Enhanced　external　counterpulsation　(EECP)　is　able　to　treat　myocardial　ischemia,　which　is　usually　caused　by　coronary　artery　stenosis.　However,　the　underlying　mechanisms　regarding　why　this　technique　is　effective　in　treating　myocardial　ischemia　remains　unclear　and　there　is　no　patient-specific　counterpulsation　mode　for　different　rates　of　coronary　artery　stenosis　in　clinic.　This　study　sought　to　investigate　the　hemodynamic　effect　of　varied　coronary　artery　stenosis　rates　when　using　EECP　and　the　necessity　of　adopting　targeted　counterpulsation　mode　to　consider　different　rates　of　coronary　artery　stenosis.　Three　3-dimensional　(3D)　coronary　models　with　different　stenosis　rates,　including　55%　(Model　1),　65%　(Model　2),　and　75%　(Model　3),　were　generated,　then　coupled　with　a　0-dimensional　(OD)　lumped　parametric　model　of　the　blood　circulatory　system.　EECP　was　applied　to　the　0D/3D　coupled　models　to　study　the　hemodynamic　response　of　the　coronary　artery.　Under　the　same　counterpulsation　mode,　the　ratio　of　diastolic　blood　pressure　to　systolic　blood　pressure　of　3　models　during　counterpulsation　was　1.4,　and　the　cardiac　output　and　coronary　artery　flow　rate　increased　significantly.　The　low　wall　shear　stress　(WSS)　and　high　oscillatory　shear　index　(OSI)　areas　were　mainly　located　at　the　posterior　end　of　the　stenosis　and　coronary　artery　bifurcation.　Moreover,　with　an　increase　in　the　rate　of　coronary　artery　stenosis,　the　increased　percentage　of　flow　rate　through　the　coronary　artery　stenosis　and　area-averaged　WSS　decreased.　The　geometric　multiscale　model　in　this　study　can　be　used　to　effectively　simulate　the　hemodynamic　characteristics　of　cardiovascular　system　following　the　application　of　EECP.　Local　precise　hemodynamic　effect　of　the　coronary　artery　stenosis　can　be　observed.　It　was　found　from　the　hemodynamic　factors　that　the　coronary　artery　with　lower　stenosis　rate　more　likely　led　to　better　vascular　endothelial　remodeling.　Thus,　it　is　necessary　to　adopt　patient-specific　counterpulsation　mode　accounting　for　different　condition　of　coronary　artery　stenosis.