ANOCA/INOCA/MINOCA: Open artery ischemia
Ischemic heart disease continues to represent a major health threat for death, disability, and poor quality of life as it also consumes enormous health-related resources. For over a century, the major clinical phenotype was taken to be obstructive atherosclerosis involving the larger coronary arteri...
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| Format: | Article |
| Language: | English |
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Elsevier
2023-02-01
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| Series: | American Heart Journal Plus |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2666602223000125 |
| _version_ | 1828035809083654144 |
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| author | Carl J. Pepine |
| author_facet | Carl J. Pepine |
| author_sort | Carl J. Pepine |
| collection | DOAJ |
| description | Ischemic heart disease continues to represent a major health threat for death, disability, and poor quality of life as it also consumes enormous health-related resources. For over a century, the major clinical phenotype was taken to be obstructive atherosclerosis involving the larger coronary arteries (e.g., coronary artery disease [CAD]). However, evolving evidence now indicates that nonobstructive CAD is the predominant phenotype. Patients within this phenotype have been termed to have angina with no obstructive CAD (ANOCA), ischemia with no obstructive CAD (INOCA), or myocardial infarction with no obstructive coronary arteries (MINOCA). But as methods to assess cardiomyocyte injury evolve, these phenotypic distinctions have begun to merge, raising concern about their usefulness.Also, considerable evidence has suggested several endotypes that link to potential mechanisms. These include coronary microvascular dysfunction, augmented vasoreactivity (failure to relax appropriately, exaggerated constriction [“spasm”], etc.), nonobstructive atherosclerosis, pre-heart failure with preserved ejection fraction, hypercoagulable states, and several others, alone or in combination.This review summarizes these syndromes and their associated clinical outcomes with an emphasis on potential mechanistic signals. These involve the endothelium, the microvasculature, and cardiomyocyte function. Biomarkers of injury/dysfunction involving these structures are discussed along with a hypothetical construct for management being tested in an ongoing trial. |
| first_indexed | 2024-04-10T15:51:54Z |
| format | Article |
| id | doaj.art-8fcc4e24460a4dc0a333255e4e0a25a4 |
| institution | Directory Open Access Journal |
| issn | 2666-6022 |
| language | English |
| last_indexed | 2024-04-10T15:51:54Z |
| publishDate | 2023-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | American Heart Journal Plus |
| spelling | doaj.art-8fcc4e24460a4dc0a333255e4e0a25a42023-02-11T04:16:33ZengElsevierAmerican Heart Journal Plus2666-60222023-02-0126100260ANOCA/INOCA/MINOCA: Open artery ischemiaCarl J. Pepine01329 SW 16th St, P.O. Box 100288, Gainesville, FL 32610-0288, United States of America.; University of Florida, Gainesville, FL, United States of AmericaIschemic heart disease continues to represent a major health threat for death, disability, and poor quality of life as it also consumes enormous health-related resources. For over a century, the major clinical phenotype was taken to be obstructive atherosclerosis involving the larger coronary arteries (e.g., coronary artery disease [CAD]). However, evolving evidence now indicates that nonobstructive CAD is the predominant phenotype. Patients within this phenotype have been termed to have angina with no obstructive CAD (ANOCA), ischemia with no obstructive CAD (INOCA), or myocardial infarction with no obstructive coronary arteries (MINOCA). But as methods to assess cardiomyocyte injury evolve, these phenotypic distinctions have begun to merge, raising concern about their usefulness.Also, considerable evidence has suggested several endotypes that link to potential mechanisms. These include coronary microvascular dysfunction, augmented vasoreactivity (failure to relax appropriately, exaggerated constriction [“spasm”], etc.), nonobstructive atherosclerosis, pre-heart failure with preserved ejection fraction, hypercoagulable states, and several others, alone or in combination.This review summarizes these syndromes and their associated clinical outcomes with an emphasis on potential mechanistic signals. These involve the endothelium, the microvasculature, and cardiomyocyte function. Biomarkers of injury/dysfunction involving these structures are discussed along with a hypothetical construct for management being tested in an ongoing trial.http://www.sciencedirect.com/science/article/pii/S2666602223000125IschemiaANOCAINOCAMINOCAMechanistic signals |
| spellingShingle | Carl J. Pepine ANOCA/INOCA/MINOCA: Open artery ischemia American Heart Journal Plus Ischemia ANOCA INOCA MINOCA Mechanistic signals |
| title | ANOCA/INOCA/MINOCA: Open artery ischemia |
| title_full | ANOCA/INOCA/MINOCA: Open artery ischemia |
| title_fullStr | ANOCA/INOCA/MINOCA: Open artery ischemia |
| title_full_unstemmed | ANOCA/INOCA/MINOCA: Open artery ischemia |
| title_short | ANOCA/INOCA/MINOCA: Open artery ischemia |
| title_sort | anoca inoca minoca open artery ischemia |
| topic | Ischemia ANOCA INOCA MINOCA Mechanistic signals |
| url | http://www.sciencedirect.com/science/article/pii/S2666602223000125 |
| work_keys_str_mv | AT carljpepine anocainocaminocaopenarteryischemia |