Key result
Autologous bone marrow stem cell transplantation significantly improved cardiac contractility (dP/dtmax 2084 vs 1290 mm Hg/s) and attenuated beta-adrenoceptor down-regulation in a rabbit model of non-ischemic heart failure.
Why the study?
Does autologous bone marrow stem cell transplantation improve beta-adrenoceptor density and cardiac contractility in a rabbit model of non-ischemic heart failure?
Does autologous bone marrow stem cell transplantation improve beta-adrenoceptor density and cardiac contractility in a rabbit model of non-ischemic heart failure?
Absolute Event Rate: 2084% vs 1290%
p-value: p=<0.05
Autologous bone marrow stem cell transplantation improves cardiac contractility and normalizes sympathoadrenal dysregulation in a rabbit model of non-ischemic heart failure.
Requires validation in larger models; leaves open translation to human non-ischemic heart failure.
BACKGROUND: Since only little is known on stem cell therapy in non-ischemic heart failure we wanted to know whether a long-term improvement of cardiac function in non-ischemic heart failure can be achieved by stem cell transplantation. METHODS: White male New Zealand rabbits were treated with doxorubicin (3 mg/kg/week; 6 weeks) to induce dilative non-ischemic cardiomyopathy. Thereafter, we obtained autologous bone marrow stem cells (BMSC) and injected 1.5-2.0 Mio cells in 1 ml medium by infiltrating the myocardium via a left anterolateral thoracotomy in comparison to sham-operated rabbits. 4 weeks later intracardiac contractility was determined in-vivo using a Millar catheter. Thereafter, the heart was excised and processed for radioligand binding assays to detect beta1- and beta2-adrenoceptor density. In addition, catecholamine plasma levels were determined via HPLC. In a subgroup we investigated cardiac electrophysiology by use of 256 channel mapping. RESULTS: In doxorubicin-treated animals beta-adrenoceptor density was significantly down-regulated in left ventricle and septum, but not in right ventricle, thereby indicating a typical left ventricular heart failure. Sham-operated rabbits exhibited the same down-regulation. In contrast, BMSC transplantation led to significantly less beta-adrenoceptor down-regulation in septum and left ventricle. Cardiac contractility was significantly decreased in heart failure and sham-operated rabbits, but was significantly higher in BMSC-transplanted hearts. Norepinephrine and epinephrine plasma levels were enhanced in heart failure and sham-operated animals, while these were not different from normal in BMSC-transplanted animals. Electrophysiological mapping revealed unaltered electrophysiology and did not show signs of arrhythmogeneity. CONCLUSION: BMSC transplantation improves sympathoadrenal dysregulation in non-ischemic heart failure.
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Dhein et al. (2006) studied Non-ischemic cardiomyopathy (heart failure) (n=38). Autologous bone marrow stem cell (BMSC) transplantation vs. Sham operation (1 ml medium) or no treatment was evaluated on Cardiac contractility (dP/dtmax in mm Hg/s) (p=<0.05). Autologous bone marrow stem cell transplantation significantly improved cardiac contractility (dP/dtmax 2084 vs 1290 mm Hg/s) and attenuated beta-adrenoceptor down-regulation in a rabbit model of non-ischemic heart failure.
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