical University of Vienna, Vienna, Austria
  • 3Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, Austria
  • 4Professor
Further Information

Publication History

Publication Date:
07 September 2005 (online)

ABSTRACT

Recently it was shown that inflammation adversely influences results obtained with the Platelet Function Analyzer System PFA-100, hypothesizing that inflammation could confound interpretation of platelet function results. We investigated the clinical relevance of these results in patients with peripheral arterial occlusive disease (PAOD), with and without signs of systemic inflammation. In 98 PAOD patients, all treated with acetylsalicylic acid (ASA), we measured PFA-100 closure times with the collagen-epinephrine test cartridges. C-reactive protein (CRP) values were measured as an indicator for systemic inflammation. Mean CRP levels were elevated in 23 patients (23%). There was no difference in mean PFA-100 results between patients with elevated CRP-levels and those without. During clinical use of the PFA system, systemic inflammation had no major influence on the performance of the collagen-epinephrine cartridge. With respect to the response to antiplatelet therapy with ASA, the results suggest that the platelet inhibitory effect of ASA is not reduced under inflammatory conditions.

REFERENCES

  • 1 Montalescot G, Collet J P, Lison L et al.. Effects of various anticoagulant treatments on von Willebrand factor release in unstable angina.  J Am Coll Cardiol. 2000;  36 110-114
  • 2 Fiotti N, Giansante C, Ponte E et al.. Atherosclerosis and inflammation. Patterns of cytokine regulation in patients with peripheral arterial disease.  Atherosclerosis. 1999;  145 51-60
  • 3 Li-Saw-Hee F L, Blann A D, Lip G J. Effects of fixed low-dose warfarin, aspirin-warfarin combination therapy, and dose-adjusted warfarin on thrombogenesis in chronic arterial fibrillation.  Stroke. 2000;  31 828-833
  • 4 Isaka N, Tanigawa T, Nishikawa M, Nakano T. High shear stress induced platelet aggregation (h-SIPA) and effects of antiplatelet therapy [in Japanese].  Nippon Rinsho. 1998;  56 2624-2629
  • 5 Turner N A, Moake J L, Kamat S G et al.. Comparative real time effects on platelets adhesion and aggregation under flowing conditions of in vivo aspirin, heparin, and monoclonal antibody fragment against glycoprotein IIbIIIa.  Circulation. 1995;  91 1354-1362
  • 6 Homoncik M, Blann A D, Hollenstein U, Pernerstorfer T, Eichler H G, Jilma B. Systemic inflammation increases shear stress-induced platelet plug formation measured by the PFA-100.  Br J Haematol. 2000;  111 1250-1252
  • 7 Gralnik H R, McKeown L P, Wilson O M, Williams S B, Elin R J. von Willebrand factor release induced by endotoxin.  J Lab Clin Med. 1989;  113 118-122
  • 8 Ridker P M, Stampfer M J, Rifai N. Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a) and standard cholesterol screening as predictors of peripheral arterial disease.  JAMA. 2001;  285 2481-2485
  • 9 Langlois M, Duprez D, Delanghe J, Buyzere M, Clement D L. Serum vitamin C concentration is low in peripheral arterial disease and is associated with inflammation and severity of atherosclerosis.  Circulation. 2001;  103 1863-1868
  • 10 Rossi E, Biasucci L M, Citterio F et al.. Risk of myocardial infarction and angina in patients with severe peripheral vascular disease: predictive role of C-reactive protein.  Circulation. 2002;  105 800-803
  • 11 Ortel T, James A H, Thames E H, Moore K D, Greenberg C S. Assessment of primary hemostasis by PFA-100 analysis in a tertiary care centre.  Thromb Haemost. 2000;  84 93-97
  • 12 von Pape K W, Aland E, Bohner J. Platelet function analysis with PFA-100 in patients medicated with acetylsalicylic acid strongly depends on concentration of sodium citrate used for anticoagulation of blood sample.  Thromb Res. 2000;  98 295-299
  • 13 Favaloro E J, Facey D, Henniker A. Use of a novel platelet function analyzer (PFA-100) with high sensitivity to disturbances in von Willebrand factor to screen von Willebrand's disease and other disorders.  Am J Hematol. 1999;  62 165-174
  • 14 Albert M A, Ridker P M. The role of C-reactive protein in cardiovascular disease risk.  Curr Cardiol Rep. 1999;  1 99-104
  • 15 McKenzie M, Gurbel P A, Levine D J, Serebruany V L. Clinical utility of available methods for determining platelet function.  Cardiology. 1999;  92 240-247
  • 16 Ziegler S, Alt E, Brunner M, Speiser W, Minar E. Influence of systemic inflammation on efficiency of antiplatelet therapy in PAOD patients.  Ann Hematol. 2004;  83 92-94
  • 17 Camici M. C-reactive protein, atherosclerosis and cardiovascular disease. An update.  Minerva Cardioangiol. 2002;  50 327-331
  • 18 Rutherford R B, Baker J D, Ernst C et al.. Recommended standards for reports dealing with lower extremity ischemia: revised version.  J Vasc Surg. 1997;  26 517-538
  • 19 Homoncik M, Jilma B, Hergovich N, Stohlawetz P, Panzer S, Speiser W. Monitoring of aspirin (ASA) pharmacodynamics with the platelet function analyzer PFA-100.  Thromb Haemost. 2000;  83 316-321
  • 20 Silva J A, White C J. Plaque instability in peripheral vessels.  Prog Cardiovasc Dis. 2002;  44 429-436
  • 21 Sestito A, Sciahbasi A, Landolfi R, Maseri A. A simple assay for platelet-mediated hemostasis in flowing whole blood (PFA-100); reproducibility and effects of sex and age.  Cardiologia. 1999;  44 661-665
  • 22 van Genderen P J, van Vliet H H, Prins F J et al.. Excessive prolongation of the bleeding time by aspirin in essential thrombocythemia is related to a decrease of large von Willebrand factor multimers in plasma.  Ann Hematol. 1997;  75 215-220
  • 23 Pernerstorfer T, Eichler H G, Stohlawetz P, Speiser W, Jilma B. Effects of heparin and aspirin on circulating P-selectin, E-selectin and von Willebrand factor levels in healthy men.  Atherosclerosis. 2001;  155 389-393
  • 24 Kaplan R C, Frishman W H. Systemic inflammation as a cardiovascular disease risk factor and as a potential target for drug therapy.  Heart Dis. 2001;  3 326-332
  • 25 Cheng T O. Salutary effects of aspirin in coronary artery disease are not limited to its platelet inhibitory effects [abstract].  Clin Cardiol. 1999;  22 A27
  • 26 Kharbanda R K, Walton B, Allen M et al.. Prevention of inflammation-induced endothelial dysfunction: a novel vasculo-protective action of aspirin.  Circulation. 2002;  105 2600-2604
  • 27 Guarnieri G. Atherosclerosis and inflammation. Patterns of cytokine regulation in patients with peripheral arterial disease.  Atherosclerosis. 1999;  145 51-60

 Dr.
Sophie Ziegler

Department of Internal Medicine II, Clinical Department of Angiology, Medical University of Vienna

Waehringer Guertel 18-20

A-1090 Wien, Austria

Email: sophie.ziegler@meduniwien.ac.at

    >