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SA JOURNAL OF DIABETES & VASCULAR DISEASE
RESEARCH ARTICLE
VOLUME 16 NUMBER 2 • NOVEMBER 2019
77
Methods
The study evaluated 95 consecutive diabetic patients undergoing
primary PCI for STEMI. Patients were recruited to receive 25 μg/kg
tirofiban bolus plus a maintenance dose of 0.15 μg/kg/min infusion
either IV (group A:
n
= 50) or IC (group B:
n
= 45) for 24 hours.
We included adult patients between 18 and 75 years with a clinical
presentation of STEMI and specific ECG criteria in the form of
ST-segment elevation ≥ 1 mm in two or more contiguous leads,
except V2 and V3 had to be ≥ 1.5 mm in females, ST-segment
elevation ≥ 2.5 mm in males less than 40 years or ≥ 2 mm in males
more than 40 years, or the presence of new-onset or presumed
new left bundle branch block.
13
The institutional ethics committee approved the study and all
patients signed informed consent.
Patients with marked uncontrolled hypertension (≥ 180/110
mmHg), rescue PCI and emergency coronary artery bypass
grafting were excluded. Other exclusion criteria included patients
presenting with cardiogenic shock, severe liver or kidney failure,
bleeding diathesis, hypersensitivity or thrombocytopaenia with
tirofiban, platelets < 150 000 cells/mm
3
, active internal bleeding,
history of ischaemic or haemorrhagic stroke within the last 30
days, atrioventricular malformation or aneurysm, neoplastic aortic
dissection, acute pericarditis, haemorrhagic retinopathy and chronic
haemodialysis.
Before the intervention all patients were treated with
acetylsalicylic acid (300 mg) and clopidogrel (600 mg). After
securing vascular access through the right femoral or radial arteries,
a total of 70–100 IU/kg unfractionated heparin IV bolus was given,
then an additional weight-adjusted unfractionated heparin was
given to achieve approximately 250 seconds of activated clotting
time (ACT).
In both groups, a bolus of 25 μg/kg of tirofiban was given
immediately after the guidewire crossed the lesion successfully
and antegrade flow was restored, aiming to secure maximum
concentration of the drug at the culprit lesion site and distal
microvascular bed. A bolus dose of tirofiban was given through
the guiding catheter in the infarct-related artery (IRA) at 30
seconds in the IC group. Maintenance IV tirofiban of 0.15 μg/kg/
min for 18 hours was started in both groups after the bolus dose.
An aspiration thrombectomy catheter was used if necessary and,
finally, a suitable drug-eluting stent (FDA approved) was employed
in the IRA in all patients.
Acetylsalicylic acid, a P2Y12 inhibitor (clopidogrel 75 mg), a
high-intensity statin, beta-blocker and an angiotensin converting
enzyme inhibitor or angiotensin II receptor blocker were prescribed
as per the guidelines. When the activated clotting time (ACT) was
< 160 seconds and/or four hours after anticoagulation, the vascular
sheath was removed by manual compression.
The time to reperfusion was recorded from the onset of chest
pain until the visualisation of at least thrombolysis in myocardial
infarction (TIMI) 2 flow in the IRA during PCI. Before and after
coronary intervention, TIMI flow grades
14
and myocardial blush
grade (MBG)
15
were evaluated blindly by two interventional
cardiologists. For evaluation of left ventricular ejection fraction
(LVEF), the biplane modified Simpson’s method was used 48 hours
after PCI and then again after 30 days.
The groups were compared for TIMI flow grades before and
after the intervention, and MBG, maximum C-reactive protein
(CRP) level, peak levels of both high-sensitivity troponin T (hs-TnT)
and CK-MB, time to peak for hs-TnT and CK-MB, time to 50% ST
resolution, and composite MACE rates at 30 days were recorded.
Safety endpoints such as significant and minor bleeding and
thrombocytopenia were noted.
According to the dye density, the MBG score was classified as
grade 3 = normal myocardial contrast density compared to contrast
density of a contra- or ipsilateral non-IRA, 2 = moderate myocardial
blush where contrast density is less than that obtained from a
contra- or ipsilateral non-IRA, 1 = minimal myocardial blush or
contrast density, and grade 0 = no myocardial blush.
16
MACE
17
included cardiovascular death, recurrent myocardial
infarction, stent thrombosis or target vessel revascularisation in
hospitalisation at one month. Thrombocytopenia was defined as
platelet count < 100 000 cells/mm
3
.
16
Intracranial haemorrhage and
decrease in haemoglobin concentration ≥ 5 g/dl were considered as
major bleeding. Minor bleeding was defined as 10 to 15% decrease
in haematocrit, blood loss with 3 to 5 g/dl decrease in haemoglobin
concentration, or ≥ 4 g/dl decrease in haemoglobin concentration
with no observed blood loss.
18
Statistical analysis
Patients’ data were collected, revised and analysed using the
statistical package for social sciences (SPSS) version 25.0 for
windows (IBM Corp, Armonk, NY, USA). Data are presented
as mean ± standard deviation (SD), frequency and percentage.
Categorical variables were compared using the chi-squared (
χ
2)
test. Continuous variables were compared with the Student’s
t
-test
(two-tailed) and one-way ANOVA test for parametric data with
Bonferroni post hoc test to detect differences between subgroups.
The level of significance was accepted if the p-value was < 0.05.
Results
The two groups showed no statistically significant differences in
cardiovascular risk factors, baseline characteristics or medication
(Table 1). The mean age was 58.5 ± 10.18 years in the IV group
and 55.90 ± 11.66 years in the IC group. The groups showed no
significant differences in baseline level of glycated haemoglobin
(HbA
1c
) (
p
= 0.08), onset-to-balloon and door-to-balloon times (
p
=
0.08, 0.3, respectively). Killip class frequency > 1 was 18% in group
A (IV) and 24% in group B (IC) (
p
= 0.33) (Table 1).
Peak CK-MB value was significantly lower in the IC group than
in the IV group (155.68 ± 121, 192.4 ± 86 U/l respectively) (
p
=
0.021). Peak hs-TnT value was significantly lower in the IC group
than in the IV group (4291 ± 334, 5342 ± 286 ng/dl;
p
= 0.035).
The percentage of patients with 50% resolution of ST-segment
was significantly higher in the IC group than in the IV group (
p
=
0.016) (Fig. 1). The maximum CRP level, peak and time to peak of
both CK-MB and hs-TnT showed statistically significant differences,
as shown in Table 2. There was no significant difference in LVEF
between the groups 48 hours after PCI (
p
= 0.632), but 30 days
after PCI, the average LVEF in the IC group was higher than in the
IV group (
p
= 0.023).
Angiographic characteristics of the two groups are presented in
Table 3. Post-procedure TIMI 3 flow (Fig. 2) andMBG3were significant
in the IC group (
p
= 0.045, 0.021, respectively). Comparison between
the groups in terms of the culprit vessel affected and multivessel
frequency showed no significant differences.
The incidence of MACE and major and minor bleeding during
the hospital stay and at follow up are shown in Table 3. Only one