CMR-Flow
Zakariye Ashkir, MD
Clinical Research Fellow
University of Oxford
Oxford, England, United Kingdom
Zakariye Ashkir, MD
Clinical Research Fellow
University of Oxford
Oxford, England, United Kingdom
Adam J. Lewandowski, PhD
Associate Professor
University of Oxford
OXFORD, England, United Kingdom
Aaron Hess, PhD
High Field Physics Lead
Oxford University, England, United Kingdom
Eleanor Wicks, MD, PhD
Clinical Lead of the Inherited Cardiac Conditions (ICC) Service
Oxford University Hospitals NHS Foundation Trust, United Kingdom
Masliza Mahmod, MD, PhD
Associate Professor
Oxford Centre for Magnetic Resonance Research, England, United Kingdom
Saul G. Myerson, MD
Professor
Oxford Centre for Clinical Magnetic Resonance Research
Oxford, England, United Kingdom
Tino Ebbers, PhD
Professor
Linköping University
Linkoping, Ostergotlands Lan, Sweden
Hugh Watkins, MD, PhD
Professor of Cardiovascular Medicine
University of Oxford, England, United Kingdom
Stefan Neubauer, MD, FSCMR
Professor of Cardiovascular Medicine
University of Oxford
Oxford, England, United Kingdom
Carl-Johan G. Carlhäll, PhD
Professor
Linköping University, Ostergotlands Lan, Sweden
Betty Raman, MD, PhD
Associate Professor
University of Oxford
Oxfordshire, England, United Kingdom
Hypertrophic cardiomyopathy (HCM) is characterised by hypercontractility and impaired ventricular relaxation which result in altered blood flow haemodynamics and have been linked with increased risk of adverse clinical events. Ventricular flow component analysis using 4D-flow cardiac magnetic resonance (4D-flow CMR) is a novel approach permitting comprehensive haemodynamic evaluation. Abnormal patterns of flow component distribution have been described in dilated and ischaemic cardiomyopathies and linked to functional limitation. This study aimed to characterise flow component changes in non-obstructive HCM (nHCM) and assess their relationship with phenotypic severity and predicted sudden cardiac death (SCD) risk.
Methods:
Fifty-one participants (37 nHCM and 14 age, sex & BMI-matched controls) underwent echocardiography and 4D-flow CMR. Left ventricular (LV) end-diastolic volume was separated into four functional components: direct flow (blood transiting the ventricle within one cycle), retained inflow (blood entering the ventricle and retained for one cycle ), delayed ejection flow (blood already in the ventricle and ejected during systole), and residual volume (ventricular blood retained for over two cycles). Flow component distribution and component end-diastolic kinetic energy/ml were calculated.
Results:
nHCM patients demonstrated greater LV ejection fraction (EF) and direct flow proportion compared to controls (47.5±9% vs 39.4±6%, p=0.003), and reduction in other flow components. Direct flow correlated with LV mass index (r=0.38, p=0.006), end-diastolic volume index (r=-0.42, p=0.010), and SCD risk (r=0.38, p=0.026). Neither LVEF, nor stroke volume correlated with markers of phenotypic severity. In contrast to controls, where there was a reliable increase in stroke volume alongside an increase in direct flow, in nHCM there was a paradoxical reduction in stroke volume (r=-0.31) with increasing direct flow, indicating a diminished cardiac reserve. There was no difference in component end-diastolic kinetic energy per ml between groups.
Conclusion:
nHCM possesses a distinctive pattern of flow component distribution typified by greater direct flow proportions at rest and direct flow-stroke volume uncoupling, in keeping with a diminished cardiac reserve. The correlation of direct flow proportion with phenotypic severity and SCD risk highlights its potential as a novel and sensitive haemodynamic measure of cardiovascular risk in patients.