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Postgrad Med J 2000;76:542-546 doi:10.1136/pmj.76.899.542
  • Review

Recent advances in ischaemic heart disease

  1. Michael Cusack,
  2. Simon Redwood,
  3. John Coltart
  1. Cardiothoracic Unit, St Thomas' Hospital, London SE1 7EH, UK
  1. Dr Cusack (email: michael.cusack{at}kcl.ac.uk)
  • Received 6 September 1999
  • Accepted 20 December 1999

Ischaemic heart disease remains a prevalent condition and continues to be associated with a significant likelihood of future major cardiac events including myocardial infarction (MI) and death. Recent years have seen considerable advances in the understanding and management of coronary artery disease. This article will attempt to focus on some of the areas of greatest interest among these, though as this represents a broad field, it cannot hope to be exhaustive.

Role of inflammation in atherosclerosis and the acute coronary syndromes

Since the “incrustation” hypothesis of von Rokitansky1 in 1852 and “lipid” hypothesis of Virchow2 in 1856 there has been great interest in the pathogenesis of atherosclerosis. Increasingly, the atherosclerotic process is seen as the response of the vessel wall to chronic, low grade injury.3 4 Initially there is dysfunction of the endothelium with accumulation of macrophages and lymphocytes subendothelially.5 The earliest discernible lesion of atherosclerosis is the “fatty streak” which histologically is an aggregation of lipid laden macrophages and T cells within the intima.5 The presence of fatty streaks are almost universal in adults and are found in the coronary arteries of 50% of children between 10 and 14 years of age.6 7 These fatty streaks precede the development of more complex lesions composed of a fibrous tissue cap containing smooth muscle cells overlying a core of lipid and necrotic material. As the volume of the plaque increases, there is initially remodelling of the arterial wall, increasing the external vessel diameter and reducing the degree of luminal narrowing.8 Plaques within the coronary circulation remain clinically “silent” until either:

(1) The process of vessel wall remodelling is overwhelmed and there is sufficient plaque encroachment into the vessel lumen to cause symptoms, or

(2) Rupture of the fibrous cap of the plaque occurs with subsequent thrombosis within the coronary artery sufficient to result in …

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