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Case Report

http://dx.doi.org/10.12997/jla.2014.3.1.43pISSN 2287-2892 • eISSN 2288-2561 JLAAcute Stent Thrombosis after Coronary Stenting in Patients with Acute Coronary SyndromeHyo-Sun Shin1,3, Sang-Hyun Kim2,3, Hack-Lyoung Kim2,3, Jae-Bin Seo2,3, Woo-Young Chung2,3, Joo-Hee Zo2,3, Myung-A Kim2,3

1Division of Cardiology, Department of Internal Medicine, Seoul National University Hospital, Seoul, 2Division of Cardiology, Department of Internal Medicine, Seoul Boramae Medical Center, Seoul, 3Seoul National University College of Medicine, Seoul, Korea

Acute stent thrombosis after percutaneous coronary intervention (PCI) is still problematic because of the subsequent development of myocardial infarction and poor prognosis. The incidence of acute stent thrombosis, occurring within 0-24hours after PCI, is relatively low, but underlying causes and treatment strategy are not well defined. Multi-vessel disease, ST-elevated myocardial infarction (STEMI), and large thrombotic burden are known risk factors of acute stent thrombosis. Thrombus aspiration, balloon angioplasty and glycoprotein IIb/IIIa receptor blocker could be therapeutic options. Recently we experienced two cases of acute stent thrombosis which developed during PCI with the aggravation of chest pain, and acute stent thrombosis were diagnosed immediately and successfully treated. Here we report two cases of acute stent thrombosis during PCI for one patient with STEMI and the other with acute coronary syndrome, which were successfully treated with thrombus aspiration and intravenous infusion of glycoprotein IIb/IIIa receptor blocker.

Key Words: Coronary thrombosis, Acute coronary syndrome, Abciximab

Received:Revised:Accepted:

March 14, 2014 May 29, 2014June 11, 2014

Corresponding Author: Sang-Hyun Kim, Division of Cardiology, Department of Internal Medicine, Seoul Boramae Medical Center, Seoul National University College of Medicine, 20, Borimae-ro, 5-gil, Dongak-gu, Seoul 156-707, KoreaTel: +82-2-870-3864, Fax: +82-2-870-3866, E-mail: shkimmd@snu.ac.kr

This is an Open Access article distributed under the terms of the creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

INTRODUCTION

After the advent of percutaneous coronary inter-

vention (PCI), mortality of acute coronary syndrome

continues to decline, but stent thrombosis (ST) after PCI

remains a residual problem of the procedure. ST occurs

about 1-2% of total PCI cases1-7 and acute stent throm-

bosis, occurring within 0-24hours after PCI, accounts for

6-25% of all ST cases.1,8 Although the incidence of ST is

relatively low, prognosis of ST is dismal; with a

case-fatality rate of 15-45%.5,7 Nonetheless underlying

causes and treatment strategy of ST are not-well defined.

Physician’s concept or suspicion of acute stent throm-

bosis can be enough for the diagnosis and improve the

prognosis of those patients. Here we report two cases

of acute stent thrombosis during PCI for one patient with

ST-elevated myocardial infarction (STEMI) and the other

with acute coronary syndrome, which were successfully

treated with thrombus aspiration and intravenous

injection of glycoprotein IIb/IIIa inhibitor.

CASE 1

A 66-year-old man visited the Emergency Department

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Fig. 1. Initial electrocardiogram showed ST-segment elevation in leads I, avL, V1, V2, V3, V4 with reciprocal changes ofST-segment in leads II, III, and aVF.

Fig. 2. Initial chest X-ray showed bilateral pulmonary edema.

with complaint of chest pain of squeezing nature which

developed 30 minutes before. On admission, his blood

pressure was 113/74 mmHg, and his heart rate was 94

beats per minute, and respiration rate was 30 /min. The

electrocardiogram (ECG) showed ST-segment elevation

in leads I, aVL, V1, V2, V3, V4 with reciprocal changes of

ST-segment in leads II, III, and aVF (Fig. 1). The chest X-ray

showed severe pulmonary edema (Fig. 2). Medical treat-

ment was started immediately including aspirin 300 mg,

clopidogrel 600 mg, intravenous nitrate infusion and bolus

injection of unfractionated heparin 6,500 units. Unfrac-

tionated heparin was administered before PCI and

repeatedly at every hour during PCI with monitoring

activated clotting time for the maintenance over 300

seconds. He received emergent coronary angiography

(CAG), and it showed total occlusion of the proximal left

anterior descending coronary artery (LAD) with thrombus

(Fig. 3-A) and segmental stenosis in left circumflex coro-

nary artery (LCX). There were stenotic lesions in middle

and distal right coronary artery (RCA). He showed severe

pulmonary edema on chest x-ray and multiple stenotic

lesions of coronary arteries, so we decided PCI on LAD

and LCX. He underwent balloon angioplasty and evero-

limus eluting stent (3.0×18 mm Xience V stent, Abbott)

was inserted in proximal LAD at first (Fig. 3-B). Two

Everolimus eluting stents were inserted in proximal and

distal LCX. After PCI, patient suddenly complained of chest

pain again. We checked the left coronary artery angiogram

again and found newly developed intraluminal filling

defect due to stent thrombosis of the proximal LAD, which

Left

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Fig. 3. (A) Left anterior oblique (LAO) projection with caudal angulation of selective left coronary angiogram showed thetotal occlusion with thrombus in the proximal part of left anterior descending artery (arrows), (B) LAO projection withcranial angulation of selective left CAG. Everolimus eluting stent (3.0×18 mm Xience V stent, Abbott, USA) was successfullyplaced in the LAD (arrows), (C) Right anterior oblique projection with cranial angulation of selective left CAG after RCAtreatment showed intraluminal filling defect of the targeted lesion of LAD (arrows), (D) After thrombus aspiration and infusionof glycoprotein IIb/IIIa receptor blocker, CAG showed recovery of coronary flow.

was treated 45 minutes before (Fig. 3-C). After intravenous

administration of a glycoprotein IIb/IIIa receptor blocker

(Abciximab), thrombus aspiration and balloon angioplasty

were done. A final angiogram revealed improved flow

through all coronary arteries (Fig. 3-D). 4 days after, a

second look CAG showed patent flow through all stented

vessels. There were no predisposing factors including

abnormal findings of coagulation system such as protein

C or S, anti-phospholipid antibody and no evidence of

malignancy. He was discharged with triple anti-platelet

therapy of aspirin 100 mg, clopidogrel 75 mg, and

cilostazol 200 mg daily. This patient was followed-up via

outpatient clinic uneventfully, and repeat CAG performed

after 12 months showed patent coronary flow.

A B

C D

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Fig. 4. (A) Right anterior oblique (RAO) projection with caudal angulation of selective left coronary angiogram showedthe long segmental concentric stenosis in proximal to middle LAD and total occlusion in proximal LCX (arrows), (B) LAOprojection with cranial angulation of selective left CAG. Two Everolimus eluting stents (2.5×28 mm and 3.0×23 mm XienceV stent, Abbott) were inserted in proximal and middle LAD, (C) LAO projection with cranial angulation of selective leftCAG after LCX treatment showed intraluminal filling defect of the distal LAD (arrows), (D) After thrombus aspiration,infusion of glycoprotein IIb/IIIa receptor blocker and balloon angioplasty, CAG showed recovery of coronary flow.

CASE 2

A 83 year-old woman was referred to our hospital with

complaints of dyspnea on exertion (New York Heart

Association functional class III) from 1 month ago and

hyponatremia with diuretic medication. Echocardiogra-

phic examination showed hypokinesia of the anterior,

inferolateral and inferior walls at base to mid-portion of

left ventricle. Under assessment of acute coronary synd-

rome, the patient was treated aspirin 300 mg, clopidogrel

600 mg and intravenous nitroglycerin infusion. Also,

unfractionated heparin was administered before PCI and

at every hour during PCI with monitoring activated clotting

time for the maintenance over 300 seconds. She

underwent CAG which showed critical stenosis in the LAD

and LCX (Fig. 4-A). Balloon angioplasty was done and

A B

C D

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two Everolimus eluting stents (2.5×28 mm and 3.0×23

mm Xience V stent, Abbott) were inserted in the proximal

and middle LAD at first (Fig. 4-B), followed by two more

Everolimus eluting stents insertion in the proximal LCX.

After successful treatment with LCX artery, she com-

plained of chest discomfort. CAG and intravenous

ultrasonography (IVUS) revealed acute stent thrombosis

in the mid-portion of LAD artery (Fig. 4-C). Thrombus

aspiration and infusion of glycoprotein IIb/IIIa receptor

blocker were done, and post-treatment CAG showed

patent coronary flow (Fig. 4-D). After PCI, pulmonary

edema disappeared and she showed the improvement

of functional status. There were no predisposing factors

including abnormal findings of coagulation system such

as protein C or S, anti-phospholipid antibody and no

evidence of malignancy. She was discharged with triple

anti-platelet therapy using aspirin 100 mg, clopidogrel

75 mg, and cilostazol 200 mg daily. The patient was

followed up via outpatient clinic without symptoms,

repeat CAG after 9 months showed patent coronary flow.

DISCUSSION

Drug-eluting stents have reduced restenosis rates and

the necessity for target-vessel revascularization. However,

ST is still problematic. ST is a rare but catastrophic

complication which frequently leads to death or myo-

cardial infarction.

Recently, multiple risk factors associated with ST were

reported. Especially, patients with STEMI, multi-vessel

coronary artery disease, Killip class≥2 on admission, low

left ventricular ejection fraction (EF), small stent diameter,

long segmental stenosis and younger age are known to

increase the risk of early ST.1,6 These two cases were

examples of myocardial infarction with multi-vessel

disease which received PCI on multi-vessel stenosis with

poor Killip class.

For these cases, the physician should be alert to new

onset or aggravation of chest pain or sudden abnormal

findings of vital signs. Immediate reexamination of

coronary flow should be recommended even during or

immediate after previous coronary angiography and PCI

bearing in mind the possibility of acute stent thrombosis.

The most important thing for the diagnosis and treatment

is clinical suspicion of acute stent thrombosis, which can

be enough for the diagnosis and improve the prognosis

of those patients. And multi-vessel PCI should be avoided

if there was no derangement of symptom, sign of poor

left ventricular function or pulmonary edema or the

evidence of cardiogenic shock.

Currently the diagnostic and treatment strategies are

not well defined. Emergent repeat PCI (thrombus aspi-

ration, balloon dilatation) is commonly employed, and

glycoprotein IIb/IIIa inhibitor is also used as ‘rescue’ therapy.

Glycoprotein IIb/IIIa inhibitor inhibited platelet aggre-

gation and thrombus formation, and furthermore,

induced lysis of fresh thrombus. In addition, treatment

such as thrombus aspiration, intracoronary tirofiban

injection has shown a favorable effect. The observational

study conducted by Akhtar MM, et al showed that the

combined use of thrombectomy with glycoprotein IIb/IIIa

inhibitor improved outcome in patients with acute stent

thrombosis.9

CONCLUSION

Acute ST during PCI was associated with multi-vessel

disease, STEMI, and large thrombotic burden. Therefore,

acute stent thrombosis can be successfully treated with

thrombus aspiration, potent platelet aggregation inhibitor

and balloon angioplasty.

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