Abstract
Left ventricular assist devices (LVAD) are currently used to either “bridge” patients with terminal congestive heart failure (CHF) until cardiac transplantation is possible or optionally for patients with contraindications for transplantation (“destination therapy”). Mechanical support is associated with a marked decrease of cardiac dilation and hypertrophy as well as numerous cellular and molecular changes (“reverse cardiac remodeling”), which can be accompanied by improved cardiac function (“bridge to recovery”) in a relatively small subset of patients with heart transplantation no longer necessary even after removal of the device (“weaning”). In the recent past, novel pharmacological strategies have been developed and are combined with mechanical support, which has increased the percentage of patients with improved clinical status and cardiac performance. Gene expression profiles have demonstrated that individuals who recover after LVAD show different gene expression compared to individuals who do not respond to unloading. This methodology holds promise for the future to develop read out frames to identify individuals who can recover after support. Aside from describing the morphological changes associated with “reverse cardiac remodeling”, this review will focus on signal transduction, transcriptional regulation, apoptosis, cell stress proteins, matrix remodeling, inflammatory mediators and aspects of neurohormonal activation in the failing human heart before and after ventricular unloading.
Highlights
Chronic heart failure (CHF) is a major cause of morbidity and mortality in both western industrialized and developing nations and causes considerable economic burden to the medical systems [1,2,3]
These results are encouraging, there is more or less consent that the clinical cardiac improvement and performance are less pronounced in the majority of cases and only a small subset of patients can be weaned from the device and live without transplantation
The approach described by Birks and coworkers consisting of combined use of mechanical support and medical treatment including clenbuterol holds promising results for the future, as the percentage of patients who can be weaned is reported to be considerably higher
Summary
Chronic heart failure (CHF) is a major cause of morbidity and mortality in both western industrialized and developing nations and causes considerable economic burden to the medical systems [1,2,3]. Birks and co-workers were able to show myocardial recovery in a percentage as high as 75% of their studied patients after combined use of ventricular unloading and an aggressive pharmacological regimen consisting of lisinopril (angiotensin converting enzyme inhibitor), carvedilol (receptor antagonist), spironolactone (aldosterone antagonist) and lorsatan (angiotensin II antagonist), which are known to reduce ventricular remodeling This approach is followed by administration of clenbuterol, a selective 2-agonist, helping to prevent cardiomyocyte atrophy in response to long-term unloading [18]. 158 Current Cardiology Reviews, 2008, Vol 4, No 3 jor morphological and molecular changes that occur in the heart during “reverse cardiac remodeling” by ventricular unloading, including some of the latest results from our group
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