Elsevier

Canadian Journal of Cardiology

Volume 30, Issue 9, September 2014, Pages 1004-1011
Canadian Journal of Cardiology

Review
Left Ventricular Remodelling in Aortic Stenosis

https://doi.org/10.1016/j.cjca.2014.04.026Get rights and content

Abstract

Aortic stenosis (AS) is a progressive condition associated with high mortality if not treated. The hemodynamic effects of AS have serious implications for the left ventricle. In this review, we describe the responses of the left ventricle to AS by highlighting the process of adaptive remodelling, which begins as a beneficial compensatory mechanism but ultimately transitions to a maladaptive process with potentially irreversible consequences. We discuss the impact of left ventricular (LV) remodelling on diastolic and systolic function and on the development of symptoms. In addition, we review the adverse consequences of maladaptive LV remodelling on clinical outcomes before and after aortic valve replacement. The relative irreversibility of maladaptive remodelling and the clear relationship between its progression and clinical outcomes suggest a need to incorporate measures of LV performance beyond simply systolic function when deciding on the timing of valve replacement.

Résumé

La sténose aortique (SA) est une affection évolutive associée à une mortalité élevée lorsqu’elle n’est pas traitée. Les effets hémodynamiques de la SA ont des conséquences sérieuses sur le ventricule gauche. Dans cette revue, nous décrivons les réponses du ventricule gauche à la SA par la mise en évidence du processus de remodelage adaptatif, qui agit au début en tant que mécanisme compensatoire bénéfique, mais finalement en tant que transition vers un processus maladaptatif ayant des conséquences potentiellement irréversibles. Nous traitons des conséquences du remodelage ventriculaire gauche (VG) sur la fonction diastolique et systolique et sur la manifestation des symptômes. De plus, nous passons en revue les conséquences indésirables du remodelage VG maladaptatif sur les résultats cliniques avant et après le remplacement valvulaire aortique. L’irréversibilité relative du remodelage maladaptatif et le lien évident entre sa progression et les résultats cliniques montrent la nécessité d’intégrer les mesures de la performance VG au-delà de la simple fonction systolique lors de la détermination du moment opportun du remplacement valvulaire.

Section snippets

Compensatory LV Response to AS

Calcific AS develops by an insidious process spanning decades, with lipid deposition and inflammation leading to calcification of the aortic valve.2, 7 The valve leaflets become thick and less mobile, resulting in a narrowed valve orifice. Early animal studies provided our initial understanding of the body's response to increased afterload. Sasayama et al.8 assessed the ventricular response to ascending aortic banding in conscious dogs by using intraventricular micromanometers and pairs of

Maladaptive Remodelling

Although LV remodelling is considered a compensatory mechanism aimed at normalization of wall stress and maintenance of systolic function in AS, it is increasingly being associated with diminished LV performance and adverse clinical outcomes.22, 23, 24, 25, 26, 27 The factors responsible for the unfavourable consequences of LV remodelling remain unclear; however, subendocardial ischemia, altered myocardial energetics, and, especially, fibrosis appear to play a role.28 As the left ventricle

Symptoms

With the realization that adaptive remodelling becomes maladaptive with increasing LV hypertrophy and consequent myocyte death, fibrosis, and diastolic dysfunction, investigators increasingly evaluated the possible relationship between LV fibrosis and the presence of symptoms in severe AS. A study evaluating patients with asymptomatic severe AS found that those with inappropriate LV hypertrophy (> 10% expected) had a 4.5-fold higher risk of death, AVR, and hospital admission.27 This suggests

LV Reverse Remodelling After Valve Replacement

Several studies have characterized the regression of maladaptive LV remodelling after AVR. Within 18 months of SAVR, marked reductions in LV mass (∼30%-40%) occur.70, 71, 72 This initial change is thought to be largely caused by regression of myocyte hypertrophy. Because fibrous content remains relatively unchanged over this period, the proportion of LV mass made up by interstitial fibrosis increases.70, 71 Although left heart filling pressures improve soon after AVR, the relative increase in

Future Directions

LV remodelling in the setting of AS begins as a compensatory process to maintain wall stress but often transitions to a maladaptive response characterized by myocyte hypertrophy, interstitial fibrosis, and apoptosis. These progressive myocardial changes frequently lead to the development of symptoms and clinical decompensation and have implications on outcomes after AVR. Although LV reverse remodelling occurs after AVR, it is clear that AVR is often performed late after irreversible maladaptive

Disclosures

The authors have no conflicts of interest to disclose.

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