LV reverse remodeling imparted by aortic valve replacement for severe aortic stenosis; is it durable? A cardiovascular MRI study sponsored by the American Heart Association

Abstract

Background: In 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.

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.

Methods: Twenty-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.

Results: All 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.

Conclusion: After 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.

Figure 1

A coronal view from a steady-state free precession acquisition demonstrating the heavily calcified (arrow) and restricted aortic valve leaflets with a intervoxel dephasing defect as depicted by the systolic turbulence (bifid arrow) radiating into the proximal ascending aorta. In itself, this is indictative of a highly velocity jet consistant with severe AS. Using phase velocity mapping to formally quantitate the mean and peak transvalvular gradients, they were 53 and 78 mmHg, respectively; severe AS.

Figure 2

Serial cardiovascular MRI mid short-axis images in diastole (top row) and systole (bottom row) in a 76 WM taken the day prior to AVR, 6 months, one year and 4 years following AVR. The LV mass decreased from 186 to 154 g over the first 6 months to only regress to 132 g over the next 3 1/2 years demonstrating the early-rapid and late-slow pattern of LVH regression. Similarly, LVEF markedly improved after afterload relief from 54% to 60% in the first 6 months with no further improvements over the ensuing 3 1/2 years (62%).

Figure 3

Demonstrating that, despite marked afterload mismatch in a 55YOWM with an LVEF 23% and LV mass of 251 g, surgical relief of afterload in a patient with demonstrated myocardial reserve (mean/peak gradients of 52 and 33 mmHg, respectively) can ensue with striking improvements in LVEF and LV mass (57%EF and 197 g at 6 months post-AVR) with minimal change by year 4 (LVEF 56% and LV mass 158 g). The initial improvements in morphometrics and volumetrics paralled marked improvements in the patients clinical response, again most evident within the first 6 months post-AVR.

Figure 4

Plots of the temporal nature of the pattern of LVH regression serially out to 4 years. Note the immediate LVH regression sparked by the massive afterload relief by AVR. However, the trajectory of initial regression at 6 months would have predicted a far greater mass reduction then evident at 4 years.

Figure 5

(Fig A, B, C) Change in mitral regurgitation that ensues upon the relief of afterload by AVR. All but 2 patients had CMR defineable reduction in their MR grade (defined herein as 0 through 7 representing no (absent) through 2+ (moderate) MR. In those 2 patients the least amount of LV remodeling was present suggesting that effective mass/volume normalization is an important mechanism towards stabilizng and eventual MR relief as it is in its initiating pathophysiology. (Note, superimposition prevents all 10 patients from being displayed).