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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 29, No 6, November/December 2018
AFRICA
359
circumference, triglycerides, high-density lipoprotein cholesterol
(HDL-C), INR and APTT (see Table 1).
As shown in Table 2, according to TEG, the inhibition of
platelet aggregation that was induced by AA% was 48.00
±
19.30% in the aspirin group, and the inhibition induced by
ADP% was 63.00
±
18.20% in the clopidogrel group. In the dual-
drug group, the inhibition of platelet aggregation was 51.00
±
16.50% for AA% and 46.00
±
15.30 for ADP%. The values in
the no-drug group were 20.00
±
19.20% for AA% and 36.00
±
19.50% for ADP%.
The values of ADP-induced platelet–fibrin clot strength of the
four groups were all between 31 mm and 47 mm, suggesting a low
risk of both bleeding and thrombosis for all subjects. The reaction
times of coagulation in the four groups were all in the normal range.
The efficacy rate (including the platelet inhibition
classifications of ‘effective’ and ‘works well’) of the dual-drug
group was higher than that of the aspirin group through the
AA pathway, but there was no statistically significant difference
(51.16 vs 45.92%;
p
>
0.05). The efficacy rate of the dual-drug
group was lower than that of the clopidogrel group through
the ADP pathway, but there was no statistically significant
difference (64.46 vs 76.32%;
p
>
0.05). The total efficacy rate of
the clopidogrel group was significantly higher than that of the
aspirin group (76.32 vs 45.92%;
p
<
0.05).
It is important to note that there were eight subjects in the
dual-drug group whose antiplatelet therapy was regarded as
ineffective in both pathways, but this group still had the highest
total efficacy rate (81.40%) of the antiplatelet therapies, through
either the AA or ADP pathway (data not shown in Table 3).
As shown in Table 4, the safety evaluation data showed
that, compared with the aspirin group, the bleeding risk of the
clopidogrel group was significantly increased (
p
<
0.05). However,
there was no significant difference in the risk of bleeding between
the dual-drug and no-drug groups. Compared with the aspirin
group or the no-drug group, the risk of thrombosis in the
Table 1. Clinical characteristics of the study population according to group randomisation
Parameters
Aspirin group (
n
=
268) Clopidogrel group (
n
=
115) Dual-drug group (
n
=
43) No-drug group (
n
=
429)
p
-value
Age, years
74.82
±
10.96
81.37
±
10.13
75.14
±
11.20
69.99
±
13.09
<
0.001
Disease history
Current smoking,
n
(%)
52 (14.13)
7 (6.09)
7 (16.28)
58 (13.52)
0.022
CHD,
n
(%)
193 (52.45)
82 (71.30)
31 (72.09)
99 (23.08)
<
0.001
Cerebrovascular events,
n
(%)
25 (6.79)
24 (20.87)
3 (6.98)
20 (4.66)
<
0.001
Diabetes mellitus,
n
(%)
158 (42.93)
44 (38.26)
15 (34.88)
84 (19.58)
<
0.001
Dyslipidaemia,
n
(%)
185 (50.27)
48 (41.74)
18 (41.86)
134 (31.24)
<
0.001
Physical examination data
Systolic blood pressure, mmHg
127.99
±
16.52
132.28
±
17.29
127.84
±
15.84
125.52
±
13.90
0.325
Diastolic blood pressure, mmHg
71.95
±
9.18
69.73
±
10.59
73.30
±
8.68
72.53
±
8.76
0.201
BMI, kg/m
2
24.91
±
2.90
24.13
±
3.08
24.58
±
2.52
24.20
±
2.79
0.104
Waist circumference, cm
91.00
±
10.18
90.68
±
15.24
89.27
±
16.01
90.87
±
9.41
0.316
Laboratory data
White blood cell count, × 10
9
cells/l
6.06
±
1.44
6.00
±
1.35
6.21
±
1.59
5.89
±
1.43
0.191
Platelet count, × 10
9
cells/l
191.28
±
50.15a
176.47
±
48.17
184.45
±
48.55
187.19
±
49.67
0.046
D-dimer,
µ
g/ml
0.60
±
0.58
0.67
±
0.99
0.53
±
0.33
0.50
±
0.74
0.192
INR
0.97
±
0.28
0.99
±
0.18
0.97
±
0.06
1.03
±
1.56
0.078
APTT, s
35.54
±
3.82
35.02
±
2.72
35.37
±
3.28
35.28
±
3.85
0.724
TC, mmol/l
4.02
±
0.79
4.05
±
1.25
4.00
±
0.86b
4.47
±
0.84
<
0.001
TG, mmol/l
1.40
±
0.68
1.34
±
0.70
1.34
±
0.64
1.45
±
0.83
0.529
HDL-C, mmol/l
1.27
±
0.35
1.34
±
0.39
1.27
±
0.28
1.32
±
0.34
0.118
LDL-C, mmol/l
2.53
±
0.73
2.43
±
0.67
2.55
±
0.76b
2.93
±
0.75
<
0.001
Fasting blood glucose, mmol/l
5.89
±
1.18
5.71
±
1.01
5.76
±
0.71
5.67
±
1.04
0.007
Serum creatinine,
µ
mol/l
87.76
±
19.01
92.98
±
23.02
92.98
±
35.84
86.12
±
16.86
0.015
eGFR, ml/min/1.73 m
2
76.87
±
20.37
71.69
±
14.48
80.52
±
46.46
80.73
±
32.02
<
0.001
HbA
1c
, %
5.98
±
0.73
5.89
±
0.88
5.89
±
0.49
5.76
±
0.64
<
0.001
CHD: coronary heart disease; cerebrovascular events included cerebral haemorrhage, cerebral ischaemia, cerebral infarction and transient ischaemic attack; BMI: body
mass index; INR: international normalised ratio; APTT: activated partial thromboplastin time; TC: total cholesterol; TG: triglycerides; HDL-C: high-density lipopro-
tein cholesterol; LDL-C: low-density lipoprotein cholesterol; eGFR: estimated glomerular filtration rate; HbA
1c
: glycated haemoglobin A
1c
.
Table 2. Parameters of platelet function in all groups
TEG data
Aspirin
group
(
n
=
268)
Clopidogrel
group
(
n
=
115)
Dual-drug
group
(
n
=
43)
No-drug
group
(
n
=
429)
AA%
48.00
±
19.30
–
51.00
±
16.50 20.00
±
19.20
ADP%
–
63.00
±
18.20 46.00
±
15.30 36.00
±
19.50
MA-AA (mm)
35.84
±
17.15 49.53
±
13.30 34.13
±
18.57 49.33
±
12.14
MA-ADP (mm) 40.61
±
13.88 34.21
±
13.71 36.64
±
13.80 41.08
±
13.17
R (min)
6.16
±
1.12 6.20
±
1.42 6.12
±
1.00 6.34
±
1.16
AA%: inhibition of platelet aggregation induced by arachidonic acid; ADP%:
inhibition of platelet aggregation induced by adenosine diphosphate; MA-AA:
maximum amplitude of arachidonic acid-induced platelet–fibrin clot strength;
MA-ADP: maximum amplitude of ADP-induced platelet–fibrin clot strength;
R: reacting time of coagulation.
Table 3.The efficacy of antiplatelet therapy through different pathways
Efficacy
AA pathway
p
-value
ADP pathway
p
-value
Aspirin
group
†
(
n
=
368)
Dual-drug
group
(
n
=
43)
Clopido-
grel group
†
(
n
=
115)
Dual-drug
group
(
n
=
43)
Ineffective,
n
, (%) 199 (54.08) 21 (48.84) 0.793 27 (23.48) 14 (32.56) 0.373
Effective,
n
, (%)
65 (17.66) 8 (18.60)
63 (54.78) 23 (53.49)
Works well,
n
, (%) 104 (28.26) 14 (32.56)
25 (21.74) 6 (13.95)
†
p
<
0.05, the effective rate of the aspirin group vs the clopidogrel group.