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Wangetal. Journal of Medical Case Reports (2023) 17:430
https://doi.org/10.1186/s13256-023-04169-5
CASE REPORT
Severe thrombocytopenia induced
bytiroban afterpercutaneous coronary
intervention: acase report
Ze‑Mu Wang1*, Bin Wang2, Ya‑Fei Li3, Bei Chen1, Qin Shen1, Dian‑Fu Li1 and Lian‑Sheng Wang1
Abstract
Background Tirofiban is a nonpeptide glycoprotein IIb/IIIa receptor antagonist used widely in patients subjected
to percutaneous coronary intervention. While the usage of tirofiban sets an important clinical benefit, severe throm‑
bocytopenia can occur with use of this agent.
Case presentation A 76‑year‑old Chinese man was admitted with 1‑month history of sudden onset of chest tight‑
ness. He was diagnosed as having subacute inferior myocardial infarction, and percutaneous coronary interven‑
tion was performed. After the procedure, patient received tirofiban at 0.15 µg/kg/minute for 4 h. A blood sample
was obtained for a complete blood count; severe thrombocytopenia was reported according to routine orders at our
hospital. All antiplatelet drugs including tirofiban, aspirin, and clopidogrel were immediately discontinued. The patient
received platelet transfusions and was treated with immunoglobulin G. Two days later, the patient’s platelet count
had increased to 75 × 109/L. There was a significant improvement after day 5, and the platelet count was 112 × 109/L.
Seven days after the acute thrombocytopenia, he was discharged with normal platelet count.
Conclusions Clinicians should be particularly aware of tirofiban‑induced thrombocytopenia in routine practice.
Keywords Glycoprotein IIb/IIIa receptor antagonists, Tirofiban, Acute coronary syndromes, Percutaneous coronary
intervention
Background
Glycoprotein IIb/IIIa receptor antagonists (GPRAs),
including abciximab, eptifibatide, and tirofiban, are
widely used in the treatment of patients with acute coro-
nary syndromes (ACS) [1]. ese agents have been exten-
sively studied in several randomized trials, which have
demonstrated that the use of GPRAs may reduce the
incidence of myocardial infarction (MI) and composite
cardiac outcomes in patients subjected to percutaneous
coronary intervention (PCI) [2]. However, severe throm-
bocytopenia can occur with use of these agents [3]. Drug-
induced thrombocytopenia may result from a number of
diverse etiologies; it is important for clinicians to make
an accurate diagnosis to guide treatment decisions and
to inform prognosis. Here, we report a case of severe
thrombocytopenia within 4 hours of tirofiban adminis-
tration after PCI for subacute inferior MI.
Case presentation
A 76-year-old Chineseman was admitted with 1-month
history of sudden onset of chest tightness. A month pre-
viously, the symptom started while he was doing exercise.
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Journal of
Medical Case Reports
*Correspondence:
Ze‑Mu Wang
zemu.wang@njmu.edu.cn
1 Department of Cardiology, The First Affiliated Hospital of Nanjing
Medical University, Nanjing, China
2 Institute of Nephrology, Zhong Da Hospital, Southeast University School
of Medicine, Nanjing, China
3 Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing
Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing
Medical University, Suzhou, China
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Wangetal. Journal of Medical Case Reports (2023) 17:430
It was associated with diaphoresis and shortness of
breath, without chest pain. e resting 12-lead electro-
cardiogram (ECG) showed abnormal Q waves in leads II,
III, and aVF, and the cardiac troponin T was elevated. He
was diagnosed as having ACS and was treated at a local
hospital. Owing to the fact that the hospital was unable
to perform coronary angiography (CAG), the patient was
discharged home several days later on aspirin (100 mg
qd), clopidogrel (75 mg qd), metoprolol (12.5 mg qd),
and rosuvastatin (10mg qn). On admission to our hos-
pital, the patient still had a mildly elevated level of high-
sensitivity cardiac troponin T (21.58 ng/L). His initial
ECG showed abnormal Q waves in the inferior (II, III,
and avF) leads (Fig.1), which may indicate subacute infe-
rior MI. His routine blood test was normal, including a
platelet count of 201 × 109/L and a white blood cell count
of 5.86 × 109/L. He had no history of blood dyscrasia and
denied any history of smoking or drinking. e patient
underwent CAG in our hospital after admission. CAG
revealed evidence of left main (LM) and three-vessel
coronary artery disease (Fig.2). Low-dose heparin (2000
units) was given during the procedure. We consider the
optimal revascularization technique for this patient to be
coronary artery bypass graft (CABG) surgery and did not
perform PCI. However, the patient decide to be treated
with PCI rather than CABG. Four days later, CAG was
performed again; multivessel coronary intervention was
performed with drug-eluting stents and drug-coated
balloon. e procedure lasted for about 2 hours, and
the dose of heparin given was 6500 units. After the
procedure, the patient was transferred in stable condi-
tion to the ward and treated by intravenous tirofiban at
0.15µg/kg/minute. Post-PCI medications included aspi-
rin 100mg qd, clopidogrel 75mg qd, metoprolol succi-
nate 12.5mg qd, rosuvastatin 10mg qn, and benazepril
5mg qd. A blood sample was obtained for a complete
blood count 4 hours after the procedure, according to
routine orders at our hospital. His platelet count was
21 × 109/L, which was confirmed by manual examina-
tion of the blood film. e patient’s hemoglobin level was
119g/L. Tirofiban infusion was stopped by 4hours, and
other antiplatelet drugs including aspirin and clopidogrel
were immediately discontinued. A heparin-induced
thrombocytopenia (HIT) platelet factor 4 antibody test
was performed, and the result was negative [4]. Over the
next 12hours, the patient received 10 unit platelet trans-
fusions to prevent hemorrhage, and his platelet count
had increased to 49 × 109/L. Another analysis completed
later indicated that his platelet count was 37 × 109/L.
Additionally, immunoglobulin G (10g) was given. Aspi-
rin and clopidogrel were resumed the next day, and the
patient received another 10 unit platelet transfusions.
Two days later, the patient’s platelet count had increased
to 75 × 109/L. e course of the patient’s platelet count
is shown in Fig.3. ere was a significant improvement
after day 5, and the platelet count was 112 × 109/L. Seven
days after the acute profound thrombocytopenia, his
platelet count was 138 × 109/L, and he was discharged
with no hemorrhagic sequelae.
Fig. 1 Initial electrocardiogram of a 76‑year‑old man admitted with 1‑month history of chest tightness
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Page 3 of 5
Wangetal. Journal of Medical Case Reports (2023) 17:430
Discussion andconclusions
Tirofiban is a nonpeptide glycoprotein (GP) IIb/IIIa
receptor antagonist used in patients subjected to PCI for
the prevention of acute stent thrombosis and reduction
of major adverse coronary events [5]. It inhibits platelet
aggregation by preventing the attachment of fibrino-
gen and von Willebrand factor to the GP IIb/IIIa recep-
tor on the thrombocyte surface [6]. While the usage of
GP IIb/IIIa inhibitors sets an important clinical benefit,
the reported incidence of thrombocytopenia induced by
tirofiban ranges from 0.4% to 5.6% [7]. us, clinicians
should be particularly aware of tirofiban-induced throm-
bocytopenia in routine practice.
Besides tirofiban, aspirin and clopidogrel are widely
used as antiplatelet agents; they have also been reported
to be associated with thrombocytopenia [8]. How-
ever, the described patient had used these two drugs for
1 month before admission, and his routine blood test
showed a normal platelet count after admission. ere-
fore, the thrombocytopenia was not caused by the dual
antiplatelet therapy.
e most well-known medication that can induce
thrombocytopenia is heparin [9]. HIT is the most impor-
tant complication of heparin therapy during PCI in car-
diac patients. ere are two types of HIT. Type I HIT is a
transient, mild drop in platelet counts 48–72hours after
initiation of heparin therapy. It occurs because of direct
heparin-induced platelet aggregation and is usually clini-
cally harmless [7]. Type II HIT is an adverse immune-
mediated reaction due to antibodies formed against
heparin–platelet factor 4 complexes, which is usually
associated with thrombosis risk. It is more severe than
type I HIT and should be suspected when patients show
Fig. 2 Coronary angiography revealed an evidence of left main and three vessel coronary artery disease
Fig. 3 Platelet count trend during hospitalization
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Wangetal. Journal of Medical Case Reports (2023) 17:430
a reduction in the platelet count to less than 100,000 per
cubic millimeter or more than 50% of the baseline value
5–15days after initiation of heparin therapy [10, 11]. e
4T’s score (theseverity of rombocytopenia, itsTiming
of heparin exposure, appearance of new rombosis, and
differential diagnosis by exclusion of oer causes) has
been utilized as a clinical assessment tool to evaluate the
likelihood of HIT [11, 12]. Our patient’s 4T’s score was 3
points. us, the suspicion for HIT was low. In addition,
we carried out an immunoassay to examine the presence
of HIT antibodies; the negative result indicated that our
patient did not have an HIT type II reaction. It is impor-
tant to exclude HIT and other causes of thrombocyto-
penia to diagnose tirofiban-induced thrombocytopenia
accurately and treat patients appropriately.
A recent study based on pre-procedural character-
istics for early prediction of thrombocytopenia before
patients were exposed to tirofiban has developed a sim-
ple risk model to predict thrombocytopenia associated
with periprocedural tirofiban exposure [7]. Five inde-
pendent risk factors, including age ≥ 65years (2 points),
white blood cell ≥ 12 × 109 /L (1 point), diabetes mel-
litus (2 points), congestive heart failure (2 points), and
chronic kidney disease (1 point), were identified as risk
factors in the scoring system. According to the scoring
system, ≥ 7 points, 3–6 points, and ≤ 2 points indicate
high risk, moderate risk and low risk. For our patient, this
score only indicates a moderate risk (4 points), calculated
based on age and congestive heart failure. erefore, a
further predictive model is still needed to help doctors
identify high-risk patients in clinical practice [7].
e efficacy of tirofiban for patients with MI who
undergo PCI was positively correlated with its dose; high
dose can enhance the clinical effects, but also increase
the hemorrhagic risk [13]. e appropriate dose could be
adopted by reference to the specific conditions of patients
under assessment of bleeding risk, and a common recom-
mended clinical dose of 10 µg/kg may be appropriate for
patients without high hemorrhagic risk, followed by con-
tinuous intravenous injection at 0.15µg/kg/minute [13].
It is important to monitor platelet counts closely after
initiation of tirofiban infusion [14]. For these patients,
testing platelet counts before treatment, 2–4 h following
the start of infusion, and at 24 h would detect most cases
of acute thrombocytopenia [1, 15]. Discontinuation of
tirofiban is usually sufficient for treatment of thrombocy-
topenia because it is cleared from the circulation within
the first hours of cessation of the drug [14, 16].
In conclusion, this report demonstrates an example of
acute severe thrombocytopenia induced by tirofiban and
endorses the importance of platelet count monitoring
after initiating therapy with this agent in clinical practice.
Abbreviations
ACS Acute coronary syndromes
CABG Coronary artery bypass graft
CAG Coronary angiography
ECG Electrocardiogram
GP Glycoprotein
GPRAs Glycoprotein IIb/IIIa receptor antagonists
HIT Heparin‑induced thrombocytopenia
hs‑cTnT High‑sensitivity cardiac troponin T
LAD Left anterior descending
LCX Left circumflex artery
LM Left main
MI Myocardial infarction
PCI Percutaneous coronary intervention
RCA Right coronary artery
Acknowledgements
Not applicable.
Author contributions
Z‑MW wrote the manuscript. Z‑MW, BW, and Y‑FL analyzed and interpreted the
patient data. BC and QS collected the relevant materials including the figures
and medical records. D‑FL performed the PCI procedure. L‑SW was a major
contributor in proof reading and manuscript correction. All authors read and
approved the final manuscript.
Funding
This work was supported by grants from the National Natural Science Founda‑
tion of China (no. 81703213) and the Natural Science Youth Foundation of
Jiangsu Province of China (no. BK20151034) to Z‑MW.
Availability of data and materials
Not applicable.
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patient for publication of
this case report and any accompanying images. A copy of the written consent
is available for review by the Editor‑in‑Chief of this journal.
Competing interests
The authors declare that they have no competing interests.
Received: 17 October 2021 Accepted: 9 September 2023
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