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• W2024170562 abstract "Coronary atherosclerosis progression is an active process involving complex interactions between inflammation, thrombosis and endothelial damage/dysfunction. Vascular intimal injury and plaque rupture exposes subepithelial collagen and von Willebrand factor (VWF), leading to prompt platelet–endothelial adhesion at the injured site and subsequent platelet activation [1Lee K.W. Lip G.Y.H. Acute coronary syndromes: Virchow's triad revisited.Blood Coagul Fibrinolysis. 2003; 14: 605-25Crossref PubMed Scopus (35) Google Scholar, 2Boos C.J. Lip G.Y. Blood clotting, inflammation, and thrombosis in cardiovascular events: perspectives.Front Biosci. 2006; 11: 328-36Crossref PubMed Scopus (25) Google Scholar]. In addition, there is simultaneous platelet–platelet aggregation and activation of the coagulation cascade, with the formation of a platelet–fibrin plug. This in turn can lead to localized and/or downstream vascular luminal compromise/obstruction, culminating ultimately in a potential acute coronary syndrome (ACS) event [1Lee K.W. Lip G.Y.H. Acute coronary syndromes: Virchow's triad revisited.Blood Coagul Fibrinolysis. 2003; 14: 605-25Crossref PubMed Scopus (35) Google Scholar, 2Boos C.J. Lip G.Y. Blood clotting, inflammation, and thrombosis in cardiovascular events: perspectives.Front Biosci. 2006; 11: 328-36Crossref PubMed Scopus (25) Google Scholar]. Platelets act to localize, amplify and sustain coagulation and inflammatory responses at the site of the ruptured plaque [1Lee K.W. Lip G.Y.H. Acute coronary syndromes: Virchow's triad revisited.Blood Coagul Fibrinolysis. 2003; 14: 605-25Crossref PubMed Scopus (35) Google Scholar, 2Boos C.J. Lip G.Y. Blood clotting, inflammation, and thrombosis in cardiovascular events: perspectives.Front Biosci. 2006; 11: 328-36Crossref PubMed Scopus (25) Google Scholar, 3Ruggeri Z.M. Platelets in atherothrombosis.Nature Med. 2002; 8: 1227-34Crossref PubMed Scopus (1374) Google Scholar]. Although the role of platelets in thrombosis is well described, it is increasingly clear that they also have a role in the pathogenesis of the underlying atherosclerotic process [3Ruggeri Z.M. Platelets in atherothrombosis.Nature Med. 2002; 8: 1227-34Crossref PubMed Scopus (1374) Google Scholar]. For example, platelet activation can occur even in the absence of plaque rupture at areas of high shear stress, such as at stenotic coronary lesions [4Jesty J. Yin W. Perrotta P. Bluestein D. Platelet activation in a circulating flow loop: combined effects of shear stress and exposure time.Platelets. 2003; 14: 143-9Crossref PubMed Scopus (98) Google Scholar, 5Lanza G.A. Sestito A. Iacovella S. Morlacchi L. Romagnoli E. Schiavoni G. Crea F. Maseri A. Andreotti F. Relation between platelet response to exercise and coronary angiographic findings in patients with effort angina.Circulation. 2003; 107: 1378-82Crossref PubMed Scopus (57) Google Scholar, 6Kawano K. Yoshino H. Aoki N. Udagawa H. Watanuki A. Hioki Y. Hasumura Y. Yasumura T. Homori M. Murata M. Ikeda Y. Ishikawa K. Shear‐induced platelet aggregation increases in patients with proximal and severe coronary artery stenosis.Clin Cardiol. 2002; 25: 154-60Crossref PubMed Scopus (19) Google Scholar]. Given the important role of platelets in both the activation and perpetuation of arterial thrombosis, there has been intense research interest in the utility of platelet function testing as an additional tool in cardiac risk stratification. Currently, there are a multitude of different methods available for the assessment of platelet function (and activation), and these include the quantification of known platelet‐specific metabolic products (e.g. platelet factor IV, β‐thrombomodulin and platelet microparticles in blood, and 11‐dehydrothromboxane β2 in urine), platelet surface receptors/proteins [e.g. soluble P‐selectin, glycoprotein (Gp) IIb/IIIa, etc. – often by flow cytometry], bleeding time, mean platelet volume, assessment of platelet shape change and platelet aggregometry (in response to known agonists) [7Harrison P. Platelet function analysis.Blood Rev. 2005; 19: 111-23Crossref PubMed Scopus (272) Google Scholar, 8Michelson A.D. Platelet function testing in cardiovascular diseases.Circulation. 2004; 110: e489-93Crossref PubMed Google Scholar, 9Kamath S. Blann A.D. Lip G.Y.H. Platelet activation: assessment and quantification.Eur Heart J. 2001; 22: 1561-71Crossref PubMed Scopus (411) Google Scholar]. However, given their often laborious processing methodology, and the need to transfer samples to a local laboratory, which is often some distance away, many of these techniques have limited applicability for widespread clinical practice or large‐scale epidemiologic studies. Consequently, there is growing interest in the ability to perform ‘near‐patient’ assessment of platelet function using whole blood, without the need for complicated specimen preparation. The PFA‐100® (Dade‐Behring, Marburg, Germany) is a simple, rapid automated point‐of‐care platelet function analyzer. Small amounts of citrated blood samples (0.8 mL per cartridge) are aspirated at high shear stress rates (5000–6000 s−1) through a capillary membrane, in the instrument cartridge, coated with the platelet agonists of either collagen/epinephrine (CEPI‐CT) or collagen/adenosine diphosphate (CADP‐CT) [10Hayward C.P. Harrison P. Cattaneo M. Ortel T.L. Rao A.K. The Platelet Physiology Subcommittee of the Scientific and Standardization Committee of the International Society on Thrombosis and HaemostasisPlatelet function analyzer (PFA)‐100 closure time in the evaluation of platelet disorders and platelet function.J Thromb Haemost. 2006; 4: 312-19Abstract Full Text Full Text PDF PubMed Scopus (354) Google Scholar]. This, in turn, triggers platelet activation, platelet–membrane adhesion and platelet–platelet aggregation, leading to occlusion of the 150 μm central aperture and the eventual cessation of blood flow. The results are expressed as closure time (CT, in seconds) for the CEPI and CAPD cartridges [10Hayward C.P. Harrison P. Cattaneo M. Ortel T.L. Rao A.K. The Platelet Physiology Subcommittee of the Scientific and Standardization Committee of the International Society on Thrombosis and HaemostasisPlatelet function analyzer (PFA)‐100 closure time in the evaluation of platelet disorders and platelet function.J Thromb Haemost. 2006; 4: 312-19Abstract Full Text Full Text PDF PubMed Scopus (354) Google Scholar]. In this issue of the Journal of Thrombosis and Haemostasis, Fuchs et al. [11Fuchs I. Frossard M. Spiel A. Riedmüller E. Laggner A.N. Jilma B. Platelet function in patients with acute coronary syndromes (ACS) predicts recurrent ACS.J Thromb Haemost. 2006; 4: 2547-52Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar] report on the ability of the PFA‐100 to predict the recurrence of ACS [recurrent non‐fatal myocardial infarction (MI), and the need for urgent revascularization or hospitalization because of recurrent angina] among a cohort of 208 patients presenting with ACS. They found that patients with a recurrence of ACS had significantly shorter baseline CADP‐CT as well as a shorter CEPI‐CT following aspirin treatment (approximately 10 min), when compared to those patients without an ACS recurrence. The use of both a CADP and a CEPI cartridge is important, as it helps determination of the responsiveness to aspirin, as although aspirin usually prolongs the CEPI‐CT, it has little effect on the CADP‐CT. In addition, Fuchs et al. [11Fuchs I. Frossard M. Spiel A. Riedmüller E. Laggner A.N. Jilma B. Platelet function in patients with acute coronary syndromes (ACS) predicts recurrent ACS.J Thromb Haemost. 2006; 4: 2547-52Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar] observed higher VWF–ristocetin cofactor (RiCo) activity (i.e. increased platelet activation) among the patients with an ACS recurrence, and a moderate, yet highly significant, correlation between VWF–RiCo and CADP‐CT. Ristocetin is a glycopeptide cofactor that is actively involved in platelet adhesion, initiating the binding of VWF to platelet GpIb. Hence, this correlation – although not unexpected by itself – does further support the conceptual dependence of VWF–platelet binding on CT values. The association of endothelial damage/dysfunction or increased platelet activation with increased future adverse cardiovascular events among patients presenting with ACS is not new [12Lee K.W. Lip G.Y. Tayebjee M. Foster W. Blann A.D. Circulating endothelial cells, von Willebrand factor, interleukin‐6, and prognosis in patients with acute coronary syndromes.Blood. 2005; 105: 526-32Crossref PubMed Scopus (200) Google Scholar, 13Trip M.D. Cats V.M. Van Capelle F.J. Vreeken J. Platelet hyperreactivity and prognosis in survivors of myocardial infarction.N Engl J Med. 1990; 322: 1549-54Crossref PubMed Scopus (548) Google Scholar]. However, the study by Fuchs et al. [11Fuchs I. Frossard M. Spiel A. Riedmüller E. Laggner A.N. Jilma B. Platelet function in patients with acute coronary syndromes (ACS) predicts recurrent ACS.J Thromb Haemost. 2006; 4: 2547-52Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar] is the first to investigate the utility of combined platelet and endothelial function assessment using CADP‐CT and VWF–RiCo levels respectively. This article also adds to the already increasing body of evidence in support of the utility of the PFA‐100 [10Hayward C.P. Harrison P. Cattaneo M. Ortel T.L. Rao A.K. The Platelet Physiology Subcommittee of the Scientific and Standardization Committee of the International Society on Thrombosis and HaemostasisPlatelet function analyzer (PFA)‐100 closure time in the evaluation of platelet disorders and platelet function.J Thromb Haemost. 2006; 4: 312-19Abstract Full Text Full Text PDF PubMed Scopus (354) Google Scholar]. For example, the same authors have shown – in a smaller cohort of 167 ACS patients – that a reduced CADP‐CT is associated with an increased amount of myocardial necrosis, particularly among those with ST elevation MI [14Frossard M. Fuchs I. Leitner J.M. Hsieh K. Vlcek M. Losert H. Domanovits H. Schreiber W. Laggner A.N. Jilma B. Platelet function predicts myocardial damage in patients with acute myocardial infarction.Circulation. 2004; 110: 1392-7Crossref PubMed Scopus (226) Google Scholar]. Hence, the present analysis by Fuchs et al. [11Fuchs I. Frossard M. Spiel A. Riedmüller E. Laggner A.N. Jilma B. Platelet function in patients with acute coronary syndromes (ACS) predicts recurrent ACS.J Thromb Haemost. 2006; 4: 2547-52Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar] clearly complements their previous work. It is of note that the quantification of platelet activation using the PFA‐100® can be related to the severity of coronary artery disease [5Lanza G.A. Sestito A. Iacovella S. Morlacchi L. Romagnoli E. Schiavoni G. Crea F. Maseri A. Andreotti F. Relation between platelet response to exercise and coronary angiographic findings in patients with effort angina.Circulation. 2003; 107: 1378-82Crossref PubMed Scopus (57) Google Scholar, 15Sestito A. Maccallini A. Sgueglia G.A. Infusino F. Larosa C. Aurigemma C. Crea F. Lanza G.A. Platelet reactivity in response to mental stress in syndrome X and in stable or unstable coronary artery disease.Thromb Res. 2005; 116: 25-31Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar] and with recurrence of ischemic events after percutaneous coronary angioplasty [16Gianetti J. Parri M.S. Sbrana S. Paoli F. Maffei S. Paradossi U. Berti S. Clerico A. Biagini A. Platelet activation predicts recurrent ischemic events after percutaneous coronary angioplasty: a 6 months prospective study.Thromb Res. 2006; 118: 487-93Abstract Full Text Full Text PDF PubMed Scopus (85) Google Scholar]. The results of this study must be interpreted with some caution, in terms of its general applicability as a widespread predictor of ACS recurrence. For example, the upstream use of aspirin 250 mg intravenously is not standard management practice in many centers, where oral aspirin (usually 300 mg) loading is usually administered. Furthermore, these results relate to ACS recurrence and not mortality per se, with a relatively low average follow‐up period (i.e. not a fixed one, such as ‘1‐year follow‐up’). Nevertheless, this is still the largest study of ACS patients using the PFA‐100® and does have important implications. We are clearly in the era of the biomarker, with a seemingly new and possibly useful marker cited in the medical literature on an almost weekly basis. In the arena of cardiovascular disease, the PFA‐100® appears to have some potential as a rapid point‐of‐care measure of platelet activation and perhaps as a tool with which to predict bleeding risk. There is indeed mounting evidence in favor of its use. Its applicability as an alternative to bleeding time and its possible use as a predictor of bleeding risk are also very attractive. It is of note that there have been a number of publications, with variable results, citing the ability of the PFA‐100® to identify aspirin‐resistant patients. However, the PFA‐100® CT is relatively insensitive to clopidogrel and ticlodipine. The ongoing Aspirin Non‐Responsiveness and Clopidogrel Endpoint Trial (ASCET) is seeking to address whether aspirin resistance – defined using the PFA‐100®– can be linked to adverse cardiovascular outcomes among 1000 coronary artery disease patients [17Pettersen A.A. Seljeflot I. Abdelnoor M. Arnesen H. Unstable angina, stroke, myocardial infarction and death in aspirin non‐responders. A prospective, randomized trial. The ASCET (ASpirin non‐responsiveness and Clopidogrel Endpoint Trial) design.Scand Cardiovasc J. 2004; 38: 353-6Crossref PubMed Scopus (65) Google Scholar]. Where do we go from here? The enthusiasts will advocate immediate use in the clinical setting, whereas the sceptics will still express many reservations. An international consensus based on an extensive overview of available evidence from use of the PFA‐100® has supported its use in the assessment of platelet disorders and function, but has suggested restricting its use to research studies and clinical trials at present [10Hayward C.P. Harrison P. Cattaneo M. Ortel T.L. Rao A.K. The Platelet Physiology Subcommittee of the Scientific and Standardization Committee of the International Society on Thrombosis and HaemostasisPlatelet function analyzer (PFA)‐100 closure time in the evaluation of platelet disorders and platelet function.J Thromb Haemost. 2006; 4: 312-19Abstract Full Text Full Text PDF PubMed Scopus (354) Google Scholar]. Consequently, optimism must be underpinned by the clear need for further data from well‐conducted, large, prospective clinical trials. The future for such a point‐of‐care device for platelet assessment still looks very promising. The authors state that they have no conflict of interest." @default.
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