Challenges and opportunities in improving left ventricular remodelling and clinical outcome following surgical and trans-catheter aortic valve replacement.
10.1007/s11684-021-0852-7
- Author:
Xu Yu JIN
1
;
Mario PETROU
2
;
Jiang Ting HU
3
;
Ed D NICOL
4
;
John R PEPPER
2
Author Information
1. Surgical Echo-Cardiology Services, Oxford Heart Centre, John Radcliffe Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, OX3 9DU, UK. xy.jin@ouh.nhs.uk.
2. Department of Cardiac Surgery, Royal Brompton Hospital, London, SW3 6NP, UK.
3. Cardiac Surgical Physiology and Genomics Group, Nuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, University of Oxford, Oxford, OX3 9DU, UK.
4. National Heart and Lung Institute, Imperial College London, London, SW3 6LY, UK.
- Publication Type:Review
- Keywords:
His-Purkinje pacing;
coronary access impairment;
left ventricular hypertrophy and fibrosis;
myocardial force-velocity relationship;
renin-angiotensin system inhibitors;
surgical aortic valve replacement;
trans-catheter aortic valve implantation
- MeSH:
Aged;
Aortic Valve/surgery*;
Aortic Valve Stenosis/surgery*;
Catheters;
Humans;
Transcatheter Aortic Valve Replacement;
Treatment Outcome;
Ventricular Remodeling
- From:
Frontiers of Medicine
2021;15(3):416-437
- CountryChina
- Language:English
-
Abstract:
Over the last half century, surgical aortic valve replacement (SAVR) has evolved to offer a durable and efficient valve haemodynamically, with low procedural complications that allows favourable remodelling of left ventricular (LV) structure and function. The latter has become more challenging among elderly patients, particularly following trans-catheter aortic valve implantation (TAVI). Precise understanding of myocardial adaptation to pressure and volume overloading and its responses to valve surgery requires comprehensive assessments from aortic valve energy loss, valvular-vascular impedance to myocardial activation, force-velocity relationship, and myocardial strain. LV hypertrophy and myocardial fibrosis remains as the structural and morphological focus in this endeavour. Early intervention in asymptomatic aortic stenosis or regurgitation along with individualised management of hypertension and atrial fibrillation is likely to improve patient outcome. Physiological pacing via the His-Purkinje system for conduction abnormalities, further reduction in para-valvular aortic regurgitation along with therapy of angiotensin receptor blockade will improve patient outcome by facilitating hypertrophy regression, LV coordinate contraction, and global vascular function. TAVI leaflet thromboses require anticoagulation while impaired access to coronary ostia risks future TAVI-in-TAVI or coronary interventions. Until comparable long-term durability and the resolution of TAVI related complications become available, SAVR remains the first choice for lower risk younger patients.
