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SUMMARIES FOR PATIENTS

Can Stem Cells Restore Cardiac Tissue after a Heart Attack?

4 May 2004 | Volume 140 Issue 9 | Page I-82

Summaries for Patients are a service provided by Annals to help patients better understand the complicated and often mystifying language of modern medicine.

Summaries for Patients are presented for informational purposes only. These summaries are not a substitute for advice from your own medical provider. If you have questions about this material, or need medical advice about your own health or situation, please contact your physician. The summaries may be reproduced for not-for-profit educational purposes only. Any other uses must be approved by the American College of Physicians.

The summary below is from the full report titled "Stem-Cell Transplantation in Myocardial Infarction: A Status Report." It is in the 4 May 2004 issue of Annals of Internal Medicine (volume 140, pages 729-737). The authors are M.S. Lee and R.R. Makkar.


What is the problem and what is known about it so far?
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Myocardial infarction, commonly called a heart attack, is the leading cause of death in developed countries. Present treatment aims to restore blood flow to the heart muscle in order to limit the extent of permanent damage. Extensive damage keeps the heart from doing its job of pumping blood to the body. This leads to a state called congestive heart failure, which may, over time, be fatal. Recent developments in stem-cell research suggest the possibility of repairing damage. Stem cells are undeveloped cells that have the potential to develop into any type of specialized cell in the body, including heart muscle cells (cardiomyocytes). Transplanted stem cells seem to be able to attach themselves to the site of injury and replace cells that have been lost. Just how they do this remains unclear. Replacing damaged heart muscle cells with healthy cells may avoid heart failure after myocardial infarction.


Why did the authors do this review?
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To learn whether stem-cell transplantation offers a practical way to reverse the effects of myocardial infarction, including heart failure.


How did the authors do this review?
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They surveyed research, both in animals and humans, on stem-cell transplantation after myocardial infarction.


What did the authors find?
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Studies in mice showed that, when fetal cardiomyocytes were placed in myocardial scar tissue, new heart muscle cells formed and heart function improved. Similarly, in a rat model of myocardial infarction, embryonic stem cells injected into heart muscle became part of the myocardium and allowed it to contract more efficiently. Small-scale studies in humans after myocardial infarction suggest that transplanting stem cells may also be feasible and might improve heart function. Although human embryonic stem cells cause little immune reaction when transplanted into other humans, supplies of these cells are limited and their use has posed difficult ethical issues. A possible alternative is to collect and use stem cells in the patient's own bone marrow that have been stimulated to grow by using chemicals called growth factors. In an experimental mouse model, these chemically stimulated bone marrow stem cells, when injected directly into the heart muscle, migrated to the injured area and formed myocardial tissue. Heart function improved, and new vessels that brought more blood to the heart developed. Another possibility is to inject stem cells into the coronary arteries that supply blood to the myocardium. A few patients have had stem cells derived from bone marrow injected into damaged heart muscle at the time of bypass surgery. Blood flow to the myocardium improved in some of these patients.


What are the implications of the review?
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While promising, it is unclear whether stem-cell transplantation will benefit patients with myocardial infarction over the long term. Too few patients have had this treatment to make any definite conclusions about its effectiveness and safety.


Related articles in Annals:

Reviews
Stem-Cell Transplantation in Myocardial Infarction: A Status Report
Michael S. Lee AND Raj R. Makkar
Annals 2004 140: 729-737. [ABSTRACT][SUMMARY][Full Text]  




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