JACC: Cardiovascular Imaging
Assessment of Subclinical Left Ventricular Dysfunction in Aortic Stenosis
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Author + information
- Jordi S. Dahl, MD, PhDa,∗,
- Julien Magne, PhDb,∗,
- Patricia A. Pellikka, MDc,
- Erwan Donal, MD, PhDd and
- Thomas H. Marwick, MBBS, PhD, MPHe,∗ (tom.marwick{at}baker.edu.au)
- aDepartment of Cardiology, Odense University Hospital, Odense, Denmark
- bCHU Limoges, Hôpital Dupuytren, Service Cardiologie, INSERM 1094, Faculté de médecine de Limoges, Limoges, France
- cDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota
- dCardiology and CIC-IT1414, CHU de Rennes LTSI, Université Rennes-1, INSERM 1099, Rennes, France
- eBaker Heart and Diabetes Institute, Melbourne, Australia
- ↵∗Address for correspondence:
Dr. Thomas H. Marwick, Baker Heart and Diabetes Institute, Melbourne, P.O. Box 6492, Melbourne, Victoria 3004, Australia.
Central Illustration
Abstract
Left ventricular (LV) systolic dysfunction is an adverse consequence of the pressure overload of severe aortic stenosis (AS). The enlargement of the interstitial space with reactive fibrosis and subsequently with replacement fibrosis and cell death has been suggested to be the main driver of the transition to symptoms, heart failure, and adverse cardiovascular events even after aortic valve replacement (AVR). Early and accurate recognition of myocardial dysfunction offers the potential to optimize the timing of intervention in severe AS. In the asymptomatic patient, an LV ejection fraction (EF) cutpoint of <50% has been used for this purpose. However, in most asymptomatic patients, an LVEF <50% is uncommon, and patients with an LVEF of 50% to 59% fare almost as badly. Moreover, the presence of a small LV cavity, the reliability and automation of the global longitudinal strain (GLS) signal, and the independent prognostic role of GLS are reasons why GLS could be expected to be a better marker of subclinical LV dysfunction in these patients. This review seeks to define whether the existing EF cutoff in AS should be modified or whether GLS should replace it as the marker of subclinical LV dysfunction.
Footnotes
↵∗ Drs. Dahl and Magne contributed equally to this work and are joint first authors.
This work was supported in part by a Partnership grant from the National Health and Medical Research Council, Canberra, Australia. Dr. Marwick has received research support from General Electric Medical Systems for an ongoing research study on the use of strain for the assessment of cardiotoxicity. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 16, 2018.
- Revision received August 19, 2018.
- Accepted August 21, 2018.
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