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Printer Friendly Print ESC Congress 2003: Bone marrow cells to repair myocardial infarction. Are they really capable of replacing injured cells and reducing infarct size?

ESC Congress 2003: Bone marrow cells to repair myocardial infarction. Are they really capable of replacing injured cells and reducing infarct size?

August 31, 2003

IMPORTANT: This press release accompanies a poster or oral session given at the ESC Congress 2003. Written by the investigator himself/herself, this press release does not necessarily reflect the opinion of the European Society of Cardiology

ESC Congress 2003: The heart is incapable of cardiocell regeneration after myocardial infarction or other injuries. After an acute myocardial infarction, non contractile scar tissue will develop with regional malefunction which may finally result in heart failure. Present treatment options include recanalization of the occluded coronary vessel to reduce the amount of injured cells and tailored medical therapy for heart failure. So far, common treatment has been unable to replace the scar tissue by contracting myocardial cells.

The new concept of cell transplantation has been addressed by two recent human investigations. Bone marrow cells of the patient are injected into the coronary circulation about one week after myocardial infarct to replace the injured cells and reduce the infarct size. This intervention seemed to be successful to reduce the contractile malefunction after myocardial infarction. The background of this observation is the new concept derived from animal experiments that some of adult bone marrow cells can home in the heart and then transdifferentiate to myocardial cells. Therefore, our goal in the present investigation was to repeat these clinical investigations in patients with large anterior myocardial infarcts.

Once the patients came into the hospital with an acute myocardial infarct the occluded vessel was mechanically recanalized with a balloon catheter to restore the blood flow instantly and the occlusion area was protected with a coronary stent.
Although blood flow is then re-established - due to the interruption of blood flow for several hours - many cells are dying and a myocardial scar is developing. Therefore, after 7 days 30 ml of bone marrow was drawn from a puncture of a hip bone and a certain subset of the cells (monocytic cells) were separated to a final volume of a about 8 - 10 ml containing 2.2 x 107 monocytic bone marrow cells. By a second catheterisation these cells were transferred into the coronary circulation over a balloon catheter into the injured tissue. The regional contractile force, the global contractile force and the regional coronary blood flow was measured at 3 month and 1 year after cell injection.

Contradictory to the previous investigations, our experiments in large myocardial infarcts do not demonstrate regional or global contractile improvement at 3 month and 1 year.

Therefore, the concept that patients bone marrow cells might replace injured myocardial cells and reduce infarct size can not be confirmed in patients with large myocardial infarctions.

Prof. Dr. Med. Hans R. Figulla
Friedrich-Schiller-University Jena, Germany






European Society of Cardiology (ESC)



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