To date, coronary artery disease is the most frequent cause of death in the Western world. Despite optimal medical therapy and advanced revascularisation strategies, 30% of the patients suffer from post-infarct heart failure due to left ventricular remodeling.
1 Ventricular remodeling induces profound changes, resulting in left ventricular dilatation and deterioration of function, which may lead to congestive heart failure.
2 Prevention of this serious complication has become a major challenge. During the last decennium, the role of bone marrow mononuclear cells (BMMCs) has been underscored in the healing process after AMI. It has been shown that the number of circulating CD34+ BMMCs, including the haematopoietic stem cells and the endothelial progenitor cells, increases after AMI.
3 These cells are recruited from the bone marrow to the infarcted area by chemokines such as stromal cell-derived factor-1.
4 The spontaneous mobilisation of these cells from the bone marrow to the infarcted area may be an important reparative mechanism. It has been suggested that these cells contribute to infarct healing by paracrine effects, i.e. inducing angiogenesis, inhibiting apoptosis, and enhancing scar tissue formation, or possibly by myocardial regeneration.
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