26 / 74
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 29, No 6, November/December 2018
358
AFRICA
group (429). Demographic and clinical data were collected
using a domestic questionnaire, which included age, regimen
of any antiplatelet drugs and combined medications, current
smoking habit, and history of hypertension, coronary heart
disease, diabetes mellitus and cerebrovascular events. Smoking
was defined as having more than one cigarette every day
for more than one year, and cerebrovascular events included
cerebral haemorrhage, cerebral ischaemia, cerebral infarction
and transient ischaemic attack.
Body height, body mass, waist circumference and blood
pressure were measured and body mass index (BMI) was
calculated. The information was collected by face-to-face
consultation, and the investigators were all trained physicians at
our hospital.
TEGwas used to measure the percentage of platelet inhibition
after anti-platelet therapy. The TEG instrument (TEG 5000
Haemoscope) and the related reagents were provided by the
Haemonetics Company in the United States. The patients took
the antiplatelet drugs as usual on the day of taking blood.
TEG parameters
7
Reaction time (R) is the time required from the start of a
blood sample test to fibrin formation. The normal range is
5–10 min, and
>
10 and
<
5 min are considered enzymatic
hypercoagulability.
Maximal amplitude (MA), which represents the maximum
strength and stability of a clot, can be ascertained by the
binding of activated platelets to a fibrin mesh. Using the TEG
instrument, 360
µ
l of heparinised blood was added to 10 ml
of activator F (reptilase and factor XIIIa) in channel 1. The
contribution of each fibrin meshwork to the clot strength
(MA-fibrin) was assessed in channel 1.
In channels 2 and 3, 360
µ
l of heparinised blood was added
to 10 ml of ADP (final concentration 2
µ
M) and 10 ml of
arachidonic acid (AA; final concentration 1 mM), respectively,
along with 10 ml of activator F to each. Channels 2 (MA-ADP)
and 3 (MA-AA) calculate the contribution of platelets, as
activated by ADP or AA, respectively, to the clot strength.
Maximal clot strength with maximally stimulated platelets
(MA-thrombin) were assessed in channel 4 by adding 360
µ
l
of kaolin-activated citrated blood to 20
µ
l of 0.2 M calcium
chloride. The normal range of MA-ADP is 31 to 47 mm; when
it was
<
31 mm, the risk of bleeding was increased, and
>
47 mm,
the risk of thrombosis was increased. When MA-ADP was
between 31 and 47 mm, the subject was considered to have the
lowest risk of bleeding and thrombosis.
8
ADP% is the percentage of platelet inhibition due to
clopidogrel, which was defined by the extent of non-response
of the platelet ADP receptor to exogenous ADP, as measured
by TEG-MA.
ADP%
=
(MA-ADP) – (MA-fibrin)
________________________
(MA-thrombin) – (MA-fibrin)
× 100%
ADP% was used as a measure of the therapeutic effect of
clopidogrel. The reference values were as follows:
<
30% was
considered to be ineffective, 30%
≤
ADP%
≤
75% was considered
to be effective, and
>
75% was considered to work well.
7
AA% is the percentage of platelet inhibition due to aspirin,
which was defined by the extent of non-response of the platelet
TXA
2
receptor to exogenous AA, as measured by TEG-MA.
AA%
=
(MA-AA) – (MA-fibrin)
________________________
(MA-thrombin) – (MA-fibrin)
× 100%
AA% was used as a measure of the therapeutic effect of aspirin.
The reference values were as follows:
<
50% was considered to
be ineffective, 50%
≤
AA%
≤
75% was considered to be effective,
and
>
75% was considered to work well.
Detection of biochemical parameters
The whole blood count was determined by an automatic
haematology analyser (Nihon Kohden MEK-7222K, Japan).
The blood lipid and glucose, and serum creatinine (SCr) values
were determined by an automatic biochemical analyser (Hitachi
7400, Japan).
Renal function was further assessed by the estimated
glomerular filtration rate (eGFR), which was calculated by the
following formula:
eGFR (ml/min/1.73 m
2
)
=
175 × standard SCr (mg/dl) – 1.234 ×
age – 0.179 (or 0.79 for females)
9
[The standard SCr (mg/dl)
=
SCr (mg/dl) (detected by an
enzymatic method) × 0.795 + 0.29]
10
Glycated haemoglobin (HbA
1c
) was measured using high-
performance liquid chromatography (Variant II from Bio-Rad,
Hercules, California, USA). The amount of D-dimer, the
international normalised ratio (INR) and the activated partial
thromboplastin time (APTT) were determined by an automatic
coagulometer (SYSMAX CA-1500, Sysmex Shanghai Ltd,
Japan).
Statistical analysis
Two data-entry clerks carried out the data input. The data were
analysed using the statistical package program SPSS (version
19.0). Categorical variables are expressed as a percentage
and continuous variables as mean
±
standard deviation (SD).
The chi-squared and Student’s
t
-tests were used to compare
categorical variables and continuous variables, respectively,
among groups. A multivariate logistic regression analysis was
applied to identify variables independently associated with
the efficacy of an antiplatelet therapy. Values of
p
<
0.05 were
regarded as statistically significant.
Results
The mean age and the prevalence of cerebrovascular events were
significantly higher in the clopidogrel group than in the other
groups, while the eGFR in the clopidogrel group was lower than
in the other groups (
p
<
0.01). Compared with the other groups,
the aspirin group had a higher prevalence of dyslipidaemia and
diabetes mellitus, and higher levels of fasting blood glucose and
HbA
1c
(
p
<
0.01), while the dual-drug group had a significantly
higher prevalence of coronary heart disease (
p
>
0.01). The
platelet count in the aspirin group was higher than that in the
clopidogrel group (
p
=
0.03).
Compared with the no-drug group, the levels of cholesterol
and low-density lipoprotein cholesterol (LDL-C) were lower
in the dual-drug group (
p
<
0.01). There was no statistically
significant difference among the four groups in indicators such
as systolic and diastolic blood pressure, body mass index, waist