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Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
  1. Thomas J Ford1,2,3,
  2. David Corcoran1,2,4,
  3. Colin Berry1,2,4
  1. 1 British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
  2. 2 West of Scotland Heart and Lung Centre, Golden Jubilee National Hospital, Clydebank, UK
  3. 3 University of New South Wales, Sydney, NSW, Australia
  4. 4 British Society of Cardiovascular Research, Glasgow, UK
  1. Correspondence to Professor Colin Berry, British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, Scotland, UK; colin.berry{at}glasgow.ac.uk

Abstract

The diagnostic management of patients with angina pectoris typically centres on the detection of obstructive epicardial CAD, which aligns with evidence-based treatment options that include medical therapy and myocardial revascularisation. This clinical paradigm fails to account for the considerable proportion (approximately one-third) of patients with angina in whom obstructive CAD is excluded. This common scenario presents a diagnostic conundrum whereby angina occurs but there is no obstructive CAD (ischaemia and no obstructive coronary artery disease—INOCA). We review new insights into the pathophysiology of angina whereby myocardial ischaemia results from a deficient supply of oxygenated blood to the myocardium, due to various combinations of focal or diffuse epicardial disease (macrovascular), microvascular dysfunction or both. Macrovascular disease may be due to the presence of obstructive CAD secondary to atherosclerosis, or may be dynamic due to a functional disorder (eg, coronary artery spasm, myocardial bridging). Pathophysiology of coronary microvascular disease may involve anatomical abnormalities resulting in increased coronary resistance, or functional abnormalities resulting in abnormal vasomotor tone. We consider novel clinical diagnostic techniques enabling new insights into the causes of angina and appraise the need for improved therapeutic options for patients with INOCA. We conclude that the taxonomy of stable CAD could improve to better reflect the heterogeneous pathophysiology of the coronary circulation. We propose the term ‘stable coronary syndromes’ (SCS), which aligns with the well-established terminology for ‘acute coronary syndromes’. SCS subtends a clinically relevant classification that more fully encompasses the different diseases of the epicardial and microvascular coronary circulation.

  • cardiac computer tomographic (ct) imaging
  • cardiac magnetic resonance (cmr) imaging
  • cardiac risk factors and prevention
  • chronic coronary disease
  • pharmacology

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

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Footnotes

  • TJF and DC contributed equally.

  • Twitter @UofGICAMS

  • Contributors CB conceived the article. TJF and DC provided the first draft, figures and revisions. All authors have approved the final manuscript.

  • Funding The British Heart Foundation has supported DC (FS/14/15/30661), TJF (RE/13/5/30177) and CB (RE/13/5/30177; FS/14/15/30661; FS172632744; PG-17-25-32884).

  • Competing interests CB is employed by the University of Glasgow, which holds consultancy and research agreements with companies that have commercial interests in the diagnosis and treatment of angina. The companies include Abbott Vascular, AstraZeneca, Boehringer Ingelheim, Menarini Pharmaceuticals and Siemens Healthcare. None of the other authors have any disclosures.

  • Ethics approval Obtained.

  • Provenance and peer review Commissioned; externally peer reviewed.

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