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Coronary Artery Disease is the leading cause of cardiovascular death worldwide and responsible for 17.3 million deaths in 2013.1,2 In 2030, it is projected that CAD in the United States reached 49,3%.3 In Indonesia, the Ministry of Health confirmed that CAD caused 12,9% of deaths from non-communicable disease.4 Early-stage of CAD is marked by endothelial injury which could progress to atherosclerosis.5 Endothelial injury repair requires colonization of EPCs derived from blood marrow-derived progenitor cells.6 Previous studies have shown the benefit of EPCs to repair damaged endothelial by differentiation into the mature endothelial cell to induce vasculogenesis. However, EPCs migration, proliferation rate, adherence capability and survival rate is greatly decreased in the patient with CAD.7,8 Several pathways were involved in the impairment of EPCs, including inflammation and oxidative stress.9 Emerging evidence showed that the decrease of EPCs number in patients with CAD is related to the long term exposure to pro-inflammatory cytokines and oxidative stress.10

High Dose Allicin with Vitamin C Improves EPCs Migration from the Patient with Coronary Artery Disease