Valvular Heart Disease

1344149 - Global Myocardial Ischemia in Severe Aortic Stenosis Reverses Early after Aortic Valve Replacement

Thursday, January 26, 2023

1:00 PM – 2:00 PM

Location: Pacific Jewel

Presenting Author(s)

GT

George D. Thornton, MBBS

Clinical Research Fellow
University College London, United Kingdom

Primary Author(s)

GT

George D. Thornton, MBBS

Clinical Research Fellow
University College London, United Kingdom

Co-Author(s)

JB

Jonathan B. Bennett, MBBS

Clinical Research Fellow
University College London, United Kingdom
FG

Francisco Gama, MD

Clinical Research Fellow
Barts Heart Centre, United Kingdom
CN

Christian Nitsche, MD, PhD

Cardiology Registrar
Barts Heart Centre at St Bartholomew's Hospital, United Kingdom
RM

Rok Mravljak, MSc

Research Cardiac Physiologist
Barts Heart Centre, United Kingdom
AA

Aderonke T. Abiodun, MBChB

Clinical Research Fellow
University College London, United Kingdom
NA

Nikoo Aziminia, MD, BSc

Clinical Research Fellow
UCL Institute of Cardiovascular Science
London, United Kingdom
SA

Salma Abdullahi, BSc

Research Practitioner
St Bartholomew's Hospital, United Kingdom
EG

Eva Gautam-Aitken

Research Project Manager
University College London, United Kingdom
HX

Hui Xue, PhD

Director, Imaging AI Program
National Institutes of Health
Bethesda, Maryland, United States
IP

Iain Pierce, PhD

Scientist
Barts Heart Centre at St Bartholomew's Hospital, United Kingdom
Rhodri Davies, MD, PhD

Associate clinical professor
University College London
London, Wales, United Kingdom
Charlotte Manisty

Consultant Cardiologist
University College London and Barts Heart Centre
London, England, United Kingdom
James C. Moon, MD

Clinical Director, Imaging
Barts Heart Centre and UCL
London, England, United Kingdom
PK

Peter Kellman, PhD

Senior Scientist
National Institutes of Health, Maryland, United States
Thomas A. Treibel, MD, PhD

Consultant Cardiologist
University College London, England, United Kingdom

Disclosure(s):

Charlotte Manisty: No relevant disclosure to display

Thomas A. Treibel, MD, PhD: No relevant disclosure to display

Background: Myocardial ischemia is common in aortic stenosis (AS) and is associated with exercise capacity, onset of symptoms and adverse myocardial remodeling. Positron emission tomography and invasive coronary studies have evaluated myocardial blood flow before and after aortic valve replacement (AVR), but these have been limited by imaging resolution, or by assessment of flow in a single coronary territory rather than the extent of the myocardium. Cardiovascular magnetic resonance (CMR) can determine myocardial function, remodeling and scar burden, and can also quantify pixel-wise stress myocardial blood flow (MBF). Using

AI-based segmentation, global and regional stress and rest MBF can be determined inline without human input with high precision and reproducibility. We aimed to evaluate the early effects of AVR on myocardial ischemia in patients with severe symptomatic AS without flow limiting coronary disease.

Methods: Patients with severe symptomatic AS undergoing either surgical or transcatheter AVR were prospectively recruited. None had flow limiting epicardial coronary stenosis by CT or invasive coronary angiography. Patients underwent baseline echocardiography, paired cardiovascular magnetic resonance (CMR) with adenosine stress (140mcg/kg/min for 4 minutes) at baseline and a median[IQR] of 10 (7-14)]weeks post-operatively.

Results:

21 patients (median [IQR] age 71 [66-74], 71% male) were included. Seventeen of 21 patients underwent paired stress perfusion (4 omitted due to safety concerns). The median [IQR] peak aortic velocity by echocardiography (Vmax) was 4.4 [4.2-4.6]m/s and AVA 0.75 [0.6-0.9]cm². At 10 weeks post-AVR, the Vmax improved to median [IQR] 2.5 [2.02-2.98]m/s and the LV mass by CMR regressed by 7%. Stress myocardial blood flow (MBF) increased by 50% from median [IQR] 1.62 [1.36-2.21]ml/g/min to 2.42 [1.66-2.74]ml/g/min,p< 0.001. Both epicardial and endocardial MBF improved after valve replacement, but the effect was mostly driven by an almost doubling of endocardial MBF from median [IQR] 1.24 [1.16-1.78] to 2.14 [1.69-2.43]ml/g/min. Likewise there was an improvement in the endocardial to epicardial ratio from median [IQR] 0.69 [0.62-0.76] to 0.83 [0.79-0.94]. Resting MBF decreased from median [IQR] 0.95 [0.76-1.10] ml/g/min to 0.82[0.74-0.88]ml/g/min, p=0.04.

Conclusion:

Severe AS results in profound subendocardial ischemia which may be a substrate for myocardial fibrosis and adverse cardiac events, but is highly and rapidly reversible by valve intervention. Myocardial blood flow improves by 50% early after AVR, driven by a near doubling of endocardial myocardial blood flow. This effect is seen even prior to substantial LV mass regression. Larger studies with histological correlation are required to determine the relative contributions of afterload and structural capillary rarefaction to ischemia in these patients.