Ariga, Rina

Bull, Sacha C

Francis, Jane M

Karamitsos, Theodoros D

Loudon, M

Mahmod, Masliza

Myerson, Saul G

Neubauer, Stefan K

Rigolli, Marzia

Sivalokanathan, S

Wijesurendra, Rohan S

JACC Cardiovascular Imaging

English

ORA - Oxford University Research Archive

A hyperdynamic RV is an early marker of clinical decompensation and cardiac recovery in aortic stenosis with normal LV ejection fraction

Oxford University Research Archive

  JIMG022518-0269 R2         A Hyperdynamic Right Ventricle is an Early Marker of Clinical Decompensation and Cardiac Recovery in Aortic Stenosis with Normal Left Ventricular Ejection Fraction  Marzia Rigolli, MBChB, MD Sanjay Sivalokanathan, MBBS, BSc Sacha Bull, MA, DPhil  Rohan S. Wijesurendra, MBBChir, MA Rina Ariga, MBBS, BSc Margaret Loudon, MBChB, DPhil Jane M. Francis, DCR(R), DNM Theodoros D. Karamitsos, MD, PhD Stefan Neubauer, SN, MD Masliza Mahmod, MBChB, DPhil* Saul G. Myerson, MBChB, MD*  Word Count: 800/800  University of Oxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, United Kingdom. This study was supported by the National Institute for Health Research, Oxford Biomedical Research Centre, Oxford, United Kingdom and the British Heart Foundation Centre of Research Excellence, Oxford, United Kingdom.  The authors have no relationship with industry to declare.  *These authors contributed equally to the work. Address for correspondence: Saul Myerson, University of Oxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, Headley Way, Oxford, OX3 9DU, United Kingdom. Fax: (+44) 01865 740449 Tel: (+44) 01865 221172 E-mail: saul.myerson@cardiov.ox.ac.uk.     JIMG022518-0269 R2         The right ventricle (RV) has been poorly studied in patients with aortic stenosis (AS) and normal left 1 ventricular (LV) function, due to the belief it is only affected by pulmonary hypertension (PH) 2 secondary to advanced LV dysfunction. Despite this, increased RV afterload is frequent in AS1, 3 difficult to assess non-invasively2, and may be present without detectable PH. The RV is extremely 4 sensitive to afterload changes and may provide an earlier marker of progression than pulmonary 5 pressures: although RV dysfunction is the typical response to acute pulmonary pressure increase, RV 6 adaptation to chronic afterload involves increasing contractility3,4. Therefore, we hypothesized that 7 in progressive AS with chronic afterload elevation, RV function would increase before detectable 8 PH, impact on symptoms and normalize after aortic valve replacement (AVR).  9 Eighty isolated AS (23 moderate, 24 severe asymptomatic, 33 severe symptomatic) and 28 controls 10 of similar age and sex distribution (18 normotensive; 10 hypertensive) were prospectively recruited. 11 Exclusions were: LV ejection fraction (EF) <55%, increased pulmonary pressures, underlying 12 cardiomyopathies and other severe valvular disease. Cardiovascular magnetic resonance (CMR) was 13 performed at baseline and, in 21 patients undergoing surgery, 8±2 months post-AVR, to assess 14 biventricular function and RV circumferential strain by ‘tissue-tracking’, a technique that may 15 overcome limitations in RV myocardial deformation5. RVEF was similar to controls in early LV 16 afterload stages (hypertensive controls: 61±4%, moderate AS: 62 ± 4%, p=0.89), but increased 17 significantly with AS severity (asymptomatic severe AS: 68 ± 7%, symptomatic AS: 74 ± 4%, 18 p<0.001; Figure). The hyperdynamic RV was accompanied by elevated RV strain (symptomatic AS: 19 -17 ± 4% vs controls: -14 ± 4%, p=0.02). RVEF correlated with peak aortic velocity (r=0.62, p<0.001, 20 Figure), symptoms of valve obstruction (r=0.66, p<0.001), and brain natriuretic peptide (BNP) values 21 (r=0.41, p=0.04). RVEF ≥71% had the best accuracy in detecting symptoms (area under the receiver 22 operator characteristics curve 0.89, p<0.001), while an RVEF ≥63% defined all symptomatic AS. 23 Baseline RVEF also correlated with LV mass regression post-AVR (r=0.61, p=0.01), and RV 24   parameters were restored towards normal post-AVR (RVEF 75 ± 4% à 61 ± 7%, p<0.001; RV strain 25 -17 ± 4 à -16 ± 4, p=0.05 in pre and post-AVR respectively).  26 We have thus demonstrated that a hyperdynamic RV is associated with increasing AS severity, 27 clinical decompensation, and LV recovery post-AVR. Right-sided compensation may play an 28 important role in adapting to chronic AS: the hypertrophic, stiff and sub-clinically impaired LV may 29 be aided by increased RV systolic function to preserve filling and maintain stroke volume across the 30 valve obstruction. A hyperdynamic RV may be a novel early objective marker of decompensated AS, 31 particularly useful for patients in whom symptoms are difficult to assess e.g. those less able to 32 mobilize or with multiple co-morbidities. If confirmed in larger-scale studies, a hyperdynamic RV 33 may result in a stimulus for consideration of valve replacement, and a new treatment target in patients 34 with right heart conditions in whom the blunted compensatory response may lead to earlier 35 decompensation. 36   JIMG022518-0269 R2                Figure – Association of RVEF with aortic stenosis  (A) RVEF in each AS group, showing increasing RVEF with worsening LV afterload. Following afterload relief by AVR, RVEF decreases towards that in the normal group. (B) Correlation of RVEF with AS severity.     1.  Johnson LW, Hapanowicz MB, Buonanno C, Bowser MA, Marvasti MA, Parker FB. Pulmonary hypertension in isolated aortic stenosis. Hemodynamic correlations and follow-up. J Thorac Cardiovasc Surg. 1988;95:603–7.  2.  Fisher MR, Forfia PR, Chamera E, Housten-Harris T, Champion HC, Girgis RE, Corretti MC, Hassoun PM. Accuracy of doppler echocardiography in the hemodynamic assessment of pulmonary hypertension. Am J Respir Crit Care Med. 2009;179:615–621.  3.  Vonk-Noordegraaf A, Haddad F, Chin KM, Forfia PR, Kawut SM, Lumens J, Naeije R, Newman J, Oudiz RJ, Provencher S, Torbicki A, Voelkel NF, Hassoun PM. Right heart adaptation to pulmonary arterial hypertension: Physiology and pathobiology. J Am Coll Cardiol. 2013;62:22–33.  4.  Aguero J, Ishikawa K, Hadri L, Santos-Gallego C, Fish K, Hammoudi N, Chaanine A, Torquato S, Naim C, Ibanez B, Pereda D, Garcia-Alvarez A, Fuster V, Sengupta PP, Leopold JA, Hajjar RJ. Characterization of right ventricular remodeling and failure in a chronic pulmonary hypertension model. Am J Physiol Heart Circ Physiol. 2014;307:H1204-15.  5.  Truong VT, Safdar KS, Kalra DK, Gao X, Ambach S, Taylor MD, Moore R, Taylor RJ, Germann J, Toro-Salazar O, Jefferies JL, Bartone C, Raman S V., Ngo T, Mazur W. Cardiac magnetic resonance tissue tracking in right ventricle: Feasibility and normal values. Magn Reson Imaging. 2017;38:189–195.   Peak transaortic velocity - echo (m/s)BA

Rigolli, M

Bull, SC

Wijesurendra, RS

Ariga, R

Francis, JM

Karamitsos, TD

Neubauer, SK

Mahmod, M

Myerson, SG

Oxford University Research Archive (ORA)

https://ora.ox.ac.uk/objects/uuid:b2b5b1ea-8dab-4860-979d-2aa445c48e76/files/me9ad91881b651528f623cc84f846b3af

A hyperdynamic RV is an early marker of clinical decompensation and cardiac recovery in aortic stenosis with normal LV ejection fraction

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