Atrioventricular mechanical coupling and major adverse cardiac events in female patients following acute ST elevation myocardial infarction.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 01 2020
Historique:
received: 13 02 2019
revised: 10 06 2019
accepted: 14 06 2019
pubmed: 14 7 2019
medline: 24 11 2020
entrez: 14 7 2019
Statut: ppublish

Résumé

Sex-specific outcome data following myocardial infarction (MI) are inconclusive with some evidence suggesting association of female sex and increased major adverse cardiac events (MACE). Since mechanistic principles remain elusive, we aimed to quantify the underlying phenotype using cardiovascular magnetic resonance (CMR) quantitative deformation imaging and tissue characterisation. In total, 795 ST-elevation MI patients underwent post-interventional CMR imaging. Feature-tracking (CMR-FT) was performed in a blinded core-laboratory. Left ventricular function was quantified using ejection fraction (LVEF) and global longitudinal/circumferential/radial strains (GLS/GCS/GRS). Left atrial function was assessed by reservoir (εs), conduit (εe) and booster-pump strains (εa). Tissue characterisation included infarct size, microvascular obstruction and area at risk. Primary endpoint was the occurrence of MACE within 1 year. Female sex was associated with increased MACE (HR 1.96, 95% CI 1.13-3.42, p = 0.017) but not independently of baseline confounders (p = 0.526) with women being older, more often diabetic and hypertensive (p < 0.001) and of higher Killip-class (p = 0.010). Tissue characterisation was similar between sexes. Women showed impaired atrial (εs p = 0.011, εe p < 0.001) but increased systolic ventricular mechanics (GLS p = 0.001, LVEF p = 0.048). While atrial and ventricular function predicted MACE in men only LV GLS and GCS were associated with MACE in women irrespective of confounders (GLS p = 0.036, GCS p = 0.04). In men ventricular systolic contractility is impaired and volume assessments precisely stratify elevated risks. In contrast, women experience reduced atrial but increased ventricular systolic strain. This may reflect ventricular diastolic failure with systolic compensation, which is independently associated with MACE adding incremental value to sex-specific prognosis evaluation.

Sections du résumé

BACKGROUND
Sex-specific outcome data following myocardial infarction (MI) are inconclusive with some evidence suggesting association of female sex and increased major adverse cardiac events (MACE). Since mechanistic principles remain elusive, we aimed to quantify the underlying phenotype using cardiovascular magnetic resonance (CMR) quantitative deformation imaging and tissue characterisation.
METHODS
In total, 795 ST-elevation MI patients underwent post-interventional CMR imaging. Feature-tracking (CMR-FT) was performed in a blinded core-laboratory. Left ventricular function was quantified using ejection fraction (LVEF) and global longitudinal/circumferential/radial strains (GLS/GCS/GRS). Left atrial function was assessed by reservoir (εs), conduit (εe) and booster-pump strains (εa). Tissue characterisation included infarct size, microvascular obstruction and area at risk. Primary endpoint was the occurrence of MACE within 1 year.
RESULTS
Female sex was associated with increased MACE (HR 1.96, 95% CI 1.13-3.42, p = 0.017) but not independently of baseline confounders (p = 0.526) with women being older, more often diabetic and hypertensive (p < 0.001) and of higher Killip-class (p = 0.010). Tissue characterisation was similar between sexes. Women showed impaired atrial (εs p = 0.011, εe p < 0.001) but increased systolic ventricular mechanics (GLS p = 0.001, LVEF p = 0.048). While atrial and ventricular function predicted MACE in men only LV GLS and GCS were associated with MACE in women irrespective of confounders (GLS p = 0.036, GCS p = 0.04).
CONCLUSION
In men ventricular systolic contractility is impaired and volume assessments precisely stratify elevated risks. In contrast, women experience reduced atrial but increased ventricular systolic strain. This may reflect ventricular diastolic failure with systolic compensation, which is independently associated with MACE adding incremental value to sex-specific prognosis evaluation.

Identifiants

pubmed: 31300172
pii: S0167-5273(19)30773-9
doi: 10.1016/j.ijcard.2019.06.036
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

31-36

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Sören J Backhaus (SJ)

University Medical Center Göttingen, Department of Cardiology and Pneumology, Georg-August University, Göttingen, Germany; German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany.

Johannes T Kowallick (JT)

German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany; University Medical Center Göttingen, Institute for Diagnostic and Interventional Radiology, Georg-August University, Göttingen, Germany.

Thomas Stiermaier (T)

University Heart Center Lübeck, Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine), University Hospital Schleswig-Holstein, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), partner site Hamburg/Kiel/Lübeck, Lübeck, Germany.

Torben Lange (T)

University Medical Center Göttingen, Department of Cardiology and Pneumology, Georg-August University, Göttingen, Germany; German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany.

Alexander Koschalka (A)

University Medical Center Göttingen, Department of Cardiology and Pneumology, Georg-August University, Göttingen, Germany; German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany.

Jenny-Lou Navarra (JL)

University Medical Center Göttingen, Department of Cardiology and Pneumology, Georg-August University, Göttingen, Germany; German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany.

Johannes Uhlig (J)

German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany; University Medical Center Göttingen, Institute for Diagnostic and Interventional Radiology, Georg-August University, Göttingen, Germany.

Joachim Lotz (J)

German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany; University Medical Center Göttingen, Institute for Diagnostic and Interventional Radiology, Georg-August University, Göttingen, Germany.

Shelby Kutty (S)

Children's Hospital and Medical Center, University of Nebraska College of Medicine, Omaha, NE 68114, USA.

Boris Bigalke (B)

Charité Campus Benjamin Franklin, University Medical Center Berlin, Department of Cardiology, Berlin, Germany.

Matthias Gutberlet (M)

Heart Center Leipzig, University of Leipzig, Institute of Diagnostic and Interventional Radiology, Leipzig, Germany.

Gerd Hasenfuß (G)

University Medical Center Göttingen, Department of Cardiology and Pneumology, Georg-August University, Göttingen, Germany; German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany.

Holger Thiele (H)

Heart Center Leipzig, University of Leipzig, Department of Internal Medicine/Cardiology, Leipzig, Germany.

Ingo Eitel (I)

University Heart Center Lübeck, Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine), University Hospital Schleswig-Holstein, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), partner site Hamburg/Kiel/Lübeck, Lübeck, Germany.

Andreas Schuster (A)

University Medical Center Göttingen, Department of Cardiology and Pneumology, Georg-August University, Göttingen, Germany; German Center for Cardiovascular Research (DZHK), partner site Göttingen, Göttingen, Germany; Department of Cardiology, Royal North Shore Hospital, The Kolling Institute, Northern Clinical School, University of Sydney, Sydney, Australia. Electronic address: andreas_schuster@gmx.net.

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