Reverse LV remodeling normalizes cardiac structure and function but leaves a persistently dysregulated HF gene program that requires prolonged unloading to fully reverse and restore normal responses to hemodynamic stress.
Short-term unloading may leave residual HF gene dysregulation despite functional recovery; leaves open optimal support duration to restore stress resilience.
, wherein there was a more complete (88%) reversal of the incident HF genes. These results demonstrate that reverse LV remodeling is associated with improvements in cardiac myocyte biology; however, the persistence of the abnormal HF gene program may be maladaptive following perturbations in hemodynamic loading conditions.
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Topkara et al. (2016) studied this question.
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