Global Longitudinal Strain as Predictor of Inducible Ischemia in No Obstructive Coronary Artery Disease in the CIAO-ISCHEMIA Study.

Echocardiography INOCA Ischemia No obstructive disease Strain Stress testing

Journal

Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography
ISSN: 1097-6795
Titre abrégé: J Am Soc Echocardiogr
Pays: United States
ID NLM: 8801388

Informations de publication

Date de publication:
16 Sep 2023
Historique:
received: 09 03 2023
revised: 18 08 2023
accepted: 05 09 2023
pubmed: 19 9 2023
medline: 19 9 2023
entrez: 18 9 2023
Statut: aheadofprint

Résumé

Global longitudinal strain (GLS) is a sensitive marker for identifying subclinical myocardial dysfunction in obstructive coronary artery disease (CAD). Little is known about the relationship between GLS and ischemia in patients with myocardial ischemia and no obstructive CAD (INOCA). To investigate the relationship between resting GLS and ischemia on stress echocardiography (SE) in patients with INOCA. Left ventricular GLS was calculated offline on resting SE images at enrollment (n = 144) and 1-year follow-up (n = 120) in the CIAO-ISCHEMIA (Changes in Ischemia and Angina over One year in International Study of Comparative Health Effectiveness with Medical and Invasive Approaches trial screen failures with no obstructive CAD on computed tomography [CT] angiography) study, which enrolled participants with moderate or severe ischemia by local SE interpretation (≥3 segments with new or worsening wall motion abnormality and no obstructive (<50% stenosis) on coronary computed tomography angiography. Global longitudinal strain values were normal in 83.3% at enrollment and 94.2% at follow-up. Global longitudinal strain values were not associated with a positive SE at enrollment (GLS = -21.5% positive SE vs GLS = -19.9% negative SE, P = .443) or follow-up (GLS = -23.2% positive SE vs GLS = -23.1% negative SE, P = .859). Significant change in GLS was not associated with positive SE in follow-up (P = .401). Regional strain was not associated with colocalizing ischemia at enrollment or follow-up. Changes in GLS and number of ischemic segments from enrollment to follow-up showed a modest but not clinically meaningful correlation (β = 0.41; 95% CI, 0.16, 0.67; P = .002). In this cohort of INOCA patients, resting GLS values were largely normal and did not associate with the presence, severity, or location of stress-induced ischemia. These findings may suggest the absence of subclinical myocardial dysfunction detectable by echocardiographic strain analysis at rest in INOCA.

Sections du résumé

BACKGROUND BACKGROUND
Global longitudinal strain (GLS) is a sensitive marker for identifying subclinical myocardial dysfunction in obstructive coronary artery disease (CAD). Little is known about the relationship between GLS and ischemia in patients with myocardial ischemia and no obstructive CAD (INOCA).
OBJECTIVES OBJECTIVE
To investigate the relationship between resting GLS and ischemia on stress echocardiography (SE) in patients with INOCA.
METHODS METHODS
Left ventricular GLS was calculated offline on resting SE images at enrollment (n = 144) and 1-year follow-up (n = 120) in the CIAO-ISCHEMIA (Changes in Ischemia and Angina over One year in International Study of Comparative Health Effectiveness with Medical and Invasive Approaches trial screen failures with no obstructive CAD on computed tomography [CT] angiography) study, which enrolled participants with moderate or severe ischemia by local SE interpretation (≥3 segments with new or worsening wall motion abnormality and no obstructive (<50% stenosis) on coronary computed tomography angiography.
RESULTS RESULTS
Global longitudinal strain values were normal in 83.3% at enrollment and 94.2% at follow-up. Global longitudinal strain values were not associated with a positive SE at enrollment (GLS = -21.5% positive SE vs GLS = -19.9% negative SE, P = .443) or follow-up (GLS = -23.2% positive SE vs GLS = -23.1% negative SE, P = .859). Significant change in GLS was not associated with positive SE in follow-up (P = .401). Regional strain was not associated with colocalizing ischemia at enrollment or follow-up. Changes in GLS and number of ischemic segments from enrollment to follow-up showed a modest but not clinically meaningful correlation (β = 0.41; 95% CI, 0.16, 0.67; P = .002).
CONCLUSIONS CONCLUSIONS
In this cohort of INOCA patients, resting GLS values were largely normal and did not associate with the presence, severity, or location of stress-induced ischemia. These findings may suggest the absence of subclinical myocardial dysfunction detectable by echocardiographic strain analysis at rest in INOCA.

Identifiants

pubmed: 37722490
pii: S0894-7317(23)00479-0
doi: 10.1016/j.echo.2023.09.006
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NHLBI NIH HHS
ID : U01 HL105462
Pays : United States

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Conflicts of Interest J.P. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. J.L.-S. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study; grants from Bayer; grants and personal fees from Pfizer; personal fees from Menarini; grants and personal fees from Sanofi; grants from Merck; grants and personal fees from Boeringher Infleheim; and grants from Amgen outside the submitted work. R.S. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study; he also reports speaker fees from Lantheus Medical Imaging, Bracco, and Philips Healthcare. M.D.S. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. He also serves on the Scientific Advisory Board for Regeneron and Amgen. P.A.P. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. K.A. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. K.A.-N. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. R.A. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. Y.X. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. D.M.K. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. J.A.S. reports grants from the National Heart, Lung, and Blood Institute, during the conduct of the study; personal fees from Bayer, Novartis, AstraZeneca, Amgen, Janssen, and United Healthcare; and grants from the American College of Cardiology, outside the submitted work. In addition, he has a patent Copyright to Seattle Angina Questionnaire with royalties paid and is on the Board of Directors for Blue Cross Blue Shield of Kansas City and Equity in Health Outcomes Sciences. J.H. is principal investigator for the ISCHEMIA trial for which, in addition to support by a National Heart, Lung, and Blood Institute grant, devices and medications were provided by Abbott Vascular, Medtronic, Abbott Laboratories (formerly St. Jude Medical), Royal Philips NV (formerly Volcano Corporation), Arbor Pharmaceuticals, AstraZeneca Pharmaceuticals, Merck Sharp & Dohme, Omron Healthcare, Sunovion Pharmaceuticals, Espero BioPharma; financial donations were provided by Arbor Pharmaceuticals LLC and AstraZeneca Pharmaceuticals LP. D.M. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. M.H.P. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. H.R.R. reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study, nonfinancial support from Abbott Vascular, Philips, SHL Telemedicine, and Siemens outside the submitted work. The remaining authors report no conflicts of interest.

Auteurs

Esther F Davis (EF)

Echocardiography Laboratory, Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts; Victorian Heart Institute and Victorian Heart Hospital, Victoria, Australia.

Daniela R Crousillat (DR)

Echocardiography Laboratory, Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiovascular Sciences, Department of Medicine, University of South Florida, Tampa, Florida; Department of Obstetrics and Gynecology, Tampa General-Heart and Vascular Institute, University of South Florida, Tampa, Florida.

Jesus Peteiro (J)

CHUAC, Universidad de A Coruña, CIBER-CV, A Coruna, Spain.

Jose Lopez-Sendon (J)

Hospital Universitario La Paz. Idipaz. UAM., Madrid, Spain.

Roxy Senior (R)

Northwick Park Hospital-Royal Brompton Hospital, London, United Kingdom.

Michael D Shapiro (MD)

Wake Forest University School of Medicine, Winston-Salem, North Carolina.

Patricia A Pellikka (PA)

Mayo Clinic, Rochester, Minnesota.

Radmila Lyubarova (R)

Albany Medical College, Albany, New York.

Khaled Alfakih (K)

King's College Hospital, London, United Kingdom.

Khaled Abdul-Nour (K)

Henry Ford Health System, Detroit, Michigan.

Rebecca Anthopolos (R)

Cardiovascular Clinical Research Center, Leon H. Charney Division of Cardiology, NYU Grossman School of Medicine, New York, New York.

Yifan Xu (Y)

Cardiovascular Clinical Research Center, Leon H. Charney Division of Cardiology, NYU Grossman School of Medicine, New York, New York.

Dennis M Kunichoff (DM)

Cardiovascular Clinical Research Center, Leon H. Charney Division of Cardiology, NYU Grossman School of Medicine, New York, New York.

Jerome L Fleg (JL)

National Institute of Health-National Heart Lung, and Blood Institute, Bethesda, Maryland.

John A Spertus (JA)

Saint Luke's Mid America Heart Institute/University of Missouri-Kansas City, Kansas City, Missouri.

Judith Hochman (J)

Cardiovascular Clinical Research Center, Leon H. Charney Division of Cardiology, NYU Grossman School of Medicine, New York, New York.

David Maron (D)

Department of Medicine, Stanford University School of Medicine, Stanford, California.

Michael H Picard (MH)

Echocardiography Laboratory, Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts.

Harmony R Reynolds (HR)

Cardiovascular Clinical Research Center, Leon H. Charney Division of Cardiology, NYU Grossman School of Medicine, New York, New York. Electronic address: harmony.reynolds@nyulangone.org.

Classifications MeSH