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Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need

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...

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Autores principales: Ford, Thomas J, Corcoran, David, Berry, Colin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5861393/
https://www.ncbi.nlm.nih.gov/pubmed/29030424
http://dx.doi.org/10.1136/heartjnl-2017-311446
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author Ford, Thomas J
Corcoran, David
Berry, Colin
author_facet Ford, Thomas J
Corcoran, David
Berry, Colin
author_sort Ford, Thomas J
collection PubMed
description 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.
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spelling pubmed-58613932018-03-22 Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need Ford, Thomas J Corcoran, David Berry, Colin Heart Review 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. BMJ Publishing Group 2018-02 2017-10-13 /pmc/articles/PMC5861393/ /pubmed/29030424 http://dx.doi.org/10.1136/heartjnl-2017-311446 Text en © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. 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/
spellingShingle Review
Ford, Thomas J
Corcoran, David
Berry, Colin
Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
title Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
title_full Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
title_fullStr Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
title_full_unstemmed Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
title_short Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
title_sort stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5861393/
https://www.ncbi.nlm.nih.gov/pubmed/29030424
http://dx.doi.org/10.1136/heartjnl-2017-311446
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