CASE REPORT
Nagoya J. Med. Sci. 85. 171–178, 2023
doi:10.18999/nagjms.85.1.171

A case of eosinophilic polyangiitis with granulomatosis thatevolved to cardiac arrest due to advanced
atrioventricular block
Yuichiro Sakurai1, Chiyako Oshikata1,2,3, Takaharu Katayama4,
Shunsuke Takagi4, Yasushi Kaneko5, Kikuo Yo5, Takeshi Kaneko2,
Hiroyuki Kubota6, Takashi Matsubara4 and Naomi Tsurikisawa1,2,3
1
Department of Allergy and Respirology, Hiratsuka City Hospital, Hiratsuka, Japan
Department of Pulmonology, Yokohama City University Graduate School of Medicine, Yokohama, Japan3
Department of Respirology, National Hospital Organization Yokohama Medical Center, Yokohama, Japan
4
Department of Cardiology, Hiratsuka City Hospital, Hiratsuka, Japan
5
Department of Emergency and Critical Care Medicine, Hiratsuka City Hospital, Hiratsuka, Japan
6
Department of Gastroenterology, Shizuoka City Shimizu Hospital, Shizuoka, Japan
2

ABSTRACT
Cardiac manifestations are the major cause of mortality in patients with eosinophilic granulomatosis withpolyangiitis (EGPA). Among these manifestations in EGPA patients, in the literature, there are fewer reports
describing bradycardia in EGPA patients than those describing tachycardia. A 50-year-old woman with ahistory of childhood-onset asthma. At age 28, she was diagnosed with eosinophilic gastroenteritis without
the diagnosis of EGPA and was started on a systemic steroid and had maintenance daily dose of 2.5 mg
after gradually tapered. She had experiencing dizziness and palpitations 2 weeks after discontinuation of
the steroid treatment. At emergency visit, electrocardiography revealed an advanced atrioventricular blockof 3:1 or less. Forty-eight minutes after the start of electrocardiography, only a P wave was observedand cardiac arrest occurred for 9 s and temporary emergency pacing was performed immediately. She wasdiagnosed as EGPA presenting leukocyte count, 16,500/µL, 42.8% of which were eosinophils and sinusitis
in computed-tomography. She could be survival by treatment of steroid, following the patient to withdraw
from an external pacemaker. She received prednisolone of 60 mg, intravenous cyclophosphamide andintravenous immunoglobulin. She had relapsed presenting peripheral eosinophilia, abdominal and numbness
in the toes of the left leg pain, but not arrythmia after tapered of prednisolone. Following additional steroid
pulse, she had an increase of prednisolone and continued by intravenous cyclophosphamide, intravenous
immunoglobulin and started mepolizumab. We presented a severe case of EGPA presenting an advanced
atrioventricular block into cardiac arrest.
Keywords: advanced atrioventricular block, eosinophilic granulomatosis with polyangiitis, eosinophilic
gastroenteritis, immunoglobulin, mepolizumab
Abbreviations:
EGPA: eosinophilic granulomatosis with polyangiitis
123
I-MIBG: iodine-123–labeled metaiodobenzylguanidine

Received: December 2, 2021; accepted: March 11, 2022
Corresponding Author: Naomi Tsurikisawa, MD
Department of Respirology, National Hospital Organization Yokohama Medical Center,
3-60-2 Harajuku, Totsuka-ku, Yokohama 245-8575, Japan
Tel: +81-45-851-2621, Fax: +81-45-851-3902, E-mail: tsurikisawa.naomi.fm@mail.hosp.go.jp
171

Yuichiro Sakurai et al

This is an Open Access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
License. To view the details of this license, please visit (http://creativecommons.org/licenses/by-nc-nd/4.0/).

INTRODUCTION
Eosinophilic granulomatosis with polyangiitis (EGPA; also known as Churg–Strauss syndrome)is a rare disease characterized by the presence of allergic granulomatosis and necrotizing vasculitis
with tissue and peripheral blood eosinophilia.1
In EGPA, mortality rate and prognosis are related to disease severity, which is assessed byusing a five-factor score (currently the 2009 Revised Five-Factor Score) where each of fivefactors (ie, age ≥ 65 years, severe cardiac involvement, severe gastrointestinal tract involvement,
renal insufficiency, and absence of sinusitis) are scored as 0 for absent or 1 for present.2 Amongthese five factors, severe cardiac involvement is the major cause of mortality in EGPA patients.
For example, survival rate at 6 years after diagnosis of myocardial involvement is reported to be
only one-third that in the absence of myocardial involvement.3 Also, EGPA patients with cardiac
involvement have a lower 5-year survival rate4 and poorer long-term prognosis than patients
without cardiac involvement.5
The most commonly reported the percentage of patients showing each cardiac involvement
among patients with EGPA are myocarditis (37.1%–89.5%), pericarditis (9.4%–50.4%), heart
failure (36.8%–51.6%), and arrhythmia (12.5%–27.4%).6-10 With respect to arrhythmia, there
are fewer reports in the literature describing bradycardia in EGPA patients—for example as aresult of bundle branch block,8 advanced atrioventricular block,9 or first-degree atrioventricular
block11—than those describing tachycardia.7-10,12-15
Here, we report a rare case of EGPA in which the patient presented with bradycardia due
to atrioventricular block that evolved into cardiac arrest; treatment by steroid pulse could be
survival, following the patient to withdraw from an external pacemaker.

CASE PRESENTATION
A 50-year-old woman with a history of childhood-onset asthma. At the age of 8, she enteredasthma remission, but at age 19 the asthma relapsed. Since age 30, she had used fluticasone plus
salmeterol (250 + 50 mg; twice daily) or fluticasone propionate (200 mg; twice daily) when she
had asthma symptoms. At age 28, she was diagnosed with eosinophilic gastroenteritis without thediagnosis of EGPA and was started on a systemic steroid (prednisolone, 30 mg per day). Overtime, the prednisolone was gradually tapered to a maintenance daily dose of 2.5 mg; however,occasional self-interruption of the steroid treatment resulted in the gastroenteritis returning. At
the time of presentation at our emergency visit, she had discontinued the steroid treatment 3
weeks previous and had experiencing dizziness and palpitations 2 weeks after discontinuation.
At presentation, her blood pressure was 136/82 mmHg and heart rate was 61 beats per min.
Electrocardiography revealed an advanced atrioventricular block of 3:1 or less (Figure 1A). Chest
X-ray revealed mild cardiac enlargement and pulmonary congestion (Figure 2). Echocardiography
revealed an ejection fraction of 52%, mild mitral regurgitation, mild tricuspid regurgitation,and inferior vena cava enlargement; a small amount of pericardial fluid was observed, but left
ventricular contractile function was good. Forty-eight minutes after the start of electrocardiography, only a P wave was observed and cardiac arrest occurred for 9 s (Figure 1B). Temporary
emergency pacing was performed immediately.

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EGPA with advanced AVB

Fig. 1 (A)Fig. 1 (B)Fig. 1 Electrocardiography at presentation at our emergency outpatient clinic
Fig. 1A: Electrocardiogram showing advanced atrioventricular block of 3: 1 or less.
Fig. 1B: At 48 min after the start of electrocardiography, a P wave only was observed and cardiac arrest occurred
for 9 s.

Fig. 2 Chest X-ray at presentation at our emergency outpatient clinic
Chest X-ray revealed mild cardiac enlargement and pulmonary congestion.
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Yuichiro Sakurai et al

At the diagnosis of EGPA, laboratory tests revealed leukocytosis (leukocyte count, 16,500/µL, 42.8% of which were eosinophils); serum total IgE, 280 IU/mL; elevated brain natriuretic
peptide, 123.8 pg/mL; elevated C-reactive protein, 0.44 mg/mL; and a negative myeloperoxidaseantineutrophil cytoplasmic antibodies. Antigen-specific serum IgE was positive at class 4 forhouse dust-mite, class 3 for cedar pollen, and class 2 for cat.
At diagnosis, enhanced computer tomography did not show cervical artery stenosis, aneurysms
or thrombosis in artery. We performed cardiac scintigraphy with iodine-123–labeled metaiodo-

Fig. 3 Cardiac scintigraphy at diagnosis
Iodine-123–labeled metaiodobenzylguanidine scintigraphy did not show decreased myocardial uptake.

Fig. 4 Abdominal contrast-enhanced computed tomography at diagnosis
Arrow indicates the location of intestinal edema.
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EGPA with advanced AVB

benzylguanidine (123I-MIBG) and the heart-to-mediastinum (H/M) ratio was determined from theimages. Also, the washout rate of MIBG within the myocardium was measured as the percent
change in left ventricular activity from the early to the delayed images. Cardiac scintigraphy
did not show any decreased uptake of 123I-MIBG in the myocardium. H/M ratio was within thenormal range at 2.27 in the early phase and 2.84 in the delayed phase, but the washout rate washigh at 27.5% (Figure 3). Abdominal contrast-enhanced computed tomography (Figure 4) reveled
intestinal edema and nasal polyps in the upper-right maxillary sinus in computed-tomography.
In line with the diagnostic criteria of Ministry of Health, Labour and Welfare for EGPA, thepatient was diagnosed with EGPA on the basis of the presence of vasculitis with asthma andelevated levels of peripheral blood eosinophils.16 Sinus rhythm returned 20 hours and 2 minutes
after cardiac arrest on the next day of starting methylprednisolone pulse therapy (1000 mg
intravenously daily for 3 consecutive days) from next day after emergency pacing.
At the end of methylprednisolone therapy, the patient was started on oral prednisolone (60mg/day); the external pacemaker was removed 6 days later. She was treated with intravenous
cyclophosphamide (600 mg/m2) every 3–4 weeks and at 2 months after the start of steroid pulse
treatment she also received intravenous immunoglobulin (400 mg/kg for 5 consecutive days).
After that, the dose of prednisolone was gradually tapered because sinus rhythm was maintained
at a mean heart rate of 70–80 beats per min. The patient reported intermittent numbness in thesole of the right foot, and one month after reduction of the dose of prednisolone to 12.5 mg,
numbness appeared in the toes of the left leg but muscle weakness did not occur. After the
prednisolone was tapered to 7.5 mg, her systolic blood pressure rose above 160 mmHg, so she
was started on 20 mg of telmisartan. She also reported gastrointestinal symptoms (diarrhea andabdominal pain) and an increased heart rate (95 beats per min) and increased leukocyte count(14,400/µL; 29.0% of which were eosinophils); in response, the prednisolone dose was increased
to 15 mg once daily, but her peripheral blood eosinophil count remained increased (leukocyte
count, 16,100/µL; 29.0% of which were eosinophils) and she had abdominal pain and diarrhea
although she did not have arrythmia. Following additional two courses of methylprednisolone
pulse therapy, the dose of prednisolone was increased to 30 mg once daily. The intravenous
cyclophosphamide was continued every 3–4 weeks, intravenous immunoglobulin was added three
weeks after another two courses of steroid pulse therapy, and the patient received mepolizumab
300 mg monthly. The vasculitis symptoms gradually improved and the prednisolone was eventually tapered to 10 mg once daily.

DISCUSSION
Increased adoption of the American College of Rheumatology criteria for the classification of
EGPA has reduced the mortality rate of patients with EGPA diagnosed after 1996 is lower thanthat of those diagnosed before 1996.4,17 More recently, the 5-, 10-, and 20-year survival rates
reported in 2011 by Guillevin et al were about 90%, 75%, and 45%, respectively,3 whereas thosereported in 2013 by Moosig et al were 97%, 89%, and 72%, respectively.5 Our group reported
in 2017 survival rates of 91.1%, 83.7%, and 68.6%, respectively.18 However, the 30-year survival
rate is reported to still be only about 55%,19 which suggests that although the 5-year survival rate
for patients with EGPA has improved, the 20- and 30-year survival rates remain poor. Patientswith EGPA with cardiac involvement show a particularly poor prognosis.3,5
FDG-PET has reportedly detected active myocardial inflammation in patients with EGPA
both before treatment and after remission.20,21 Cardiac sympathetic nerve function was damaged
in EGPA patients with cardiac involvement. We showed 123I-MIBG scintigraphy was useful in
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detecting cardiac involvement and in predicting cardiac events.22 123I-MIBG scintigraphy can evaluate the viability of the myocardium by the value of H/M and the function of the myocardiumby the value of WR. In one case we reported, 123I-MIBG scintigraphy showed a mild decreasein accumulation and FDG-PET of EGPA with a mild increase in WR of 22.14% did not show
significant accumulation in the heart.23 We considered that EGPA has less accumulation of FDPPET in the heart as reported in cardiac sarcoidosis.24 Therefore, in EGPA, 123I-MIBG scintigraphy
is considered to be more suitable for screening including mild cardiac involvement.
Compared to EGPA with cardiac involvement, AVB is more frequent in cardiac sarcoidosis, andthere are cases of permanent pacemaker insertion and heart transplantation even after treatment
with steroids and immunosuppressants, and there are many reports of sudden death25 or fibrosis
to the myocardium.26 There are few reports of EGPA presenting with arrhythmia, and among
them, there are even fewer reports of bradyarrhythmia or AVB, but there are reports that steroids
and immunosuppressive agents have been successful.13,15
The conventional treatment for EGPA is combined corticosteroid–cyclophosphamide therapy;
however, this approach sometimes has little effect in EGPA patients with mononeuritis multiplex
or heart failure.27 Previously, we reported that intravenous immunoglobulin therapy was effective
for the treatment of EGPA in patients with severe mononeuritis multiplex or heart failure who
did not respond to combined corticosteroid–cyclophosphamide treatment.28 In addition, we havereported that the long-term efficacy of intravenous immunoglobulin in EGPA patients with severemononeuritis multiplex or heart failure is a result of an increased regulatory T-cell population(as FOXP3+CD4+ T cells) in the peripheral blood,29 suggesting that intravenous immunoglobulin
may improve prognosis in these patients.18 Patients with EGPA in remission often relapse whenprednisolone is tapered to below 10 mg.30 Our group has also reported that EGPA patients withmyocardial or gastrointestinal tract involvement show frequent relapses.18
In addition to conventional combined corticosteroid (prednisolone)–cyclophosphamide therapy,
our patient received intravenous immunoglobulin but still showed relapse of vasculitis symptoms
and an increased peripheral eosinophil count after reduction of the prednisolone dose. However,after the addition of mepolizumab her peripheral eosinophil count did not increase, suggestingthat she might have entered remission. In EGPA patients, there are reports of sudden death due
to coronary artery dissection,31 coronary artery stenosis,32 or arrhythmia.33
We presented a survival case of EGPA presenting an advanced atrioventricular block into
cardiac arrest. A case with severe cardiac involvement may be need treatment not only corticosteroids, intravenous cyclophosphamide, intravenous immunoglobulin, but mepolizumab.
We obtained the patient’s written informed consent to publish details of her case.

CONFLICTS OF INTEREST
No author has any conflict of interest to disclose.

REFERENCES
1
2

Churg J, Strauss L. Allergic granulomatosis, allergic angiitis, and periarteritis nodosa. Am J Pathol.
1951;27(2):277–301.
Guillevin L, Pagnoux C, Seror R, et al. The five-factor score revisited: assessment of prognosis of systemic
necrotizing vasculitides based on the French Vasculitis Study Group (FVSG) Cohort. Medicine (Baltimore).
2011;90(1):19–27. doi:10.1097/MD.0b013e318205a4c6.

Nagoya J. Med. Sci. 85. 171–178, 2023

176

doi:10.18999/nagjms.85.1.171

EGPA with advanced AVB

3

4

5

6
7

8
9

10
11

12

13
14

15

16
17

18

19

20

21

22

23

Guillevin L, Cohen P, Gayraud M, Lhote F, Jarrousse B, Casassus P. Churg-Strauss syndrome. Clinical study
and long-term follow-up of 96 patients. Medicine (Baltimore). 1999;78(1):26–37. doi:10.1097/00005792199901000-00003.
Comarmond C, Pagnoux C, Khellaf M, et al. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss):
clinical characteristics and long-term followup of the 383 patients enrolled in the French Vasculitis Study
Group cohort. Arthritis Rheum. 2013;65(1):270–281. doi:10.1002/art.37721.
Moosig F, Bremer JP, Hellmich B, et al. A vasculitis centre based management strategy leads to improved
outcome in eosinophilic granulomatosis and polyangiitis (Churg-Strauss, EGPA): monocentric experiencesin 150 patients. Ann. Rheum. Dis. 2013;72(6):1011–1017. doi:10.1136/annrheumdis-2012-201531.
Pakbaz M, Pakbaz M. Cardiac involvement in eosinophilic granulomatosis with polyangiitis: a meta-analysisof 62 case reports. J Tehran Heart Cent. 2020;15(1):18–26.
Szczeklik W, Miszalski-Jamka T, Mastalerz L, et al. Multimodality assessment of cardiac involvementin Churg-Strauss syndrome patients in clinical remission. Circ J. 2011;75(3):649–655. doi:10.1253/circj.
cj-10-0772.
Dennert RM, van Paassen P, Schalla S, et al. Cardiac involvement in Churg-Strauss syndrome. Arthritis
Rheum. 2010;62(2):627–634. doi:10.1002/art.27263.
Vinit J, Bielefeld P, Muller G, et al. Heart involvement in Churg-Strauss syndrome: retrospective study
in French Burgundy population in past 10 years. Eur J Intern Med. 2010;21(4):341–346. doi:10.1016/j.
ejim.2010.05.004.
Neumann T, Manger B, Schmid M, et al. Cardiac involvement in Churg-Strauss syndrome: impact ofendomyocarditis. Medicine (Baltimore). 2009;88(4):236–243. doi:10.1097/MD.0b013e3181af35a5.
Zampieri M, Emmi G, Beltrami M, et al. Cardiac involvement in eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome): prospective evaluation at a tertiary referral centre. Eur J Intern
Med. 2021;85:68–79. doi:10.1016/j.ejim.2020.12.008.
Ikeda S, Usami K, Tomita M, et al. An autopsy case of eosinophilic granulomatosis with polyangiitis
with sudden cardiac death presenting cardiomyopathy and neuropathy [in Japanese]. Peripher Nerve
2014;25(1):115–120.
Sharpley FA. Missing the beat: arrhythmia as a presenting feature of eosinophilic granulomatosis withpolyangiitis. BMJ Case Rep. 2014;2014:bcr2013203413. doi:10.1136/bcr-2013-203413
Chin JY, Yi JE, Youn H. Churg-Strauss syndrome associated with rapid deterioration of left ventricular
diastolic dysfunction and conduction disturbance. J. Echocardiography. 2013;30(9):E269-E273 doi:10.1111/
echo.12314.
Budanova M, Mitrofanova L, Kozlenok A, Ryzhkova D, Maslyanskiy A, Moiseeva O. Ventricular tachycardia
as the first manifestation of Churg-Strauss syndrome. J Cardiol Cases. 2016;15(2):61–64. doi:10.1016/j.
jccase.2016.10.011.
Ozaki S. ANCA-associated vasculitis: diagnostic and therapeutic strategy. Allergol Int. 2007;56(2):87–96.
doi:10.2332/allergolint.R-07-141.
Masi AT, Hunder GG, Lie JT, et al. The American College of Rheumatology 1990 criteria for the classification of Churg-Strauss syndrome (allergic granulomatosis and angitis). Arthritis Rheum. 1990;33(8):1094–1100.
doi:10.1002/art.1780330806.
Tsurikisawa N, Oshikata C, Kinoshita A, Tsuburai T, Saito H. Longterm prognosis of 121 patients witheosinophilic granulomatosis with polyangiitis in Japan. J Rheumatol. 2017;44(8):1206–1215. doi:10.3899/
jrheum.161436.
Jardel S, Puéchal X, Quellec AL, et al. Mortality in systemic necrotizing vasculitides: A retrospective
analysis of the French Vasculitis Study Group registry. Autoimmun Rev. 2018;17(7):653–659. doi:10.1016/j.
autrev.2018.01.022.
Morita H, Yokoyama I, Yamada N, Uno K, Nagai R. Usefulness of 18FDG13N-ammonia PET imaging for evaluation of the cardiac damage in Churg-Strauss syndrome. Eur J Nucl Med Mol Imaging.
2004;31(8):1218. doi:10.1007/s00259-004-1550-9.
Marmursztejn J, Guillevin L, Trebossen R, et al. Churg-Strauss syndrome cardiac involvement evaluated bycardiac magnetic resonance imaging and positron-emission tomography: a prospective study on 20 patients.
Rheumatology (Oxford). 2013;52(4):642–650. doi:10.1093/rheumatology/kes155.
Horiguchi Y, Morita Y, Tsurikisawa N, Akiyama K. 123I-MIBG imaging detects cardiac involvement andpredicts cardiac events in Churg-Strauss syndrome. Eur J Nucl Med Mol Imaging. 2011;38(2):221–229.
doi:10.1007/s00259-010-1617-8.
Horiguchi Y, Tsurikisawa N, Harasawa A, et al. Detection of pulmonary involvement in eosinophilic
granulomatosis with polyangiitis (Churg-Strauss, EGPA) with 18F-fluorodeoxyglucose positron emission

Nagoya J. Med. Sci. 85. 171–178, 2023

177

doi:10.18999/nagjms.85.1.171

Yuichiro Sakurai et al

24

25
26

27
28
29

30

31

32
33

tomography. Allergol Int. 2014;63(1):121–123. doi:10.2332/allergolint.13-LE-0550.
Ohira H, Birnie DH, Pena E, et al. Comparison of 18F-fluorodeoxyglucose positron emission tomography(FDG PET) and cardiac magnetic resonance (CMR) in corticosteroid-naive patients with conduction systemdisease due to cardiac sarcoidosis. Eur J Nucl Med Mol Imaging. 2016;43(2):259–269. doi:10.1007/s00259015-3181-8.
Nordenswan HK, Lehtonen J, Ekström K, et al. Outcome of Cardiac sarcoidosis presenting with high-grade
atrioventricular block. Circ Arrhythm Electrophysiol. 2018;11(8):e006145. doi:10.1161/CIRCEP.117.006145.
Okada DR, Xie E, Assis F, et al. Regional abnormalities on cardiac magnetic resonance imaging andarrhythmic events in patients with cardiac sarcoidosis. J Cardiovasc Electrophysiol. 2019;30(10):1967–1976.
doi:10.1111/jce.14082.
Renaldini E, Spandrio S, Cerudelli B, Affatato A, Balestrieri GP. Cardiac involvement in Churg–Strauss
syndrome: a follow-up of three cases. Eur Heart J. 1993;14(12):1712–1716. doi:10.1093/eurheartj/14.12.1712.
Tsurikisawa N, Taniguchi M, Saito H, et al. Treatment of Churg-Strauss syndrome with high-dose intravenous
immunoglobulin. Ann Allergy Asthma Immunol. 2004;92(1):80–87. doi:10.1016/S1081-1206(10)61714-0.
Tsurikisawa N, Saito H, Oshikata C, Tsuburai T, Akiyama K. High-dose intravenous immunoglobulin
treatment increases regulatory T cells in patients with eosinophilic granulomatosis with polyangiitis. J
Rheumatol. 2012;39(5):1019–1025. doi:10.3899/jrheum.110981.
Samson M, Puéchal X, Devilliers H, et al. Long-term outcomes 118 patients with eosinophilic granulomatosis
with polyangiitis (Churg–Strauss syndrome) enrolled in two prospective trials. J Autoimmun. 2013;43:60–69.
doi:10.1016/j.jaut.2013.03.003.
Hunsaker JC 3rd, O’Connor WN, Lie JT. Spontaneous coronary arterial dissection and isolated eosinophiliccoronary arteritis: sudden cardiac death in a patient with a limited variant of Churg-Strauss syndrome. Mayo
Clin Proc. 1992;67(8):761–766. doi:10.1016/s0025-6196(12)60801-5.
Setoguchi M, Okishige K, Sugiyama K, et al. Sudden cardiac death associated with Churg-Strauss syndrome.
Circ J. 2009;73(12):2355–2359. doi:10.1253/circj.cj-08-0926.
Groh M, Masciocco G, Kirchner E, et al. Heart transplantation in patients with eosinophilic granulomatosis
with polyangiitis (Churg-Strauss syndrome). J Heart Lung Transplant. 2014;33(8):842–850 doi:10.1016/j.
healun.2014.02.023.

References End

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