BACKGROUND: It has been reported that granulocyte colony-stimulating factor (G-CSF) can promote angiogenesis by mobilizing bone marrow stem cells to blood vessels. The purpose of this study is to clarify whether low-dose and long-term G-CSF treatment can improve severe myocardial ischemia. METHODS: We studied 40 patients (M/F = 29/11, age = 68 ± 9 years) who had severe coronary artery disease (7 with and 5 without old myocardial infarction; 3VD/2VD/1VD = 17/17/6) and severe myocardial ischemia with no indication for revascularization. G-CSF (1.5 μg/kg) was injected for 14 consecutive days. All patients were evaluated using stress myocardial scintigraphy, the Canadian Cardiovascular Society (CCVS) score, and cardiopulmonary exercise testing before and after 3 months of treatment. On 17 SPECT segments, the total defect score (TDS) and delta TDS (TDS (stress) minus TDS (resting)) were evaluated to assess the severity of myocardial ischemia. RESULTS: The changes in stress TDS, delta TDS, and regional wall motion score were significantly greater in the G-CSF group than the control group (P < .0001). The CCVS score improved significantly from baseline to the 3-month follow-up assessment in the G-CSF group (P < .0001). The increase of peak VO2 was significantly larger in the G-CSF group than the control group (P = .015). CONCLUSION: Low-dose and long-term G-CSF treatment can improve severe ischemia in patients with severe coronary artery disease.
BACKGROUND: It has been reported that granulocyte colony-stimulating factor (G-CSF) can promote angiogenesis by mobilizing bone marrow stem cells to blood vessels. The purpose of this study is to clarify whether low-dose and long-term G-CSF treatment can improve severe myocardial ischemia. METHODS: We studied 40 patients (M/F = 29/11, age = 68 ± 9 years) who had severe coronary artery disease (7 with and 5 without old myocardial infarction; 3VD/2VD/1VD = 17/17/6) and severe myocardial ischemia with no indication for revascularization. G-CSF (1.5 μg/kg) was injected for 14 consecutive days. All patients were evaluated using stress myocardial scintigraphy, the Canadian Cardiovascular Society (CCVS) score, and cardiopulmonary exercise testing before and after 3 months of treatment. On 17 SPECT segments, the total defect score (TDS) and delta TDS (TDS (stress) minus TDS (resting)) were evaluated to assess the severity of myocardial ischemia. RESULTS: The changes in stress TDS, delta TDS, and regional wall motion score were significantly greater in the G-CSF group than the control group (P < .0001). The CCVS score improved significantly from baseline to the 3-month follow-up assessment in the G-CSF group (P < .0001). The increase of peak VO2 was significantly larger in the G-CSF group than the control group (P = .015). CONCLUSION: Low-dose and long-term G-CSF treatment can improve severe ischemia in patients with severe coronary artery disease.
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