Rapid Fire Abstracts
Jonathan Bennett, MBBS
Dr
University College London
Jonathan Bennett, MBBS
Dr
University College London
Bryce Watson, MD
Research Assistant
Institute of Cardiovascular Science, University College London, United Kingdom
Nikoo Aziminia, BMBS, BSc
Clinical Research Fellow
University College London and Barts Heart Centre, United Kingdom
George d. Thornton, MBBS PhD
NIHR Academic Clinical Lecturer
Institute of Cardiovascular Science, University College London, United Kingdom
Abhishek Shetye, MBChB BSc
Cardiology Registrar
Barts Heart Centre, St Bartholomew’s Hospital, London, United Kingdom, United Kingdom
Kush P. Patel, MD
Cardiologist Registrar
Barts Heart Centre, United Kingdom
Iain Pierce, PhD
CMR Physiicist
University College London and Barts Heart Centre, United Kingdom
Benjamin Meredith, BSc
Research Data Manager
University College London, United Kingdom
Rhodri H. Davies, MD, PhD
Doctor
University College London and Barts Heart Centre, United Kingdom
James C. Moon, MD
Professor of Cardiology
University College London, United Kingdom
Alun D. Hughes, MD, PhD
Professor
University College London, United Kingdom
Peter Kellman, PhD
Director of the Medical Signal and Image Processing Program
National Heart, Lung, and Blood Institute, National Institutes of Health
Thomas A. Treibel, MD, PhD
Associate Professor
University College London, United Kingdom
Aortic stenosis (AS) is characterized by impaired myocardial perfusion, particularly in the sub-endocardium, which can be detected non-invasively through cardiovascular magnetic resonance (CMR) quantitative stress perfusion mapping. Elevated left ventricular end-diastolic pressure (LVEDP), resulting from left ventricular hypertrophy and fibrosis, reduces coronary perfusion pressure (CPP) impairing myocardial perfusion. This study aims to evaluate whether impaired myocardial perfusion in AS is associated with invasively measured LVEDP.
Methods:
Single-centre prospective cohort study of patients with severe symptomatic AS with clinical decision for transcatheter aortic valve replacement (TAVR). Patients underwent pre-TAVR cardiovascular magnetic resonance (CMR) (1.5T Aera, Siemens Healthineers, Germany) with adenosine stress quantitative perfusion mapping(1). Aortic diastolic blood pressure (DBP) was measured during stress and rest using a validated device (USCOM BP+, Australia)(2). During TAVR invasive assessment of LVEDP was measured. Stress and rest CPP was calculated using DBP – LVEDP.
Results:
A total of 23 patients (age 78.3 ±7, male 15 [65%]) with severe AS (aortic valve area [AVA] 0.84 ±0.19cm2) were recruited. Mean LVEDP was 23.9 (10.7mmHg) with 20 (86%) having elevated LVEDP >15mmHg. Stress myocardial blood flow (sMBF) was 1.66 ±0.45mL/g/min, which was significantly lower in the endocardium compared to epicardium (1.4 ±0.43 vs 1.84 ±0.49mL/g/min, p < 0.001). The ratio of endocardial sMBF to epicardial sMBF was 0.76 ±0.14mL/g/min. Mean rest MBF (rMBF) was 1.00 ±0.29mL/g/min without difference between endo- and epicardium values.
Higher LVEDP was associated with higher systolic blood pressure (r= 0.50, p < 0.01), reduced AVA (R -0.42, p 0.04), females (28.9 ±9.9mmHg vs 21.2 ±10.4mmHg, p=0.04), and reduced stress endo-epicardial ratio (r=-0.42, p=0.04). Mean stress CPP was 44.8 ±12.7mmHg and was positively associated with stress endo-epicardial ratio (R 0.66, p < 0.001) but not absolute measures of sMBF. Rest CPP (53.5 ±14.5mmHg) was not associated with rMBF (r= -0.32, p=0.14).
Conclusion:
Reduced subendocardial perfusion, indicated by lower endocardial-to-epicardial sMBF ratio, in people with AS, is associated with higher systolic blood pressure, lower AVA, female sex, and higher LVEDP. The inclusion of CPP calculations enhanced the association with endocardial-to-epicardial sMBF ratio. However, absolute measures of sMBF and rMBF showed no significant association with either LVEDP or CPP.