Ate Cox proportional hazards model showed that PM carriers were an independent predictor of 1-year ST (HR = 5.268, 95 CI = 1.528?8.164, P = 0.009). Table 6 shows the detailed results of the multivariate analysis. There was a decreased adverse-event ree survival rate (including ST, MI, death, and total adverse events) among patients carrying the CYP2C19 PM phenotypes when compared with the EMs (Fig. 2).Statistical AnalysisAll analyses were carried out using SPSS version 17.0 (SPSS Inc., Chicago, IL, USA). The Hardy-Weinberg equilibrium was assessed using chi-square analysis. Discrete variables, expressed as counts or percentages, were compared by chi-square or Fisher’s exact test, as appropriate. Continuous inhibitor variables were expressed as mean 6 standard deviation (SD). Normally distributed continuous variables were compared by t-test, and non-normally distributed data were compared by nonparametric test. The 
independent association between the presence of the CYP2C19*2 or *3 allele and its outcome was assessed after adjusting for other potential confounding factors by using multivariate Cox regression analysis and a Cox proportional hazards model for event-free survival. All variables associated with P,0.1 in the univariate analysis were entered into the multivariate model as covariates. A value of P,0.05 was considered as statistically significant.DiscussionIn the present study, we reported the associations of CYP2C19 loss-of-function polymorphisms with the incidences of adverse outcomes of CAD patients after PCI. We found that 15900046 patients with PMs have much higher incidences of ST, MI, and death when compared with EMs of CYP2C19. Several studies have provided evidences linking CYP2C19 genetic variation to reduced exposure to the active drug metabolite, lower inhibitor platelet inhibition, and less protection from recurrent ischemic events in people receiving clopidogrel [21]. According to previous reports, common polymorphisms in the CYP2C19 gene were approximately 30 in whites, 40 in blacks, and .55 in East Asians [22]. As described earlier, according to CYP2C19 genotype, individuals can be divided into three groups: PMs, IMs, and EMs. Our results indicate that PMs accounted for 9.36 and IMs for 48.12 of the Chinese CAD patients. Our result is in line with that reported in previous studies [22]. Although several studies have shown that CYP2C19*2 and CYP2C19*3 polymorphisms influence the platelet response to Table 5. Accumulated Major Adverse Events During the Oneyear Period After Intervention.Results Patient Characteristics and CYP2C19 GenotypeAmong the 1068 patients, there were 524 (49.06 ) with wild homozygous, 465 (43.54 ) with heterozygous, and 79 (7.40 ) with mutant homozygous CYP2C19*2, and there were 947 (88.67 ) with wild homozygous, 100 (9.36 ) with heterozygous, and 11 (1.97 ) with mutant homozygous CYP2C19*3. We divided these 1068 patients into three phenotypes based on CYP2C19*2 and CYP2C19*3 genotypes. Accordingly, there were 454 (42.51 ) EMs, 514 (48.13 ) IMs, and 100 (9.36 ) PMs in the present study. Table 1 and Table 2 describe the baseline characteristics of the studied population according to CYP2C19 phenotype. All these variables were well balanced among these three groups (all P.0.05). Table 3 shows the angiographic and procedural characteristics, which were also well balanced among the three groups (all P.0.05).Clinical outcomesPhenotypes EMs (n = 454) IMs (n = 514) 24 (4.67) 18 (3.50) 20 (3.89) 50 (9.73) PMs (n = 100) 10 (.Ate Cox proportional hazards model showed that PM carriers were an independent predictor of 1-year ST (HR = 5.268, 95 CI = 1.528?8.164, P = 0.009). Table 6 shows the detailed results of the multivariate analysis. There was a decreased adverse-event ree survival rate (including ST, MI, death, and total adverse events) among patients carrying the CYP2C19 
PM phenotypes when compared with the EMs (Fig. 2).Statistical AnalysisAll analyses were carried out using SPSS version 17.0 (SPSS Inc., Chicago, IL, USA). The Hardy-Weinberg equilibrium was assessed using chi-square analysis. Discrete variables, expressed as counts or percentages, were compared by chi-square or Fisher’s exact test, as appropriate. Continuous variables were expressed as mean 6 standard deviation (SD). Normally distributed continuous variables were compared by t-test, and non-normally distributed data were compared by nonparametric test. The independent association between the presence of the CYP2C19*2 or *3 allele and its outcome was assessed after adjusting for other potential confounding factors by using multivariate Cox regression analysis and a Cox proportional hazards model for event-free survival. All variables associated with P,0.1 in the univariate analysis were entered into the multivariate model as covariates. A value of P,0.05 was considered as statistically significant.DiscussionIn the present study, we reported the associations of CYP2C19 loss-of-function polymorphisms with the incidences of adverse outcomes of CAD patients after PCI. We found that 15900046 patients with PMs have much higher incidences of ST, MI, and death when compared with EMs of CYP2C19. Several studies have provided evidences linking CYP2C19 genetic variation to reduced exposure to the active drug metabolite, lower platelet inhibition, and less protection from recurrent ischemic events in people receiving clopidogrel [21]. According to previous reports, common polymorphisms in the CYP2C19 gene were approximately 30 in whites, 40 in blacks, and .55 in East Asians [22]. As described earlier, according to CYP2C19 genotype, individuals can be divided into three groups: PMs, IMs, and EMs. Our results indicate that PMs accounted for 9.36 and IMs for 48.12 of the Chinese CAD patients. Our result is in line with that reported in previous studies [22]. Although several studies have shown that CYP2C19*2 and CYP2C19*3 polymorphisms influence the platelet response to Table 5. Accumulated Major Adverse Events During the Oneyear Period After Intervention.Results Patient Characteristics and CYP2C19 GenotypeAmong the 1068 patients, there were 524 (49.06 ) with wild homozygous, 465 (43.54 ) with heterozygous, and 79 (7.40 ) with mutant homozygous CYP2C19*2, and there were 947 (88.67 ) with wild homozygous, 100 (9.36 ) with heterozygous, and 11 (1.97 ) with mutant homozygous CYP2C19*3. We divided these 1068 patients into three phenotypes based on CYP2C19*2 and CYP2C19*3 genotypes. Accordingly, there were 454 (42.51 ) EMs, 514 (48.13 ) IMs, and 100 (9.36 ) PMs in the present study. Table 1 and Table 2 describe the baseline characteristics of the studied population according to CYP2C19 phenotype. All these variables were well balanced among these three groups (all P.0.05). Table 3 shows the angiographic and procedural characteristics, which were also well balanced among the three groups (all P.0.05).Clinical outcomesPhenotypes EMs (n = 454) IMs (n = 514) 24 (4.67) 18 (3.50) 20 (3.89) 50 (9.73) PMs (n = 100) 10 (.
