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Effects of different doses of tirofiban combined with dual antiplatelet drugs on platelet indices, vascular endothelial function, and major adverse cardiovascular events in patients with acute ST-segment elevated myocardial infarction undergoing percutaneous coronary intervention

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Abstract

This trial targeted to analyze the effects of different doses of tirofiban combined with dual antiplatelet drugs on platelet indices, vascular endothelial function, and major adverse cardiovascular events (MACE) in patients with acute ST-segment elevated myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). A total of 180 patients with STEMI who underwent PCI were divided into Group A, Group B, and Group C (60 cases per group). Group A was given conventional medication, and Groups B and C were given a standard dose (10 μg/kg) and a high dose (20 μg/kg) of tirofiban on the basis of Group A, respectively. Thrombolysis in myocardial infarction (TIMI) myocardial perfusion grade and TIMI blood flow grade were compared. Myocardial enzymes, platelet indices, vascular endothelial function, inflammatory factors, and cardiac function indices were detected. In-hospital bleeding events and follow-up MACE were recorded. After PCI, Group C had a higher number of TIMI myocardial perfusion grade III and TIMI blood flow grade III versus Group A. Group C achieved the greatest changes in myocardial enzymes, platelet indices, vascular endothelial function-related factors, inflammatory factors, and cardiac function indices, followed by Group B and Group A. The incidence of bleeding events was higher in Group C than in Group A, and that of MACE in Group C was lower than in Group A. The addition of high-dose tirofiban to PCI and dual antiplatelet drugs for STEMI patients can improve myocardial blood perfusion, cardiac function, and vascular endothelial function, inhibit platelet activation and aggregation, and reduce the occurrence of MACE.
RESEARCH ARTICLE
Effects of different doses of tirofiban combined with dual antiplatelet
drugs on platelet indices, vascular endothelial function, and major
adverse cardiovascular events in patients with acute ST-segment elevated
myocardial infarction undergoing percutaneous coronary intervention
Xia Li, Xiaofan Guo, Naijin Zhang, Ye Chang, & Yingxian Sun
Cardiovascular Medicine, First Hospital of China Medical University, Shenyang, Liaoning Province, China
Abstract
This trial targeted to analyze the effects of different doses of tirofiban combined with dual antiplatelet
drugs on platelet indices, vascular endothelial function, and major adverse cardiovascular events
(MACE) in patients with acute ST-segment elevated myocardial infarction (STEMI) undergoing percuta-
neous coronary intervention (PCI). A total of 180 patients with STEMI who underwent PCI were divided
into Group A, Group B, and Group C (60 cases per group). Group A was given conventional medication,
and Groups B and C were given a standard dose (10 μg/kg) and a high dose (20 μg/kg) of tirofiban on
the basis of Group A, respectively. Thrombolysis in myocardial infarction (TIMI) myocardial perfusion
grade and TIMI blood flow grade were compared. Myocardial enzymes, platelet indices, vascular
endothelial function, inflammatory factors, and cardiac function indices were detected. In-hospital
bleeding events and follow-up MACE were recorded. After PCI, Group C had a higher number of TIMI
myocardial perfusion grade III and TIMI blood flow grade III versus Group A. Group C achieved the
greatest changes in myocardial enzymes, platelet indices, vascular endothelial function-related factors,
inflammatory factors, and cardiac function indices, followed by Group B and Group A. The incidence of
bleeding events was higher in Group C than in Group A, and that of MACE in Group C was lower than in
Group A. The addition of high-dose tirofiban to PCI and dual antiplatelet drugs for STEMI patients can
improve myocardial blood perfusion, cardiac function, and vascular endothelial function, inhibit platelet
activation and aggregation, and reduce the occurrence of MACE.
Plain Language Summary
What is the context?
Acute myocardial infarction is a branch of acute coronary syndromes, which can be categorized
into ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial
infarction. Percutaneous coronary intervention is a non-surgical, invasive treatment used to
improve blood flow to ischemic tissues and relieve coronary artery stenosis or occlusion.
Despite the fact that percutaneous coronary intervention allows for timely mechanical reperfusion,
patients with myocardial infarction have to face an increased risk of adverse cardiovascular events.
What is the new?
The addition of high-dose tirofiban to percutaneous coronary intervention and dual antiplate-
let drugs for ST-segment elevation myocardial infarction patients can improve myocardial
blood perfusion, cardiac function, and vascular endothelial function, inhibit platelet activa-
tion and aggregation, and reduce the occurrence of major adverse cardiovascular events.
What is the impact?
These findings favor the future application of tirofiban combination therapies and can
improve patients’ conditions alone.
Keywords
Acute ST-segment elevated myocardial
infarction, dual antiplatelet drugs, major
adverse cardiovascular events, percutaneous
coronary intervention, platelet index,
tirofiban, vascular endothelial function
History
Received 4 April 2024
Revised 28 August 2024
Accepted 4 September 2024
Correspondence: Yingxian Sun Cardiovascular Medicine, First Hospital
of China Medical University, No. 155 Nanjing North Street, Heping
District, Shenyang, Liaoning Province 110001, China.
E-mail: Sunyingxian3150@163.com
This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/
4.0/), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited. The terms on
which this article has been published allow the posting of the Accepted
Manuscript in a repository by the author(s) or with their consent.
http://www.tandfonline.com/iplt
ISSN: 0953-7104 (print), 1369-1635 (electronic)
Platelets, 2024; 35(1): 2402301
© 2024 The Author(s). Published with license by Taylor & Francis Group, LLC.
DOI: https://doi.org/10.1080/09537104.2024.2402301
Introduction
Heart attacks caused by plaque forming in the arteries are called
myocardial infarction (MI), which results in reduced blood flow
to the heart and thereafter damage to the heart.
1
As acute MI
(AMI) progresses, mechanical complications may occur including
cardiogenic shock, interventricular septal rupture, free wall rup-
ture, acute mitral regurgitation, and right ventricular infarction.
2
AMI is a subset of acute coronary syndromes, which can be
divided into an ST-segment elevation myocardial infarction
(STEMI) or a non-ST-elevation myocardial infarction
(NSTEMI).
3
Systemic activation chain, antithrombotic drugs,
and rapid reperfusion are some of the current treatments
available.
4
Percutaneous coronary intervention (PCI) is a non-
surgical and invasive procedure used to improve blood flow to
ischemic tissue and relieve coronary artery stenosis or occlusion.
5
Despite timely mechanical reperfusion under PCI, patients with
MI are forced to challenge an increased risk of adverse cardio-
vascular events.
6,7
Antiplatelet therapy is key to reducing local thrombotic com-
plications and systemic ischemic events in patients undergoing
PCI, but it is inevitably associated with increased bleeding.
8
Current antiplatelet drugs target different platelet activation path-
ways and exhibit specific pharmacodynamic and pharmacokinetic
characteristics. Early treatment strategies with intravenous anti-
platelet drugs may be able to fill the gap of insufficient platelet
inhibition.
9
Dual antiplatelet therapy (DAPT) with aspirin plus
a P2Y
12
inhibitor has been the standard antithrombotic treatment
after PCI, but this therapy has a narrow treatment window due to
a significant increase in major bleeding.
10
A comparative study
has shown that combination therapy with tirofiban and DAPT
neither affects platelet counts nor increases the incidence of
symptomatic bleeding or thromboembolic complications.
11
This
suggests the application value of tirofiban and DAPT in disease
treatment. Tirofiban is a small non-peptide ligand-glycoprotein
IIb/IIIa inhibitor,
12
which can competitively impede the binding
of fibrinogen and GP IIb/IIIa receptor, thus inhibiting platelet
function, prolonging bleeding time, and inhibiting thrombosis.
Currently, tirofiban has been widely used in the treatment of
acute coronary syndrome, which can relieve the thrombus load
at the lesion site, better restore coronary blood flow and myocar-
dial perfusion, and reduce the occurrence of adverse cardiovas-
cular events.
13–16
Although numerous studies have indicated that
the application of platelet glycoprotein IIb/IIIa receptor antago-
nists improves clinical outcomes in patients after PCI,
17–19
the
efficacy of their application in patients with acute STEMI under-
going direct PCI is uncertain. This may be highly related to the
timing of drug administration as well as drug dosage. Meanwhile,
concerning the current treatment limitations of monotherapy, this
trial was implemented to explore the efficacy of tirofiban at
different doses and DAPT in STEMI patients undergoing PCI
and further evaluated associated effects on platelet indices, vas-
cular endothelial function, and major adverse cardiovascular
events (MACE).
Materials and methods
Ethical statement
This trial was conducted with the approval of the Ethical
Committee of the First Hospital of China Medical University
(approval number: 20180325) and patients provided written
informed consent. The study was conducted in accordance with
the Declaration of Helsinki.
Study subjects
Acute STEMI patients (n = 180) who underwent PCI in First
Hospital of China Medical University were selected as the study
subjects, and they were randomly divided into three groups using
a computer-generated random-number list and a 1:1:1 allocation
ratio: Group A, Group B, and Group C, with 60 cases in each
group. All patients met the following inclusion criteria: ① Patients
met the diagnostic criteria outlined in the “2019 Guidelines for
the Diagnosis and Treatment of Acute ST-segment Elevation
Myocardial Infarction”
20
; Patient had obvious symptoms of
chest pain, and the time from onset to admission was <12 h;
Patients underwent emergency PCI; ④ Patients had no history of
allergy or contraindications to the drug in this study; Patients
with normal cognitive and mental state, treatment compliance,
and examination cooperation; Patients with complete ethical
approval materials, informed consent documents, clinical data,
and follow-up data. Exclusion criteria included Patients with
a history of MI; Patients with coagulation dysfunction;
Patients with cardiogenic shock; Patients with abnormal liver
and kidney function; ⑤ Patients with a previous history of heart
surgery and major trauma; Patients who had taken platelet
glycoprotein IIb/IIIa receptor inhibitors and immunosuppressants
in the past 1 month that may affect the results of this study;
Patients with diseases of the blood system, inflammatory dis-
eases, malignant tumors, and mental diseases; ⑧ Patients treated
by other means.
Research methods
The patients in the three groups were treated with PCI and were
given symptomatic supportive treatments such as vital signs
monitoring and oxygen cardioprotection after admission to the
hospital. Group A was given conventional drug treatment.
Patients were taken orally 300 mg aspirin enteric-coated tablet
(20170215, Staldson (Beijing Biopharmaceuticals Co., Ltd.,
China) + 180 mg Ticagrelor Tablets (J20130020, AstraZeneca,
Sweden) before PCI. During PCI, Groups B and C were treated
with tirofiban (20170101, Huadong Medicine, Hangzhou,
China) on the basis of Group A. Group B was treated with
a standard dose (10 μg/kg) intracoronary administration of tiro-
fiban, and then maintained with 0.15 μg/(kg · min) intravenous
drip until 24 h after PCI, and Group C was treated with high
dose (20 μg/kg) intracoronary administration of tirofiban, and
maintained with 0.15 μg/(kg-min) intravenous drip until 24
h after surgery. Every 12 h, low molecular weight heparin was
injected subcutaneously for anticoagulation within 3–5 days after
PCI. Oral aspirin enteric-coated tablets (100 mg/d) and
Ticagrelor Tablet (90 mg/time, 2 times/d) were continued for 6
months after PCI.
Observation indices
(1) Thrombolysis in myocardial infarction (TIMI) blood flow:
Coronary angiography was performed in all three groups
after PCI to evaluate TIMI myocardial perfusion
21
and
TIMI blood flow
22
of the infarct-related artery.
(2) Myocardial enzyme spectrum: 4 ml of venous blood was
extracted from the left upper arm of patients and centrifuged
at 3000 r/min for 12 min. The separated serum was stored at
−80°C. Lactate dehydrogenase (LDH), creatine kinase (CK),
creatinine kinase-myocardial band (CK-MB), aspartate ami-
notransferase (AST), and α-hydroxybutyric-dehydrogenase
(α-HBD) before and 24 h after PCI were assessed by an
2X. Li et al. Platelets, 2024; 35(1): 1–8
automatic biochemical analyzer (Celercare M1, Tianjin
Mnchip Technologies Co., Ltd., Tianjin, China) and corre-
sponding kits.
(3) Platelet indices: 4 ml blood was collected with the same method
as before. An automatic blood cell analyzer (BC6800-Plus,
Shenzhen Mindray Bio-Medical Electronics Co., Ltd.,
Shenzhen, China) was employed to examine platelet count
(PLT), mean platelet volume (MPV), platelet distribution
width (PDW), and platelet aggregation rate (PAR) before and
24 h after PCI. The positive expression rates of P-selectin
(CD62P), CD63, and mycophenolate acid (MPA) before and
24 h after PCI were evaluated by a flow cytometer (FACSCanto
II, BD, USA) and monoclonal immunofluorescence.
(4) Vascular endothelial function: 3 ml blood was acquired with
the same method as before. Before and 24 h after PCI, rocket
immunoelectrophoresis was applied to test von Willebrand
factor (vWF) levels, enzyme-linked immunosorbent assay
(ELISA) method to evaluate endothelin-1 (ET-1) levels, and
Griess reagent method to measure NO level. The kits were
available from Shanghai Institute Of Biological Products
Limited Liability Company (Shanghai, China), Sangon
(Shanghai, China), and Beyotime (Shanghai, China),
respectively.
(5) Inflammatory factors: 3 ml blood was acquired, and
C-reactive protein (CRP), procalcitonin (PCT), and interleu-
kin-6 (IL-6) before and 24 h after PCI were tested by ELISA
kits (Beyotime).
(6) Cardiac function indicators: Left ventricular ejection fraction
(LVEF), left ventricular end-diastolic diameter (LVEDD), and
left ventricular end-systolic diameter (LVESD) were observed
by echocardiography before and 30 days after PCI.
(7) Bleeding events and MACE: In-hospital bleeding events (ure-
thral hemorrhage and gastrointestinal hemorrhage) were
recorded. MACE during the 1-year follow-up was recorded,
including recurrent angina pectoris, recurrent MI, heart fail-
ure, malignant arrhythmia, cardiogenic shock, etc.
Statistical analysis
The data analysis software is SPSS 22.0 (IBM Corp, Armonk,
NY, USA). Measurement data were described as
x ± s, and the
data meeting the normal distribution by the Kolmogorov–
Smirnov test were performed by paired sample t-test or one-
way analysis of variance. Enumeration data were described by
n (%) and comparisons between groups were analyzed by the
χ
2
test. p < .05 was considered statistically significant.
Results
Baseline data
No significant difference was found in age, BMI, time of onset,
gender, percentage of smoking history, percentage of hyperten-
sion history, percentage of diabetes history, and percentage of
hyperlipidemia history among Group A, Group B, and Group
C (all p > .05, Table I).
TIMI myocardial perfusion grade and TIMI blood flow grade
Post-procedure TIMI myocardial perfusion and TIMI blood flow
grades of Group A, Group B, and Group C had statistical sig-
nificance (p < .05); the number of TIMI myocardial perfusion
grades 0 and TIMI blood flow grades I-II was less in Group
C than in Group A; and the number of TIMI myocardial perfusion
grade III and TIMI blood flow grade III in Group C was higher
than that in Group A (p < .05/9 = 0.0056) (Table II).
Myocardial enzyme profile indices
The comparison of Group A, Group B, and Group C did not show
any statistical significance in LDH, CK, CK-MB, AST, or α-HBD
before PCI (p > .05), and after PCI, these indices of the three groups
were decreased, and Group B and Group C were lower than Group
A, and Group C was lower than Group B (p < .05, Table III).
Table I. Comparison of three groups of baseline data.
Projects Group A Group B Group C P value
Age (x ± s, years) 62.92 ± 6.79 63.05 ± 7.01 63.42 ± 6.70 .917
Body mass index (x ± s, kg/m
2
) 24.15 ± 2.42 23.92 ± 2.40 24.03 ± 2.27 .869
Time of onset (x ± s, h) 6.45 ± 1.45 6.28 ± 1.45 6.37 ± 1.34 .813
Gender [n(%)] .746
Male 33 (55.00) 32 (53.33) 36 (60.00)
Female 27 (45.00) 28 (46.67) 24 (40.00)
Smoking history [n (%)] 26 (43.33) 31 (51.67) 28 (46.67) .655
Hypertension history [n (%)] 33 (55.00) 29 (48.33) 32 (53.33) .749
Diabetes history [n (%)] 22 (36.67) 19 (31.67) 19 (31.67) .799
Hyperlipidemia history [n (%)] 38 (63.33) 35 (58.33) 40 (66.67) .637
Table II. Comparison of TIMI myocardial perfusion grade and TIMI blood flow grade among the three groups [n (%)].
Groups Group A Group B Group C P value
TIMI myocardial perfusion grade <.001
0 11 (18.33) 5 (8.33) 0 (0.00)
I-II 19 (31.67) 14 (23.33) 9 (15.00)
III 30 (50.00) 41 (68.33) 51 (85.00)
TIMI blood flow grade <.001
0 6 (10.00) 4 (6.67) 0 (0.00)
I-II 18 (30.00) 10 (16.67) 5 (8.33)
III 36 (60.00) 46 (76.67) 55 (91.67)
Compared with group A,
p < .0056 (0.05/9). TIMI, Thrombolysis in myocardial infarction.
DOI: https://doi.org/10.1080/09537104.2024.2402301 Platelets 3
Platelet indices
PLT, MPV, PDW, PAR, CD62P, CD63, and MPA among Group
A, Group B, and Group C were not significantly different before
the procedure (p > .05). After PCI, these parameters were all
decreased in the three groups, and Group B and Group C were
lower than Group A, and Group C was lower than Group B
(p < .05, Table IV).
Vascular endothelial function
Group A, Group B, and Group C did not show statistical signifi-
cance in vWF, ET-1, or NO before the procedure (p > .05). After
PCI, vWF and ET-1 were decreased while NO was increased in
all three groups; among them, vWF and ET-1 were lower in
Groups B and C than in Group A, and vWF and ET-1 were
lower in Group C than in Group B; NO in Groups B and C was
higher than in Group A, and NO in Group C was higher than in
Group B (p < .05, Table V).
Inflammatory factors
In Group A, Group B, and Group C, CRP, PCT, and IL-6
levels were not significantly different before the procedure
(p > .05). After PCI, CRP, PCT, and IL-6 levels of the three
groups were all decreased, Group B and Group C were lower
than Group A, and Group C was lower than Group B (p < .05,
Table VI).
Cardiac function indices
LVEF, LVEDD, and LVESD did not differ statistically in
Group A, Group B, and Group C before the procedure
(p > .05). On the 30
th
day after PCI, LVEF was increased
whereas LVEDD and LVESD were decreased in the three
groups than those before the procedure; among them,
LVEDD and LVESD were lower in Groups B and C than in
Group A, and LVEDD and LVESD were lower in Group
C than in Group B; LVEF in Groups B and C was higher
than in Group A, and LVEF in Group C was higher than in
Group B (p < .05, Table VII).
Incidence of bleeding events and MACE
The comparison of the incidence of bleeding events during hos-
pitalization in patients of Group A, Group B, and Group
C revealed that the incidence of bleeding events during
Table III. Comparison of myocardial enzyme profiles among the three groups.
Groups Group A Group B Group C P value
Before procedure
LDH (IU/L) 682.32 ± 102.29 681.67 ± 100.20 684.06 ± 102.08 .990
CK (IU/L) 456.54 ± 96.73 453.72 ± 96.35 458.40 ± 93.81 .964
CK-MB (IU/L) 46.02 ± 5.78 46.46 ± 6.11 45.77 ± 6.16 .816
AST (IU/L) 94.65 ± 15.88 93.98 ± 14.26 94.16 ± 14.93 .968
α-HBD (IU/L) 506.55 ± 48.27 508.93 ± 43.33 506.79 ± 43.94 .951
After procedure
LDH (IU/L) 488.77 ± 45.53
454.47 ± 44.79
①③
420.62 ± 43.34
①②③
<.001
CK (IU/L) 221.10 ± 48.72
196.48 ± 46.49
①③
176.34 ± 37.71
①②③
<.001
CK-MB (IU/L) 42.30 ± 4.19
38.48 ± 4.56
①③
34.75 ± 4.08
①②③
<.001
AST (IU/L) 82.29 ± 7.75
76.43 ± 8.32
①③
65.67 ± 8.14
①②③
<.001
α-HBD (IU/L) 385.91 ± 34.50
324.64 ± 26.03
①③
274.58 ± 24.44
①②③
<.001
Compared with group A after procedure,
p < .05; compared with group B after procedure,
p < .05; compared with the
same group before procedure,
p < .05. LDH, lactate dehydrogenase; CK, creatine kinase; CK-MB, creatinine kinase-
myocardial band; AST, aspartate aminotransferase; α-HBD, α-hydroxybutyric-dehydrogenase.
Table IV. Comparison of platelet indices among the three groups.
Groups Group A Group B Group C P value
Before procedure
PLT (×10
9
/L) 189.70 ± 26.72 190.17 ± 24.93 191.36 ± 24.81 0.935
MPV (fL) 13.25 ± 2.12 13.15 ± 2.14 13.22 ± 2.09 0.965
PDW (%) 19.15 ± 1.96 19.05 ± 2.02 19.12 ± 2.07 0.962
PAR (%) 57.48 ± 10.58 56.87 ± 9.89 57.52 ± 9.42 0.923
CD62P (%) 7.20 ± 1.14 7.18 ± 1.15 7.22 ± 1.15 0.982
CD63%) 6.94 ± 0.24 6.95 ± 0.25 6.97 ± 0.21 0.777
MPA (%) 20.89 ± 2.42 21.26 ± 2.38 21.10 ± 2.40 0.698
After procedure
PLT (×10
9
/L) 171.52 ± 27.26
156.24 ± 25.46
①③
122.68 ± 26.31
①②③
<0.001
MPV (fL) 11.86 ± 2.00
10.64 ± 2.22
①③
8.93 ± 2.17
①②③
<0.001
PDW (%) 17.68 ± 1.50
16.34 ± 1.34
①③
15.40 ± 1.42
①②③
<0.001
PAR (%) 32.66 ± 8.35
24.95 ± 9.17
①③
16.94 ± 8.40
①②③
<0.001
CD62P (%) 2.89 ± 0.50
2.33 ± 0.52
①③
1.81 ± 0.35
①②③
<0.001
CD63%) 2.44 ± 0.16
2.06 ± 0.23
①③
1.58 ± 0.20
①②③
<0.001
MPA (%) 15.02 ± 1.47
13.36 ± 1.50
①③
11.94 ± 1.34
①②③
<0.001
Compared with group A after procedure,
p < .05; compared with group B after procedure,
p < .05; compared with the
same group before procedure,
p < .05. PLT, platelet count; MPV, mean platelet volume; PDW, platelet distribution
width; PAR, platelet aggregation rate; CD62P, P-selectin; MPA, mycophenolate acid.
4X. Li et al. Platelets, 2024; 35(1): 1–8
hospitalization was higher in Group C than in Group A
(p < .05/3 = 0.0167). The incidence of MACE during the 1-year
postoperative follow-up period was compared among the three
groups of patients, which demonstrated that the incidence of
MACE in Group C was lower than that in Group A
(p < .05/3 = 0.0167) (Table VIII).
Table VI. Comparison of inflammatory factors among the three groups.
Groups Group A Group B Group C P value
Before procedure
CRP (mg/L) 11.88 ± 2.41 11.65 ± 2.42 12.01 ± 2.37 .707
PCT (μg/L) 2.74 ± 0.42 2.77 ± 0.40 2.75 ± 0.43 .922
IL-6 (ng/L) 8.47 ± 1.30 8.42 ± 1.22 8.39 ± 1.25 .939
After procedure
CRP (mg/L) 9.06 ± 1.30
7.45 ± 1.27
①③
4.39 ± 1.24
①②③
<.001
PCT (μg/L) 1.97 ± 0.44
1.68 ± 0.31
①③
1.15 ± 0.26
①②③
<.001
IL-6 (ng/L) 5.92 ± 1.03
4.25 ± 0.97
①③
3.72 ± 0.94
①②③
<.001
Compared with group A after procedure
p < .05; compared with group B after procedure,
p < .05; compared
with the same group before procedure,
p < .05. CRP, C-reactive protein; PCT, procalcitonin; IL-6, inter-
leukin-6.
Table VII. Comparison of cardiac function indices among the three groups.
Groups Group A Group B Group C P value
Before procedure
LVEF (%) 41.60 ± 6.05 42.07 ± 5.96 41.88 ± 6.11 .913
LVEDD (mm) 58.30 ± 4.23 58.82 ± 4.44 58.57 ± 4.81 .821
LVESD (mm) 44.92 ± 3.79 45.18 ± 3.77 45.60 ± 3.65 .601
After procedure
LVEF (%) 50.27 ± 5.25
54.10 ± 5.93
①③
57.57 ± 5.33
①②③
<.001
LVEDD (mm) 52.43 ± 5.52
47.40 ± 5.67
①③
42.03 ± 5.82
①②③
<.001
LVESD (mm) 37.18 ± 2.07
35.42 ± 2.13
①③
32.42 ± 2.03
①②③
<.001
Compared with group A after procedure,
p < .05; compared with group B after procedure,
p < .05; compared
with the same group before procedure,
p < .05. LVEF, left ventricular ejection fraction; LVEDD, left
ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter.
Table V. Comparison of vascular endothelial function among the three groups.
Groups Group A Group B Group C P value
Before procedure
vWF (%) 162.37 ± 19.10 163.54 ± 18.30 162.85 ± 19.34 .944
ET-1 (ng/L) 97.62 ± 4.27 96.74 ± 4.53 96.80 ± 4.26 .467
NO (μmol/L) 51.34 ± 8.11 50.83 ± 7.41 50.91 ± 8.14 .930
After procedure
vWF (%) 145.80 ± 17.26
130.52 ± 17.79
①③
106.32 ± 12.15
①②③
<.001
ET-1 (ng/L) 84.46 ± 4.56
77.14 ± 5.33
①③
63.05 ± 5.82
①②③
<.001
NO (μmol/L) 60.64 ± 11.73
65.45 ± 10.04
①③
72.21 ± 9.81
①②③
<.001
Compared with group A after procedure,
p < .05; compared with group B after procedure,
p < .05; compared with the
same group before procedure,
p < .05. vWF, von Willebrand factor; ET-1, endothelin-1; NO, nitric oxide.
Table VIII. Comparison of bleeding events and MACE incidence among the three groups [n (%)].
Groups Group A Group B Group C P value
Bleeding events 2 (3.33) 4 (6.67) 11 (18.33)
.013
Urethral hemorrhage 1 (1.67) 2 (3.33) 4 (6.67)
Gastrointestinal hemorrhage 1 (1.67) 2 (3.33) 7 (11.67)
MACE 18 (30.00) 9 (15.00) 5 (8.33)
.006
Recurrent angina pectoris 6 (10.00) 3 (5.00) 3 (5.00)
Recurrent myocardial infarction 2 (3.33) 1 (1.67) 1 (1.67)
Heart failure 5 (8.33) 2 (3.33) 0 (0.00)
Malignant arrhythmia 5 (8.33) 3 (5.00) 1 (1.67)
Compared with group A
p < .0167 (0.05/3). MACE, major adverse cardiovascular events.
DOI: https://doi.org/10.1080/09537104.2024.2402301 Platelets 5
Discussion
The prognosis of AMI has improved due to recent advances in early
reperfusion and drug therapy. Even so, there are still a lot of improve-
ments to be made.
23
PCI reduces the risk of spontaneous MI and
revascularization and improves angina status. However, there is
a risk of myocardial injury during PCI.
24
Antiplatelet therapy is the
main drug therapy for preventing thrombotic or ischemic events in
patients with coronary artery disease after PCI. The use of antiplatelet
therapy comes at the cost of an increased risk of bleeding complica-
tions. Therefore, modulating antiplatelet therapy is often considered to
balance the risk of thrombotic or ischemic events with the risk of
bleeding.
25
Tirofiban has historically been used as a bridge for anti-
platelet therapy (clopidogrel) to inhibit platelets during PCI to prevent
stent thrombosis.
26
Regarding this, combination therapy with tirofiban
and antiplatelet therapy may be considered if antiplatelet therapy is
inadequate in STEMI patients undergoing PCI. As for this trial, the
effect of tirofiban was mainly studied in combination with DAPT on
STEMI patients undergoing PCI.
TIMI grade flow evaluates epicardial blood flow and TIMI
myocardial perfusion grade evaluates microvascular perfusion. It
has been identified that higher odds of survival can be achieved if
TIMI grade 3 flow is achieved early during thrombolytic reperfu-
sion or PCI.
27
This trial found that high-dose tirofiban combined
with DAPT could effectively improve myocardial blood perfusion
during the perioperative period of PCI. As reported, intracoronary
administration with tirofiban can improve the incidence of TIMI
III at a high dose in patients with STEMI.
28
Further, intracoronary
tirofiban bolus can improve TIMI II-III in patients with acute
STEMI.
29
Measurements of myocardial enzymes have been taken as
a quantitative method to assess myocardial injury.
30
This trial
supported that LDH, CK, CK-MB, AST, and α-HBD were all
decreased after treatment, with high-dose tirofiban showing the
highest inhibition effect. A current report has measured the
inhibition of CK and CK-MB in AMI patients receiving com-
bined therapy of Danhong injection and tirofiban.
31
Tirofiban
has a high affinity and short plasma half-life and specific
inhibition of ongoing platelet aggregation and thrombosis.
32
Consistently, this trial found that a high dose of tirofiban most
effectively suppressed platelet activation and aggregation. In
addition to that, tirofiban protected against endothelial dysfunc-
tion, inflammation, and cardiac dysfunction and prevented
MACE. After PCI, tirofiban can reduce platelet activation and
endothelial dysfunction,
33
as well as improve myocardial perfu-
sion and recover cardiac function.
34
A tirofiban regimen can
improve cardiac function and reduce inflammation in AMI
patients after emergency PCI.
35
Moreover, after PCI, tirofiban,
in combination with anisodamine, can improve postoperative
myocardial perfusion and accelerate cardiac function recovery
in AMI patients.
36
For AMI patients undergoing PCI, tirofiban
combined with ticagrelor and aspirin can improve left ventricu-
lar function and reduce platelet aggregation and serum inflam-
mation without causing significant changes in MACE.
37
As indicated, the dose of tirofiban used in the trial was varied,
and high-dose tirofiban achieved a greater improvement effect on
STEMI patients undergoing PCI. In patients with acute coronary
syndrome who underwent PCI, high-dose intravenous tirofiban
reduces infarct size compared with low-dose infusion,
38
further
confirming the dose-dependent improvement effect of tirofiban.
However, another paper illustrates that a high dose of tirofiban is
associated with hemorrhagic risk on the scene of STEMI
treatment.
39
Therefore, given the patient’s condition and hemor-
rhagic risk, the rational dosage application of tirofiban becomes
essential. There are some studies discussing the clinical efficacy
of tirofiban combined with conventional DAPT in patients
undergoing PCI. For instance, Guo et al. have divided ACS
patients into the high-dose group (0.10–0.15 μg/kg/min), the mod-
erate-dose group (0.05–0.10 μg/kg/min), and the low-dose group
(<0.05 μg/kg/min), which concluded that periprocedural adminis-
tration of low-dose tirofiban offers a favorable efficacy outcome
in patients with pre-treatment of dual traditional antiplatelet
therapy.
40
Another study has demonstrated that for patients who
suffered from AMI and were treated with PCI, the application of
tirofiban plus ticagrelor and aspirin could effectively improve
myocardial perfusion function, decrease the incidence of no-
reflow or slow blood flow, and have marked curative effects.
37
Moreover, Liu et al. have supported that DAPT could effectively
diminish the incidence of major complications in aged female
patients with diabetes and STEMI.
41
Compared with this pub-
lished article, our subject was STEMI patients who underwent
PCI, and our focus was on myocardial enzymes, platelet indices,
vascular endothelial function, inflammatory factors, and cardiac
function indices, which are all innovative points of our research.
PCI in patients with AMI is a common method to improve
long-term prognosis because it can open the infarcted blood
vessels, restore myocardial reperfusion, and save ischemic myo-
cardium. However, at the same time, PCI may lead to the aggra-
vation of endothelial function damage and local thrombus in
a coronary artery, which may increase the risk of recurrent infarc-
tion after the procedure. Therefore, it is important to take active
measures against platelet coagulation in PCI. At present, clinical
antiplatelet therapy is often carried out with aspirin, P2Y12
inhibitors, and platelet GP IIb/IIIa receptor antagonists. Among
them, aspirin and P2Y12 inhibitors can only inhibit some of the
platelet-related enzyme/receptor activities and have no obvious
antiplatelet agglutination effects. Platelet GP IIb/IIIa receptor
antagonists specifically block the GP IIb/IIIa receptors in the
channel, thereby inhibiting platelet activation while also eliminat-
ing activator-induced platelet aggregation.
42
Therefore, this study
aimed to further investigate the clinical efficacy and safety of
different doses of tirofiban combined with DAPT therapy given
during PCI. The results of the study revealed that the combination
of different doses of tirofiban in PCI could improve myocardial
perfusion, cardiac function, and vascular endothelial function,
inhibit platelet activation and aggregation, and reduce the occur-
rence of MACE in STEMI patients.
In brief, the addition of high-dose tirofiban to PCI and DAPT for
STEMI patients can improve myocardial blood perfusion, cardiac
function, and vascular endothelial function, inhibit platelet activa-
tion and aggregation, and reduce the occurrence of MACE. These
findings benefit the future application of combined therapy with
tirofiban and individually improve patients' conditions. However,
the sample size was relatively small and no sample size calculation
was performed, which might be considered a limitation of the study
and the fact that this study was not registered in clinical trial
databases (e.g., ClinicalTrials.gov) is also a limitation. Meanwhile,
this study did not use the drug before PCI, and the optimal timing of
tirofiban administration can be discussed in the future. Furthermore,
we did not consider the application of the Kaplan–Meier method to
analyze the 12-month MACE-free survival rate, which should be
further explored in future work.
Acknowledgments
We would like to give our sincere gratitude to the reviewers for their
constructive comments.
Disclosure statement
The authors have no conflicts of interest to declare that are relevant to the
content of this article.
6X. Li et al. Platelets, 2024; 35(1): 1–8
Funding
No funds, grants, or other support was received.
Supplementary material
Supplemental data for this article can be accessed online at https://doi.
org/10.1080/09537104.2024.2402301
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ResearchGate has not been able to resolve any citations for this publication.
Article
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Introduction Platelets play a key role in arterial thrombosis and antiplatelet therapy is pivotal in the treatment of cardiovascular disease. Current antiplatelet drugs target different pathways of platelet activation and show specific pharmacodynamic and pharmacokinetic characteristics, implicating clinically relevant drug-drug interactions. Areas covered This article reviews the role of platelets in hemostasis and cardiovascular thrombosis, and discusses the key pharmacodynamics, drug-drug interactions and reversal strategies of clinically used antiplatelet drugs. Expert opinion Antiplatelet therapies target distinct pathways of platelet activation: thromboxane A2 synthesis, adenosine diphosphate-mediated signaling, integrin αIIbβ3 (GPIIb/IIIa), thrombin-mediated platelet activation via the PAR1 receptor and phosphodiesterases. Key clinical drug-drug interactions of antiplatelet agents involve acetylsalicylic acid – ibuprofen, clopidogrel – omeprazole, and morphine – oral P2Y12 inhibitors, all of which lead to an attenuated antiplatelet effect. Platelet function and genetic testing and the use of scores (ARC-HBR, PRECISE-DAPT, ESC ischemic risk definition) may contribute to a more tailored antiplatelet therapy. High on-treatment platelet reactivity presents a key problem in the acute management of ST-elevation myocardial infarction (STEMI). A treatment strategy involving early initiation of an intravenous antiplatelet agent may be able to bridge the gap of insufficient platelet inhibition in high ischemic risk patients with STEMI.
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