Clinical Review

ABC of interventional cardiology

Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarction

BMJ 2003; 326 doi: 10.1136/bmj.326.7401.1259 (Published 5 June 2003)
Cite this as: BMJ 2003;326:1259

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  1. Ever D Grech, consultant cardiologist, assistant professor,
  2. David R Ramsdale, consultant cardiologist
  1. Health Sciences Centre and St Boniface Hospital, Winnipeg, Manitoba, Canada and University of Manitoba, Winnipeg
  2. Cardiothoracic Centre, Liverpool

    Introduction

    The term acute coronary syndrome refers to a range of acute myocardial ischaemic states. It encompasses unstable angina, non-ST segment elevation myocardial infarction (ST segment elevation generally absent), and ST segment elevation infarction (persistent ST segment elevation usually present). This article will focus on the role of percutaneous coronary intervention in the management of unstable angina and non-ST segment elevation myocardial infarction; the next article will address the role of percutaneous intervention in ST segment elevation infarction.

    Although there is no universally accepted definition of unstable angina, it has been described as a clinical syndrome between stable angina and acute myocardial infarction. This broad definition encompasses many patients presenting with varying histories and reflects the complex pathophysiological mechanisms operating at different times and with different outcomes. Three main presentations have been described—angina at rest, new onset angina, and increasing angina.

    Spectrum of acute coronary syndromes according to electrocardiographic and biochemical markers of myocardial necrosis (troponin T, troponin I, and creatine kinase MB), in patients presenting with acute cardiac chest pain

    Pathogenesis

    The process central to the initiation of an acute coronary syndrome is disruption of an atheromatous plaque. Fissuring or rupture of these plaques—and consequent exposure of core constituents such as lipid, smooth muscle, and foam cells—leads to the local generation of thrombin and deposition of fibrin. This in turn promotes platelet aggregation and adhesion and the formation of intracoronary thrombus.

    Diagram of an unstable plaque with superimposed luminal thrombus

    Unstable angina and non-ST segment elevation myocardial infarction are generally associated with white, platelet-rich, and only partially occlusive thrombus. Microthrombi can detach and embolise downstream, causing myocardial ischaemia and infarction. In contrast, ST segment elevation (or Q wave) myocardial infarction has red, fibrin-rich, and more stable occlusive thrombus.

    Distal embolisation of a platelet-rich thrombus causing occlusion of intramyocardial arteriole (arrow). Such …

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