Volume 11 Supplement 1
Incongruity of LVH regression with persistent inopportune diastolic dysfunction; results following AVR for severe aortic stenosis. Sponsored by the American Heart Association
© Biederman et al; licensee BioMed Central Ltd. 2009
Published: 28 January 2009
Very elegant invasive animal and human studies have demonstrated that in subjects with pressure overload due to severe aortic stenosis (AS), following aortic valve replacement (AVR), while myocyte regression is quite rapid, interstitial collagen content regression lags.
We hypothesize that this discord manifests as a thwarted improvement in diastolic function as related to LVH regression after AVR for AS.
All patients survived AVR and were available for serial follow-up over 4 time periods (mean 3 ± 1) out to 4 years. E:A ratios and/or morphology almost uniformly improved (9/10 pts) from 0.9:1 to 1.7:1 (p < 0.005), including 4 patients improving one complete grade. This was moderately well correlated with LV mass index regression (r = 0.55, p = < 0.05). Deceleration time also improved (233 vs. 192 ms, p < 0.005). While EF improved (55 ± 22 to 65 ± 11%, p < 0.05), as did LV geometry (1.07 ± 0.2 to 0.94 ± 0.24 g/m2, p < 0.05), neither were tightly correlated with improvements in diastolic function. However, using predictive modeling from historic controls, the improvement seen in diastolic function was incomplete and tardy. Specifically, while there were 4 patients that returned to normal diastolic function as per morphologic criteria, even these patients did not return to pre-morbid e:a ratios or deceleration times of the normal historic cohort. It followed that the remaining patients, except for one, improved only in arithmatic metrics. Importantly, while the LVH regresssed quickly, most occured within the first 6 months, there was a lag in diastolic function improvement by >12 months.
Following AVR for severe AS, as expected, marked improvements in LV mass regression occur; however, improvements in diastolic physiology are incomplete and quite tardy, not paralleling structural changes. Pathophysiologically, it is likely that the interstitium, failing to be as heavily modulated by relief of pressure overload as are the myocytes, contributes to a paradoxical increase in diastolic stiffness. This interplay between collagen content and myocyte results in a less than expected improvement in myocardial diastolic properties following afterload relief contributing to residual dyspnea.
This article is published under license to BioMed Central Ltd.