Table 1.
Characteristics | No cilostazol (n = 22) |
Cilostazol (n = 24) |
All patients (n = 46) |
p-Value |
---|---|---|---|---|
Medical history | ||||
Age, years | 72 ± 8 | 71 ± 9 | 72 ± 9 | 0.56 |
Females | 11 (50) | 18 (75) | 29 | 0.08 |
BMI, kg/m2 | 28 ± 5 | 29 ± 8 | 28 ± 7 | 0.73 |
Hypertension | 21 (95) | 22 (92) | 43 | 1.00 |
DM | 17 (77) | 18 (75) | 35 | 0.86 |
Dyslipidemia | 18 (82) | 20 (83) | 38 | 1.00 |
Active smoker | 5 (23) | 5 (21) | 10 | 0.88 |
Platelet reactivity (PRU) | 224 ± 45 | 191 ± 55 | 207 ± 53 | 0.03 |
Laboratory results | ||||
WBC, ×103/μL | 7.5 ± 2.0 | 8.9 ± 2.5 | 8.3 ± 2.4 | 0.04 |
Hgb, g/dL | 13.2 ± 2.2 | 13.0 ± 1.5 | 13.1 ± 1.8 | 0.74 |
Hct, % | 39.1 ± 6.0 | 38.8 ± 3.8 | 39.0 ± 5.0 | 0.83 |
Platelet count, ×103/μL | 249 ± 86 | 252 ± 78 | 251 ± 81 | 0.89 |
BUN, mg/dL | 22 ± 8 | 20 ± 7 | 21 ± 8 | 0.34 |
Creatinine, mg/dL | 1.0 ± 0.3 | 0.9 ± 0.3 | 0.9 ± 0.3 | 0.23 |
Concomitant therapy | ||||
Aspirin | 11 (50) | 15 (63) | 26 | 0.39 |
PPIs | 3 (14) | 5 (21) | 8 | 0.70 |
Statins | 17 (77) | 19 (79) | 36 | 0.88 |
CCBs | 7 (32) | 7 (29) | 14 | 1.00 |
Genotypes | ||||
CYP2C19*2 (G681A) (rs4244285) | ||||
Wild | 17 (77) | 17 (71) | 34 (74) | 0.61 |
Mutant | 5 (23) | 7 (29) | 12 (26) | |
CYP2C19*17(C806T) (rs12248560) | ||||
Wild | 13 (59) | 20 (83) | 33 (72) | 0.10 |
Mutant | 9 (41) | 4 (17) | 13 (28) | |
ABCB1 (C3435T) (rs1045642) | ||||
Wild | 8 (36) | 7 (29) | 15 (33) | 0.60 |
Mutant | 14 (64) | 17 (71) | 31 (67) | |
PON1 (A575G) (rs662) | ||||
Wild | 5 (23) | 3 (13) | 8 (17) | 0.45 |
Mutant | 17 (77) | 21 (87) | 38 (83) | |
P2RY12 (T744C) (rs2046934) | ||||
Wild | 17 (77) | 20 (83) | 37 (80) | 0.72 |
Mutant | 5 (23) | 4 (17) | 9 (20) |
Values are mean ± SD or n (%). BMI, Body mass index; WBC, white blood cells; Hgb, hemoglobin; BUN: blood urea nitrogen. The alleles CYP2C19*3 and CYP2C19*4 were not observed in the study population. p-Values indicate significance of effects of genotype groups on the results of comparisons between the cilostazol and non-cilostazol groups.