Reversal of Myocyte Hypertrophy by Ventricular Unloading: Cardiac Improvement Without Adrenergic Receptor Upregulation and Relocalization

Pippa M. Schnee, BA; Naeema Shah, MS; Marianne Bergheim, BA; Brian J. Poindexter, MS; L. Max Buja, MD; Timothy J. Myers, BS; Branislav Radovancevic, MD; O. Howard Frazier, MD; Roger J. Bick, PhD

Disclosures

May 16, 2006

Abstract

In previous studies, we found that the improved contractile ability of cardiac myocytes from patients who have had left ventricular assist device (LVAD) support was due to a number of beneficial changes, most notably in calcium handling (increased sarcoplasmic reticulum calcium binding and uptake), improved integrity of cell membranes due to phospholipid reconstruction (reduced lysophospholipid content), and an upregulation of adrenoreceptors (increased adrenoreceptor numbers). However, in the case presented here, there was no increase in adrenoreceptor number, which is something that we usually find in core tissue at the time of LVAD removal or organ transplantation; also, there was no homogeneous postassist device receptor distribution. However, the patient was well maintained for 10 months following LVAD implantation, until a donor organ was available, regardless of the lack of adrenoreceptor improvement.

We conclude from these studies that cardiac recovery is the result of the initiation of multiple repair mechanisms, and that the lack of expected changes, in this case increased adrenoreceptors, is not always an accurate indicator of anticipated outcome. We suggest that interventions and strategies have to consider multiple, beneficial changes due to unloading and target a number of biochemical and structural areas to produce improvement, even if not all of these improvements occur.


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