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P3 Novel insights into diminished cardiac reserve in hypertrophic cardiomyopathy from 4D flow CMR component analysis
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  1. Z Ashkir1,
  2. AJ Lewandowski2,
  3. CJ Carlhäll3,
  4. E Wicks1,4,
  5. S Johnson1,
  6. A Hess5,
  7. M Mahmod1,
  8. S Myerson1,
  9. T Ebbers3,
  10. H Watkins6,
  11. S Neubauer1,
  12. B Raman1
  1. 1Oxford Centre for Clinical Magnetic Resonance Imaging (OCMR), University of Oxford, Oxford, UK
  2. 2Oxford Cardiovascular Clinical Research Facility (CCRF), University of Oxford, Oxford, UK
  3. 3Division of Diagnostics and Specialist Medicine, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden
  4. 4Inherited Cardiovascular Conditions (ICC) Service, Oxford University Hospitals NHS Foundation Trust and the University of Oxford, Level 6, West Wing, John Radcliffe Hospital, Headley Way, Headington, Oxford, UK
  5. 5Nuffield Department of Clinical Neurosciences (NDCN), University of Oxford, Oxford, UK
  6. 6Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK

Abstract

Objective 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 have been linked to functional limitation. This study aimed to characterise ventricular flow component changes in hypertrophic cardiomyopathy (HCM) and assess their relationship with phenotypic severity and predicted sudden cardiac death (SCD) risk.

Methods Fifty-one participants (37 non-obstructive HCM and 14 age, sex & BMI-matched controls) underwent 4D-flow CMR. Left ventricular (LV) end-diastolic volume was separated into four components: direct flow (blood transiting the ventricle within one cycle), retained inflow (blood entering the ventricle and retained for one cycle), delayed ejection flow (retained ventricular blood ejected during systole), and residual volume (ventricular blood retained for over two cycles).

Results HCM patients demonstrated greater direct flow compared to controls (47.5±9% vs 39.4±6%, p=0.003), and reduction in other components. In contrast to controls, HCM exhibited a paradoxical reduction in stroke volume (r=-0.31) with increasing direct flow suggesting diminished cardiac reserve. This direct flow component proportion correlated with LV mass index (r=0.38), end-diastolic volume index (r=-0.42), and SCD risk (r=0.38). Neither LV ejection fraction, nor stroke volume correlated with markers of phenotypic severity.

Conclusion HCM possesses a distinctive pattern of flow component distribution typified by direct flow-stroke volume decoupling, and 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.

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