Thorac Cardiovasc Surg 2006; 54 - V_101
DOI: 10.1055/s-2006-925765

Cardioprotective effect of percutanous intramyocardial stem cell injection in hibernating myocardium

K Krause 1, K Jaquet 2, S Geidel 2, M Nauerz 2, J Ostermeyer 2, KH Kuck 2
  • 1AK St. Georg, Herzklinik, Hamburg, Germany
  • 2AK St. Georg, Hamburg, Germany

Aims: Intramyocardial and intracoronary stem cell injection has been shown to improve myocardial function in preclinical and clinical studies. These effects have been desribed in acute myocardial infarction so far, although the mechanism is still unclear. We investigated the effects of bone marrow derived stem cells in a porcine model of chronic progressive myocardial ischemia.

Methods: A circumflex ameroid constrictor was placed off-pump by minimally-invasive surgery in 11 pigs. Constrictor occlusion was documented angiographically after 2 weeks. At week 2 and 6, endocardial electromechanical NOGA-system (Biosense Webster, Inc., California, USA) mapping of the left ventricle, coronary and ventricular angiography, as well as echocardiography were performed. Two weeks after ameroid placement, 11 pigs were randomized with 4 pigs receiving mesenchymal or hematopoietic bone marrow dereived stem cells and 7 pigs receiving placebo at 10 injection sites into the ischemic region of the myocardium. Injections were performed using a NOGATM guided percutaneous transendocardial injection catheter, MYOSTARTM. After 6 weeks, histology (Elastica-van-Giesson, Masson's Trichrome) of ischemic and non-ischemic regions was analyzed.

Results: Endocardial electromechanical mapping showed a significantly reduced ischemic endocardial surface area compared to the control group (5% vs. 41%) at week 6 suggesting a decline in ischemia. Morphometric quantitative histological analysis of the ischemic regions revealed a reduction of myocardial fibrosis (14% vs. 28%) in the stem cell treated group.

Conclusion: Endocardial stem cell injection may induce cardioprotective effects in hibernating myocardium and may attenuate the progression of ischemic tissue damage.