Valvular Heart Disease
Jonathan B. Bennett, MBBS
Clinical Research Fellow
University College London, United Kingdom
Jonathan B. Bennett, MBBS
Clinical Research Fellow
University College London, United Kingdom
George D. Thornton, MBBS
Clinical Research Fellow
University College London, United Kingdom
Christian Nitsche, MD, PhD
Cardiology Registrar
Barts Heart Centre at St Bartholomew's Hospital, United Kingdom
Francisco Gama, MD
Clinical Research Fellow
Barts Heart Centre, United Kingdom
Rok Mravljak, MSc
Research Cardiac Physiologist
Barts Heart Centre, United Kingdom
Iain Pierce, PhD
Scientist
Barts Heart Centre at St Bartholomew's Hospital, United Kingdom
Aderonke T. Abiodun, MBChB
Clinical Research Fellow
University College London, United Kingdom
Salma Abdullahi, BSc
Research Practitioner
St Bartholomew's Hospital, United Kingdom
Eva Gautam-Aitken
Research Project Manager
University College London, United Kingdom
Nikoo Aziminia, MD, BSc
Clinical Research Fellow
UCL Institute of Cardiovascular Science
London, United Kingdom
Peter Kellman, PhD
Senior Scientist
National Institutes of Health, Maryland, United States
Charlotte Manisty
Consultant Cardiologist
University College London and Barts Heart Centre
London, England, United Kingdom
Rhodri Davies, MD, PhD
Associate clinical professor
University College London
London, Wales, United Kingdom
James C. Moon, MD
Clinical Director, Imaging
Barts Heart Centre and UCL
London, England, United Kingdom
Thomas A. Treibel, MD, PhD
Consultant Cardiologist
University College London, England, United Kingdom
Left ventricular (LV) hypertrophy and myocardial fibrosis are the hallmarks of myocardial remodeling in severe aortic stenosis (AS) and they predict outcome after aortic valve replacement (AVR). Whereas focal replacement scar is irreversible after AVR, both left ventricular mass (LVM) and diffuse fibrosis regress at 1 year. Cardiac magnetic resonance (CMR) T1 mapping allows attribution of LVM regression to changes of cellular volume (CellVol) and extracellular volume (ECVol). Whether early post-AVR LVM regression is driven by CellVol or ECVol is unknown. We sought to investigate the components of early LVM regression at 8-12 weeks post-AVR.
Methods:
Patients with symptomatic severe AS recruited as part of the MASTER study (NCT04627987) underwent pre-AVR echocardiography (AS severity) and paired CMR (volumes, function, and diffuse fibrosis) early (8-12 weeks) post-AVR. CellVol was derived from total LVM (LVM/1.05 [specific gravity of myocardium]) and extracellular volume fraction (ECV%) via pre- and post-contrast T1 mapping and synthetic ECV calculation. Segments with focal fibrosis on late gadolinium enhancement (LGE) were excluded from ECV% calculation.
Results:
21 patients (age 70.8 ±9.5, male 68%) were imaged prior to and at median of 10 (IQR 3.1) weeks post-AVR (surgical AVR 63% / transcatheter AVR 37%). Aortic valve peak velocity improved (4.5±0.4 m/s to 2.5±0.4 m/s; p < 0.001) with significant improvement in NYHA class. Indexed LVM regressed 10.6% (87.3±16.9 g/m2 to 78.0±16.2 g/m2; p< 0.001) accompanied by 14.3% reduction in indexed CellVol (62.6±12.2 ml/m2 to 53.6 ±11.5 ml/m2; p< 0.001). ECV% increased from 24.6±2.5% to 27.9±2.0% (p < 0.001); but indexed ECVol did not significantly change at follow up (20.5±4.5 ml/m2 to 20.7±4.3 ml/m2; p=0.65). There was no new LGE present at follow-up.
Conclusion:
For the first time we show that early after AVR LVH reduction is caused by isolated cellular regression. Diffuse fibrosis is unchanged early post-AVR and as a percentage of the myocardium increases. This may be a contributing mechanism for early heart failure after valve replacement in AS and could be a target for adjunct medical therapy.