Rapid Fire Abstracts
Bryce Watson, MD
Research Assistant
Institute of Cardiovascular Science, University College London, United Kingdom
Bryce Watson, MD
Research Assistant
Institute of Cardiovascular Science, University College London, United Kingdom
Jonathan Bennett, MBBS
Dr
University College London
Nikoo Aziminina, MD
Clinical Research Fellow
University College London, United Kingdom
Abhishek Shetye, MBChB BSc
Cardiology Registrar
Barts Heart Centre, St Bartholomew’s Hospital, London, United Kingdom, United Kingdom
George d. Thornton, MBBS PhD
NIHR Academic Clinical Lecturer
Institute of Cardiovascular Science, University College London, United Kingdom
Rhodri H. Davies, MD, PhD
Doctor
University College London and Barts Heart Centre, United Kingdom
Iain Pierce, PhD
CMR Physiicist
University College London and Barts Heart Centre, United Kingdom
Rebecca Kozor, MD, PhD
Associate Professor
Kolling Institute, Department of Cardiology, Royal North Shore Hospital, and University of Sydney, Australia
James C. Moon, MD
Professor of Cardiology
University College London, United Kingdom
Martin Ugander, MD, PhD
Professor of Cardiac Imaging
Kolling Institute, Royal North Shore Hospital and University of Sydney/ Karolinska University Hospital and Karolinska Institutet, Australia
Thomas A. Treibel, MD, PhD
Associate Professor
University College London, United Kingdom
Diastolic dysfunction in the setting of aortic stenosis (AS) before and following aortic valve replacement (AVR) is incompletely understood, with diastolic function improving in some individuals following AVR and not others (1)(2). The contribution of hydraulic force to left ventricular filling is yet to be assessed in individuals with AS before and after AVR. The aim of this study was to assess the atrioventricular area difference (AVAD) (3) as a surrogate for the net hydraulic force of left ventricular filling in a cohort of participants with severe symptomatic AS before and 1-year after AVR.
Methods: This was a single-centre prospective observational cohort study of patients with severe, symptomatic AS undergoing AVR between January 2012 and January 2015 (RELIEF-AS study, NCT02174471) (4). Recruited patients underwent clinical assessment and CMR at 1.5T (Avanto, Siemens Healthineers, Germany) prior to AVR and 1 year after AVR. In addition to routine ventricular and atrial analysis, AVAD at mid-diastole was measured as the difference between a validated machine learning (5) measurement of left ventricular short-axis area and manual measurement of left atrial short-axis area (Figure 1). AVAD correlations with cardiac structure, function, and myocardial remodeling were assessed.
Results: AS participants with paired CMR scans were included (n=110, 54% male, age 69±10 years, AVA 0.74±0.25 cm2, Vmax 4.4±0.6 m/s). AVAD was positive at baseline consistent with a net hydraulic force assisting LV filling. There was no difference between baseline and post-operative AVAD (2.8±6.5 vs 2.6±5.2 cm2, p=0.77). Echocardiographic diastolic function improved following AVR. After AVR, E/e’ decreased (median [interquartile range] 12.5 [9.1-16.0] vs 10.3 [7.8-12.6], p < 0.01) and e’ increased (6.6±2.1 vs 8.1±2.7 cm/s, p< 0.01). In multivariable linear regression, improvement in AVAD was weakly associated with the combination of lower baseline values of left ventricular mass index and extracellular volume fraction (global R2=0.16, p< 0.001, Table 1). Post-operative AVAD was weakly associated with increased post-operative 6-minute walk test distance (R2=0.15, p< 0.01).
Conclusion:
There is a net positive hydraulic force assisting LV filling in AS at baseline and following AVR. Improvement in AVAD, as a surrogate for hydraulic force, following AVR is associated with less severe myocardial remodeling at baseline.