Author + information
- Received September 12, 2018
- Revision received January 31, 2019
- Accepted February 1, 2019
- Published online August 5, 2019.
- aBarts Heart Centre, St Bartholomew’s Hospital, London, United Kingdom
- bInstitute of Cardiovascular Science, University College London, London, United Kingdom
- ↵∗Address for correspondence:
Prof. James C. Moon, Barts Heart Centre, St Bartholomew’s Hospital, 2nd Floor, King George V Block, London EC1A 7BE, United Kingdom.
• AS is a disease of the valve, vasculature, and myocardium, causing left ventricular remodeling (hypertrophy, remodeling, fibrosis) and other cardiac changes (left atrial dilatation, pulmonary artery and right ventricular changes).
• Multimodality imaging plays a key role in assessment of cardiac changes to aortic stenosis afterload and to determine if they are adaptive and reversible, or maladaptive and irreversible.
• Myocardial remodeling and other cardiac changes are major determinants of symptoms and outcome from transcatheter or surgical aortic valve replacement.
Aortic stenosis (AS) causes left ventricular remodeling (hypertrophy, remodeling, fibrosis) and other cardiac changes (left atrial dilatation, pulmonary artery and right ventricular changes). These changes, and whether they are reversible (reverse remodeling), are major determinants of timing and outcome from transcatheter or surgical aortic valve replacement. Cardiac changes in response to AS afterload can either be adaptive and reversible, or maladaptive and irreversible, when they may convey residual risk after intervention. Structural and hemodynamic assessment of AS therefore needs to evaluate more than the valve, and, in particular, the myocardial remodeling response. Imaging plays a key role in this. This review assesses how multimodality imaging evaluates AS myocardial hypertrophy and its components (cellular hypertrophy, fibrosis, microvascular changes, and additional features such as cardiac amyloid) both before and after intervention, and seeks to highlight how care and outcomes in AS could be improved.
Drs. Treibel and Moon are directly and indirectly supported by the University College London Hospitals NIHR Biomedical Research Centre and Biomedical Research Unit at Barts Hospital, respectively. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received September 12, 2018.
- Revision received January 31, 2019.
- Accepted February 1, 2019.
- 2019 American College of Cardiology Foundation
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