Abstract
BackgroundIn patients with severe aortic stenosis (AS), long-term data tracking surgically induced effects of afterload reduction on reverse LV remodeling are not available. Echocardiographic data is available short term, but in limited fashion beyond one year. Cardiovascular MRI (CMR) offers the ability to serially track changes in LV metrics with small numbers due to its inherent high spatial resolution and low variability.HypothesisWe hypothesize that changes in LV structure and function following aortic valve replacement (AVR) are detectable by CMR and once triggered by AVR, continue for an extended period.MethodsTweny-four patients of which ten (67 ± 12 years, 6 female) with severe, but compensated AS underwent CMR pre-AVR, 6 months, 1 year and up to 4 years post-AVR. 3D LV mass index, volumetrics, LV geometry, and EF were measured.ResultsAll patients survived AVR and underwent CMR 4 serial CMR's. LVMI markedly decreased by 6 months (157 ± 42 to 134 ± 32 g/m2, p < 0.005) and continued trending downwards through 4 years (127 ± 32 g/m2). Similarly, EF increased pre to post-AVR (55 ± 22 to 65 ± 11%,(p < 0.05)) and continued trending upwards, remaining stable through years 1-4 (66 ± 11 vs. 65 ± 9%). LVEDVI, initially high pre-AVR, decreased post-AVR (83 ± 30 to 68 ± 11 ml/m2, p < 0.05) trending even lower by year 4 (66 ± 10 ml/m2). LV stroke volume increased rapidly from pre to post-AVR (40 ± 11 to 44 ± 7 ml, p < 0.05) continuing to increase non-significantly through 4 years (49 ± 14 ml) with these LV metrics paralleling improvements in NYHA. However, LVmass/volume, a 3D measure of LV geometry, remained unchanged over 4 years.ConclusionAfter initial beneficial effects imparted by AVR in severe AS patients, there are, as expected, marked improvements in LV reverse remodeling. Via CMR, surgically induced benefits to LV structure and function are durable and, unexpectedly express continued, albeit markedly incomplete improvement through 4 years post-AVR concordant with sustained improved clinical status. This supports down-regulation of both mRNA and MMP activity acutely with robust suppression long term.
Highlights
In patients with severe aortic stenosis (AS), compensatory left ventricular hypertrophy (LVH) is the predominate mechanism manifest to attempt to normalize the markedly elevated afterload imposed at the aortic valve level [1]
After initial beneficial effects imparted by aortic valve replacement (AVR) in severe AS patients, there are, as expected, marked improvements in LV reverse remodeling
Overtime this initially beneficial response leads to deleterious downstream effects not limited to mismatched neovascularization relative to the extent of left ventricular (LV) hypertrophy, supranormal LV performance likely due to geometic remodeling and marked interstial fibrosis due to collagen deposition that eventually leads to codominant explanations for the often pronounced hypertrophy often seen in late stage AS [2,3,4,5]
Summary
In patients with severe aortic stenosis (AS), compensatory left ventricular hypertrophy (LVH) is the predominate mechanism manifest to attempt to normalize the markedly elevated afterload imposed at the aortic valve level [1] Overtime this initially beneficial response leads to deleterious downstream effects not limited to mismatched neovascularization relative to the extent of left ventricular (LV) hypertrophy, supranormal LV performance likely due to geometic remodeling and marked interstial fibrosis due to collagen deposition that eventually leads to codominant explanations for the often pronounced hypertrophy often seen in late stage AS [2,3,4,5]. Hypothesis: We hypothesize that changes in LV structure and function following aortic valve replacement (AVR) are detectable by CMR and once triggered by AVR, continue for an extended period
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