Heart Ischemia Increases Endothelial Precursor Cells, Promoting Collateralization

Exercise-induced ischemia in coronary artery disease patients appears to trigger a substantial increase in the number of circulating endothelial precursor cells (EPCs), which may contribute to neovascularization, according to a report in the April issue of Arteriosclerosis, Thrombosis, and Vascular Biology.

EPCs may promote neovascularization, the authors explain, but the mechanisms stimulating the increase in circulating EPC numbers are poorly understood.

Dr. Volker Adams from University Leipzig, Germany and colleagues investigated the time course of circulating EPC numbers after a single symptom-limited exercise stress test in 28 patients with stable coronary artery disease and in 11 healthy subjects.

Sixteen of the patients experienced exercise-induced ischemia lasting a mean of 5.7 minutes, the report indicates.

Circulating EPC counts showed a 2.9-fold increase 24 hours after the single ischemic episode and a 3.3-fold increase at 48 hours, compared with the control group and with patients who did not experience exercise-induced ischemia, the authors report. EPC counts returned to normal within 72 hours.

In patients with exercise-induced ischemia, but not in the other groups, vascular endothelial growth factor (VEGF) increased a maximum 4-fold 2 hours after the maximal exercise test, the results indicate. In contrast, GM-CSF, TNF-alpha, and b-FGF did not differ among the 3 groups.

“In conclusion,” the investigators write, “the present study demonstrates for the first time to our knowledge that a short episode of myocardial ischemia in coronary artery disease patients is sufficient to induce a considerable increase in the number of circulating EPCs, most likely resulting from enhanced differentiation of EPCs from circulating pluripotent bone marrow-derived progenitor cells. This increase seems to be related to the increase of plasma VEGF.”

Arterioscler Thromb Vasc Biol 2004;24:684-690.