Since thrombus formation is a very complex procedure in vivo, platelet function testing methods in vitro might only reflect the degree of inhibition of platelet from a certain level, which do't reflect the functional status of platelets in vivo adequately. There are a variety of signal transduction pathways involved in the formation of platelet activation and thrombosis. Gurbel et al. first reported individuals with variability on clopidogrel treatment response in 2003, and proposed the concept of clopidogrel resistance. Different patients received the same dose of aspirin or other anti -platelet drug such as clopidogrel , due to various reasons bound to lack some patients antithrombotic efforts to increase the incidence of thrombotic events , while another part of the patient easily understood antithrombotic excessive bleeding events, " antithrombotic individualized treatment , " according to differences in patient against platelet drugs or anticoagulant drug reactions and adjust the treatment plan , is the direction of antithrombotic therapy in the future.

There are a number of studies have shown that patients with no response Clopidogrel , measuring the relationship between high platelet reactivity and clinical adverse ischemic events displayed between platelet activity . However, there is still lack of quantitative threshold high platelet reactivity and the risks associated with the clinical consensus . In addition, there are only limited data support, to measure platelet function -based therapy to improve the clinical efficacy of the concept . Over the years, more than 20,000 cases reported in patients with numerous studies confirm that high platelet reactivity after PCI with stent thrombosis , including cardiovascular events , including an increased risk of significant correlation . Pharmacodynamic analysis GRVITAS trial showed significantly lower platelet reactivity associated with a lower risk of adverse cardiovascular events . Brar in more than 3000 cases of patients published in JACC Meta-analysis showed that "high platelet reactivity " of patients whose cardiovascular death, heart attack and stent thrombosis occurred more than twice the rate of " non-high platelet reactivity " patients .

Two new anti-platelet drugs (Prasugrel and Ticagrelor) in several recent randomized trials have considerable persuasive , and has included some guidance in the current guidelines. Ticagrelor even more than Prasugrel in pharmacodynamic studies more effectively inhibit platelet , and has a lower risk of bleeding. Cilostazol is an old drug , mostly for the treatment of intermittent claudication , in recent years there are also some testing and coronary stents prevent restenosis after angioplasty , however, so far , there is little direct comparison Cilostazol and Ticagrelor related articles .

We designed this test , in addition to testing for high yellow people treat DAPT (dual anti-platelet therapy) under the platelet reactivity (high on-treatment platelet reactivity) ratio , this population of patients with ticagrelor instead for a month or cilostazol treatment after its platelet reactivity changes and compare between the two groups , and even track six months after the bleeding and adverse cardiovascular events rate? Through this test we can compare the treatment for patients with high platelet reactivity of what strategies more appropriate.

Inclusion Criteria:

1 under DAPT (dual antiplatelet therapy) of stable angina patients for elective stent implantation.

2. DAPT 24 hours, 7d and 30d after treatment PRU (platelet activity units) values. (Drug unresponsive patients was defined as PRU> 235).

Exclusion Criteria:

1.Not suitable for the treatment of patients with DAPT. (Active peptic ulceration or bleeding) 2 patients of aspirin, clopidogrel, ticagrelor, cilostazol medication intolerance.

3 contraindications for aspirin, clopidogrel, ticagrelor, cilostazol drug usage (such as heart failure patients not suitable for use cilostazol).

stable angina who received routine dual antiplatelet agents therapy.