Valvular Heart Disease

1342258 - Myocardial edema in aortic stenosis: insights from multiparametric SASHA

Friday, January 27, 2023

10:20 AM – 11:00 AM

Location: Pacific Jewel

Presenting Author(s)

CN

Christian Nitsche, MD, PhD

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

Primary Author(s)

CN

Christian Nitsche, MD, PhD

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

Co-Author(s)

GT

George D. Thornton, MBBS

Clinical Research Fellow
University College London, United Kingdom
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
JA

Jessica Artico, MD

Clinical Research Fellow
St Bartholomew's Hospital, England, United Kingdom
GJ

George Joy, MBBS

Research Fellow
University College London, United Kingdom
HK

Hibba Kurdi, MD, BSc

Cardiology Fellow
Barts Health NHS Trust, London, UK
London, United Kingdom
IP

Iain Pierce, PhD

Scientist
Barts Heart Centre at St Bartholomew's Hospital, United Kingdom
KC

Kelvin Chow, PhD

Staff Scientist
Siemens Healthineers
Chicago, Illinois, United States
PK

Peter Kellman, PhD

Senior Scientist
National Institutes of Health, Maryland, United States
HX

Hui Xue, PhD

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

Disclosure(s):

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

Background: Aortic stenosis (AS) causes dramatic adverse myocardial remodelling. Beyond myocardial hypertrophy and fibrosis, low-grade myocardial inflammation has been implicated, but is difficult to detect with conventional imaging. Recent data proposed a role of myocardial edema/inflammation in AS. ¹ Quantitative cardiac magnetic resonance (CMR) mapping by saturation-recovery single-shot acquisition (SASHA) generates more accurate T1 and T2 values compared to modified look-locker inversion recovery, which are less biased by magnetization transfer and T1/2 interdependence. ² We hypothesized that jointly acquired T1/T2 multiparametric SASHA (mSASHA) ³ can detect myocardial edema in AS and differentiate this from fibrosis.

Methods: Patients with severe AS and healthy volunteers (HV) underwent CMR on a 1.5T scanner (MAGNETOM Aera, Siemens) including non-contrast prototype mSASHA. AS patients also had post-contrast mSASHA acquired, allowing for calculation of extracellular volume fraction (ECV%). Segmentation of the myocardium (endo- and epicardial borders) and blood pool was performed automatically using an artificial intelligence (AI) approach fully integrated on the scanner (Gadgetron in-line AI, Figure 1).

Results: Twenty-eight AS patients (68±10years, 89% male) and 70 HV (39±11years, 44% male) underwent CMR with hematocrit on the day (no difference in hematocrit between groups). Compared to HV, AS patients had higher native T2_SASHA(45±5 vs.43±2ms, p=0.03; Figure 2A), but comparable T1_SASHA (1208±64 vs. 1209±30ms, p=0.8). In AS, native T2_SASHA correlated more strongly with ECV_SASHA(R²=0.72, p< 0.001; Figure 2B) than native T1_SASHA(R²=0.44, p< 0.001). By multiple linear regression analysis, only native T2_SASHA(adj. beta 0.008, 95% CI 0.005 to 0.011, p< 0.001) but not native T1_SASHA (p=0.2) remained significantly associated with ECV_SASHA.

Conclusion:

In AS, mSASHA offers new insights into left ventricular remodelling. Elevation of T2 in AS and its strong correlation with ECV indicate that myocardial edema/inflammation may play a small but important role in left ventricular adaptation to the increased afterload posed by AS.