Foreword

Platelet aggregation is a major factor in acute ischaemic syndromes (unstable angina and myocardial infarction) and excessive platelet aggregation can complicate coro- nary interventions. In clinical practice, platelet aggregation is usually initiated by spontaneous rupture of a coronary plaque, or by iatrogenic rupture (dissection) during coro- nary intervention. Current treatment of unstable angina and myocardial infarction includes aspirin, a weak plate- let aggregation inhibitor, and heparin as anticoagulant. Similarly aspirin and heparin are used routinely to avoid thrombotic complications during coronary intervention. In spite of such combination therapy, platelet aggregation remains a major clinical problem in subgroups of patients with unstable angina and during coronary intervention.