Left ventricular remodelling in bicuspid aortic valve disease

Author:

Butcher Steele C12ORCID,Pio Stephan M1ORCID,Kong William K F13ORCID,Singh Gurpreet K1ORCID,Ng Arnold C T4ORCID,Perry Rebecca5,Sia Ching-Hui3ORCID,Poh Kian Keong6ORCID,Almeida Ana G7,González Ariana8,Shen Mylène9,Yeo Tiong Cheng3,Shanks Miriam10,Popescu Bogdan A11ORCID,Galian Gay Laura12,Fijałkowski Marcin13,Liang Michael314,Tay Edgar4,Ajmone Marsan Nina1ORCID,Selvanayagam Joseph5,Pinto Fausto6,Zamorano Jose L7,Pibarot Philippe8ORCID,Evangelista Arturo11,Bax Jeroen J115,Delgado Victoria1ORCID

Affiliation:

1. Department of Cardiology, Leiden University Medical Center, Heart Lung Center, Albinusdreef 2, 2300 RC Leiden, The Netherlands

2. Department of Cardiology, Royal Perth Hospital, Perth, Western Australia, 197 Wellington St, Perth WA 6000, Australia

3. Department of Cardiology, National University Heart Centre, National University Health System, 5 Lower Kent Ridge Rd, Singapore 119074, Singapore

4. Department of Cardiology, Princess Alexandra Hospital, The University of Queensland, Brisbane, 199 Ipswich Rd, Woolloongabba QLD 4102, Australia

5. Department of Cardiovascular Medicine, Flinders Medical Centre, Flinders Dr, Bedford Park SA 5042, Adelaide, Australia

6. Yong Loo Lin School of Medicine, National University of Singapore, 10 Medical Dr, Singapore 117597, Singapore

7. Cardiology Department, Santa Maria University Hospital (CHLN), CAML, CCUL, Lisbon School of Medicine of the Universidade de Lisboa, Av. Prof. Egas Moniz MB, 1649-028 Lisboa, Portugal

8. Department of Cardiology, Hospital Universitario Ramón y Cajal, M-607, 9, 100, 28034 Madrid, Spain

9. Quebec Heart and Lung Institute, Laval University, 2725 Ch Ste-Foy, Québec, QC G1V 4G5, Canada

10. Division of Cardiology, University of Alberta, Mazankowski Alberta Heart Institute, 11220 83 Ave NW, Edmonton, AB T6G 2B7, Canada

11. University of Medicine and Pharmacy ‘Carol Davila’—Euroecolab, Institute of Cardiovascular Diseases ‘Prof. Dr. C. C. Iliescu’, Bulevardul Eroii Sanitari 8, București 050474, Romania

12. Department of Cardiology, Hospital Universitari Vall d’Hebrón, Passeig de la Vall d'Hebron, 119, 08035 Barcelona, Spain

13. First Department of Cardiology, Medical University of Gdansk, Marii Skłodowskiej-Curie 3a, 80-210 Gdańsk, Poland

14. Department of Cardiology, Khoo Teck Puat Hospital, 90 Yishun Central, Singapore 768828, Singapore

15. Heart Center, University of Turku and Turku University Hospital, Kiinamyllynkatu 4-8, 20521 Turku, Finland

Abstract

Abstract Aims Characterization of left ventricular (LV) geometric pattern and LV mass could provide an important insight into the pathophysiological adaptations of the LV to pressure and/or volume overload in patients with bicuspid aortic valve (BAV) and significant (≥moderate) aortic valve (AV) disease. This study aimed to characterize LV remodelling and its prognostic impact in patients with BAV according to the predominant type of valvular dysfunction. Methods and results In this international, multicentre BAV registry, 1345 patients [51.0 (37.0–63.0) years, 71% male] with significant AV disease were identified. Patients were classified as having isolated aortic stenosis (AS) (n = 669), isolated aortic regurgitation (AR) (n = 499) or mixed aortic valve disease (MAVD) (n = 177). LV hypertrophy was defined as a LV mass index >115 g/m2 in males and >95 g/m2 in females. LV geometric pattern was classified as (i) normal geometry: no LV hypertrophy, relative wall thickness (RWT) ≤0.42, (ii) concentric remodelling: no LV hypertrophy, RWT >0.42, (iii) concentric hypertrophy: LV hypertrophy, RWT >0.42, and (iv) eccentric hypertrophy: LV hypertrophy, RWT ≤0.42. Patients were followed-up for the endpoints of event-free survival (defined as a composite of AV repair/replacement and all-cause mortality) and all-cause mortality. Type of AV dysfunction was related to significant variations in LV remodelling. Higher LV mass index, i.e. LV hypertrophy, was independently associated with the composite endpoint for patients with isolated AS [hazard ratio (HR) 1.08 per 25 g/m2, 95% confidence interval (CI) 1.00–1.17, P = 0.046] and AR (HR 1.19 per 25 g/m2, 95% CI 1.11–1.29, P < 0.001), but not for those with MAVD. The presence of concentric remodelling, concentric hypertrophy and eccentric hypertrophy were independently related to the composite endpoint in patients with isolated AS (HR 1.54, 95% CI 1.06–2.23, P = 0.024; HR 1.68, 95% CI 1.17–2.42, P = 0.005; HR 1.59, 95% CI 1.03–2.45, P = 0.038, respectively), while concentric hypertrophy and eccentric hypertrophy were independently associated with the combined endpoint for those with isolated AR (HR 2.49, 95% CI 1.35–4.60, P = 0.004 and HR 3.05, 95% CI 1.71–5.45, P < 0.001, respectively). There was no independent association observed between LV remodelling and the combined endpoint for patients with MAVD. Conclusions LV hypertrophy or remodelling were independently associated with the composite endpoint of AV repair/replacement and all-cause mortality for patients with isolated AS and isolated AR, although not for patients with MAVD.

Funder

European Society of Cardiology

Publisher

Oxford University Press (OUP)

Subject

Cardiology and Cardiovascular Medicine,Radiology, Nuclear Medicine and imaging,General Medicine

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