Determination of Optimal Duration of Mechanical Unloading for Failing Hearts to Achieve Bridge to Recovery in a Rat Heterotopic Heart Transplantation Model

Ventricular Assist Device: Emerging Modality for Long Term Cardiac Support

“…35 Cellular structure and function also improves and reverts back toward normal. [36][37][38][39] Thus, the reduction in left ventricular volumes is not just a function of the unloading provided by the VAD but actually reflects alterations in the dynamics of myocyte function.…”

“…To date, an average of only 5%-10% of patients who undergo mechanical circulatory support demonstrate adequate recovery of ventricular function to allow device explantation. 33,34 There is also concern that prolonged mechanical unloading reduces cardiac cell function, as well as cell size, in a time-dependent manner [35][36][37][38][39][40] which may lead to myocardial atrophy. Unloading induced atrophy can be an important impediment to myocardial recovery and removal of the VADs for bridge-to-recovery, limiting the efficacy of VAD treatment.…”

Myocardial Recovery Following Left Ventricular Assist Device Therapy

“…Clinical and experimental studies have shown recovery (Takaseya et al 2004), as well as no change (Chaudhary et al 2004) to occur with MU, in addition to a biphasic response, i.e. initial recovery followed by subsequent decline coinciding with contractile function deterioration (Oriyanhan et al 2007). Similarly, phospholamban (PLB) PLB:Serca2a ratio a key determinant of contractile function (Koss et al 1997), known to be elevated in HF, displays a similar short term recovery (decreased ratio), with later resurgence of ratio coinciding with prolonged support and decline in contractile function (Ogletree et al 2010).…”

“…Improvement of beta-AR (β-AR) responsiveness and density occurs during LVAD therapy (Dipla et al 1998;Klotz, S. et al 2005a;Milting et al 2006;Ogletree-Hughes et al 2001), as well as mechanically unloaded failing rat hearts (Oriyanhan et al 2007). LVAD induced β-AR "recovery" is independent of cessation of systemic β-AR agonist therapy (OgletreeHughes et al 2001), of greater magnitude than that caused by pharmacotherapy alone (Klotz, S. et al 2005a), and unrelated to duration of support (Ogletree-Hughes et al 2001).…”

Reversible Dilated Cardiomyopathy: Into the Thaumaturgy of the Heart—Part 1

“…67 Several animal and clinical studied have investigated myocyte changes following LV unloading from LVAD and have documented regression of cardiac hypertrophy, 68 some suggesting to a point of myocardial atrophy. 69 Diakos et al 70 have prospectively assessed morphological myocardial changes in 44 LVAD patients. They found regression of cardiomyocyte size, but not beyond that of normal donor hearts.…”