ReviewLeft Ventricular Remodelling in Aortic Stenosis
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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