Article Text

Download PDFPDF
The central role of platelet activation in determining the severity of acute coronary syndromes
  1. S Kennon1,
  2. C P Price2,
  3. P G Mills1,
  4. M Macey3,
  5. J Cooper4,
  6. H Clarke2,
  7. A D Timmis1
  1. 1Department of Cardiology, Bart’s and the London NHS Trust, London, UK
  2. 2Department of Clinical Biochemistry, Bart’s and the London NHS Trust
  3. 3Department of Haematology, Bart’s and the London NHS Trust
  4. 4MRC Epidemiology and Medical Care Unit, Charterhouse Square, London, UK
  1. Correspondence to:
    Dr S Kennon, Cardiac Catheterisation Laboratory, St Vincents Private Campus, 59–61 Victoria Parade, Fitzroy, Melbourne, Victoria 3065, Australia;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Recent observational studies in acute coronary syndromes have shown that factors influencing the degree of platelet activation also influence the mode of presentation. Prior aspirin treatment and smoking—with directionally opposite effects on platelet function—were found to be independently associated with unstable angina and myocardial infarction, respectively.1 However, the few studies involving direct measurement of activation parameters in acute coronary syndromes have not provided a consensus regarding this.2,3 To clarify whether there is differential activation in unstable angina and acute myocardial infarction we have prospectively assessed platelet activation in a cohort of patients presenting with acute coronary syndromes by using a light scattering technology to determine mean platelet component, a marker of platelet degranulation.


Consecutive patients admitted to an east London hospital with acute coronary syndromes were recruited. Myocardial infarction was diagnosed if two of the following criteria were fulfilled: (a) cardiac chest pain lasting at least 30 minutes; (b) ⩾ 0.1 mV ST elevation in at least one standard lead or ⩾ 0.2 mV ST elevation in two or more contiguous chest leads; and (c) creatine kinase concentration ⩾ 400 IU/l (upper limit of reference range 200 IU/l). ECG criteria were not required for the diagnosis of unstable angina; however, patients were recruited only if they fulfilled criteria for Braunwald class 3B unstable angina. Patients …

View Full Text