Molecular biology of myocardial recovery.
The use of LVADs that leads to a dramatic mechanical and hemodynamic unloading of the failing left ventricle offers a unique opportunity to investigate the mechanisms of remodeling and reverse remodeling. Although it is being increasingly realized that the LVAD unloading results in regression of hypertrophy and improvement of myocyte function and LV geometry, the cellular and molecular mechanisms responsible for these beneficial effects remain undefined. The favorable alterations in geometry that occur in parallel fashion at the organ, cellular, and molecular levels are most likely caused by the reduced LV wall stress/stretch as a consequence of the mechanical support provided by LVAD. If it is confirmed that LVAD unloading can contribute significantly to reverse remodeling, the role of LVADs may graduate from bridge-to-transplantation or destination therapy to bridge-to-recovery.
Zhang
Jianyi
J
University of Minnesota Health Science Center, Minneapolis, MN 55455, USA. zhang047@maroon.tc.umn.edu
Narula
Jagat
J
D017209:Apoptosis / Q000502:physiology; D015415:Biomarkers; D001707:Biopsy, Needle; D003402:Creatine Kinase / Q000032:analysis / Q000378:metabolism*; D005260:Female; D006333:Heart Failure / Q000473:pathology* / Q000628:therapy*; D006353:Heart-Assist Devices; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000032:analysis / Q000378:metabolism; D008967:Molecular Biology; D011379:Prognosis; D012720:Severity of Illness Index; D018487:Ventricular Dysfunction, Left / Q000473:pathology* / Q000628:therapy; D020257:Ventricular Remodeling / Q000502:physiology*
D015415:Biomarkers; D020928:Mitogen-Activated Protein Kinases; D003402:Creatine Kinase