Aspirin Dose and Prevention

of Coronary Abnormalities
in Kawasaki Disease
Frederic Dallaire, MD, PhD,a Zoe Fortier-Morissette, MD,a Samuel Blais, BSc,a Anita Dhanrajani, DNB,b
Dania Basodan, MBBS,c Claudia Renaud, MD,c Mathew Mathew, BSc,d Astrid M. De Souza, MSc,e Audrey Dionne,
MD,f Joel Blanchard, BSc,a Harrison Saulnier, BSc,c Kimberley Kaspy, MDCM,c Soha Rached-dAstous, MD,f
Nagib Dahdah, MD,f Brian W. McCrindle, MD, MPH,d Derek G. Human, BM,e Rosie Scuccimarri, MDc

BACKGROUND: Acetylsalicylic acid (ASA) is part of the recommended treatment of Kawasaki abstract
disease (KD). Controversies remain regarding the optimal dose of ASA to be used. We aimed
to evaluate the noninferiority of ASA at an antiplatelet dose in acute KD in preventing
coronary artery (CA) abnormalities.
METHODS: This is a multicenter, retrospective, nonrandomized cohort study including
children 0 to 10 years of age with acute KD between 2004 and 2015 from 5 institutions, of
which 2 routinely use low-dose ASA (35 mg/kg per day) and 3 use high-dose ASA (80 mg/
kg per day). Outcomes were CA abnormalities defined as a CA diameter with a z score 2.5.
We assessed the risk difference of CA abnormalities according to ASA dose. All subjects
received ASA and intravenous immunoglobulin within 10 days of fever onset.
RESULTS: There were 1213 subjects included, 848 in the high-dose and 365 in the low-
dose ASA group. There was no difference in the risk of CA abnormalities in the low-dose
compared with the high-dose ASA group (22.2% vs 20.5%). The risk difference adjusted
for potential confounders was 0.3% (95% confidence interval [CI]: 4.5% to 5.0%). The
adjusted risk difference for CA abnormalities persisting at the 6-week follow-up was 1.9%
(95% CI: 5.3% to 1.5%). The 95% CI of the risk difference of CA abnormalities adjusted for
confounders was within the prespecified 5% margin considered to be noninferior.
CONCLUSIONS: In conjunction with intravenous immunoglobulin, low-dose ASA in acute KD is
not inferior to high-dose ASA for reducing the risk of CA abnormalities.

aDepartment of Pediatrics, Faculty of Medicine and Health Sciences, Centre de recherche du centre Whats Known on This Subject: Controversies
hospitalier universitaire de Sherbrooke, University of Sherbrooke, Sherbrooke, Canada; Divisions of bPediatric
remain regarding the appropriate acetylsalicylic
Rheumatology and eCardiology, Department of Pediatrics, University of British Columbia, British Columbia
Childrens Hospital, Vancouver, Canada; cDepartment of Pediatrics, Montreal Childrens Hospital, McGill acid (ASA) dose to be used during treatment of
University Health Centre, Montreal, Canada; dLabatt Family Heart Center, The Hospital for Sick Children and Kawasaki disease (KD). The anti-inflammatory dose
Department of Pediatrics, University of Toronto, Toronto, Canada; and fDivision of Pediatric Cardiology, Centre of ASA is recommended in acute KD, but it has never
Hospitalier Universitaire Sainte-Justine, Montreal, Canada been proven to reduce the incidence of coronary
Dr Dallaire conceptualized and designed the study, conducted analyses, designed the data artery abnormalities.
collection instruments, drafted the initial manuscript, and supervised manuscript revision; Dr What This Study Adds: This multicenter study
Fortier-Morissette contributed to the study design, helped design the data collection instruments, suggests that an antiplatelet dose of ASA is not
coordinated and supervised data collection at 1 of the 4 sites, and critically reviewed the
inferior to higher doses in reducing the risk of
manuscript; Mr Blais helped design the data collection instruments, coordinated and supervised
data collection at 1 of the 4 sites, contributed to the data management and cleaning, contributed
coronary artery abnormalities when administered
to data analysis, and critically reviewed the manuscript; Mr Mathew, Ms De Souza, Dr Dhanrajani, concomitantly with intravenous immunoglobulin in
Dr Basodan, and Dr Renaud supervised data collection and participated in database cleanup acute KD.
at 1 of the 4 sites and critically reviewed the manuscript; Dr Dionne, Mr Blanchard, Dr Kaspy,
Mr Saulnier, and Dr Rached-dAstous contributed to data collection and data abstraction and
To cite: Dallaire F, Fortier-Morissette Z, Blais S, et al.
critically reviewed the manuscript; Drs Dahdah and McCrindle and Human contributed to the
Aspirin Dose and Prevention of Coronary Abnormalities in
Kawasaki Disease. Pediatrics. 2017;139(6):e20170098

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PEDIATRICS Volume 139, number 6, June 2017:e20170098 Article
Kawasaki disease (KD), an acute,
self-limited vasculitis of unknown
origin, is the most common
cause of acquired heart disease in
children in developed countries.1,2
Coronary artery (CA) dilatation
and aneurysms may develop in
15% to 25% of untreated children,
putting them at risk for future CA
complications such as thrombosis
and myocardial infarction.1,2 Prompt
diagnosis and early treatment with
intravenous immunoglobulin (IVIg)
significantly reduce the risk of CA
involvement. Studies in the 1980s
demonstrated that IVIg combined
with acetylsalicylic acid (ASA) had
a significant impact on morbidity,
mortality, and CA aneurysm risk.3 5
ASA was used before the IVIg era
for both its anti-inflammatory and
antithrombotic effects.4 Studies to
date have failed to demonstrate any
benefit of the anti-inflammatory
dose of ASA in preventing CA
abnormalities.69
Two separate
meta-analyses showed that CA
abnormalities were dependent on the
total IVIg dose but were independent
of the ASA dose.10,11
A Cochrane
review boldly stated that there was
insufficient evidence to indicate
whether children with KD should
continue to receive ASA as part of
their treatment regimen.12 Despite
all this, controversies remain on the
appropriate dose of ASA to be used
in the treatment of acute KD.13,14
Avoiding an anti-inflammatory dose
of ASA has the theoretical advantage
of preventing serious side effects
from high-dose ASA therapy, such as
Reye syndrome, raised liver enzymes,
gastrointestinal bleeding, and
sensorineural hearing loss.14 On the
other hand, the anti-inflammatory
effect of high-dose ASA could reduce
the duration of fever, which has been
shown by some authors,7,15
but not
all.6,8,9
In Canada, ASA dose varies from
institution to institution. At least
2 Canadian pediatric tertiary
care institutions routinely and
2 Dallaire et al
systematically use ASA at an anti-
platelet dose during treatment
of acute KD, whereas most other
medical centers use an anti-
inflammatory dose. We therefore
included these institutions in a
multicenter retrospective cohort
study and sought to evaluate if
the routine use of low-dose ASA
during treatment of acute KD was
noninferior to high-dose ASA in
reducing the risk of CA abnormalities.
Methods
Study Design and Patient Population
This was a multicenter,
nonrandomized, retrospective,
noninferiority cohort study. The
target population comprised all
children between 0 and 10 years
of age diagnosed with complete or
incomplete acute KD between 2004
and 2015 in 1 of the 5 Canadian
participating institutions. Two
of these institutions have been
routinely prescribing low-dose ASA
(35 mg/kg per day) in acute KD. The
3 remaining institutions have been
routinely prescribing high-dose ASA
(80 mg/kg per day). There was no
change in the routine dose of ASA
prescribed during treatment of acute
KD throughout the study period in
any of the participating institutions.
All KD cases were identified through
local clinical databases and medical
archives and then screened for
eligibility. Eligible subjects were
children with a first episode of KD
diagnosed and treated with IVIg and
ASA within 10 days of fever onset.
Given that the diagnosis of KD cannot
be confirmed, subjects were eligible if
the clinical suspicion of KD was such
that treatment with IVIg was deemed
clinically indicated by the treating
physician. Subjects were followed
from diagnosis until 12 months
postdiagnosis.
Exclusion criteria were as follows:
subjects whose final diagnosis of KD
was clearly rejected by the treating
physician; subjects with structural
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cardiac disease at baseline other
than cardiac disease secondary to
KD; subjects with recurrence of KD
(second episode not included); and
subjects with follow-up <6 weeks or
with incomplete echocardiographic
studies during follow-up.
Research ethics board approval
was granted at each participating
institution. Only anonymous
retrospective data were gathered for
this study, and the requirement for
patient consent was waived by the
research ethics boards.
ASA Treatment Definition
To test our main hypothesis, we
used an approach analogous to an
intent-to-treat analysis in which the
treatment group was based on the
dose of ASA routinely used by the
institution where the subject was
admitted.16 In this analysis, subjects
admitted in 1 of the 2 institutions
routinely prescribing low-dose
ASA (35 mg/kg per day) during
treatment of acute KD were assigned
to the low-dose group, irrespective
of the actual dose received. Patients
admitted to 1 of the 3 institutions
routinely prescribing high-dose ASA
(80 mg/kg per day) during treatment
of acute KD were assigned to the
high-dose group.
Additionally, we compared the
risk of CA abnormalities according
to the dose of ASA that was
actually prescribed, irrespective
of the institution where they were
admitted. In this analysis, low-dose
ASA was defined as a prescribed dose
<10 mg/kg per day during the acute
febrile phase. Prescribed ASA doses
10 mg/kg per day were defined
as high dose. There were <1% of
subjects who received a moderate
ASA dose (1079 mg/kg per day) and
these were included in the high ASA
dose category.
Primary and Secondary Outcomes
The primary outcome was the risk
of any CA abnormalities, defined
as any main CA segment with an
internal diameter z score 2.5 at
any time during follow-up (thus
including small, medium, and giant
CA aneurysms). CA z scores were
calculated as previously described.17
Our secondary outcomes were as
follows: any CA abnormalities except
mild dilatation of the left main CA
(isolated left main CA z scores <5
were not considered abnormal);
persistent CA abnormalities (any
CA segment z score 2.5 present
at the 6-week follow-up or later);
medium or larger CA aneurysms (any
CA segment z score 5.0); giant CA
aneurysms (z score 10.0 or absolute
diameter >8 mm); resistance
to treatment (defined as the
requirement for further treatment
after the first dose of IVIg); and fever
duration.
Data Collection
The following data were collected
from the medical charts:
demographic information (sex, age
at diagnosis), clinical information
at diagnosis (KD symptoms, date of
fever onset, duration of fever, routine
laboratory results), initial treatment
(IVIg doses and treatment course,
IVIg brand, initial ASA dose, any
other rescue treatment), follow-up
treatment, and echocardiography
data from diagnosis until follow-up
at 12 months (weight and height at
echocardiography, and all coronary
internal diameter measurements).
Information on side effects of ASA
was not specifically collected. Data
collected were entered by using the
web-based data capture tool REDCap
(Vanderbilt University, Nashville,
TN).18
Statistical Analysis
We used a noninferiority design to
assess whether the risk difference
of CA abnormalities between
treatment groups would stay within
the 95% confidence interval (CI) of
a predefined clinically acceptable
margin.19 Low-dose ASA was
considered noninferior to high-dose
PEDIATRICS Volume 139, number 6, June 2017
ASA if the 95% CI of the risk
difference for CA abnormalities was
5.0%.
Adjusted risk differences between
treatments were computed by using
binomial regression risk analysis.20
Only confounding variables that
influenced the final adjusted risk
difference by >5% were kept in the
final model. Potential confounding
variables considered for inclusion in
the models were as follows: type of
KD (complete versus incomplete),
sex, need for retreatment (any rescue
treatment after the first IVIg), young
age (<12 months of age at diagnosis),
and IVIg brand. All were kept in the
final model, except IVIg brand, which
had no influence on the adjusted risk
difference. Differences in patients
characteristics between treatment
groups were assessed by using
Students t test or an 2 test, where
appropriate. We used SAS (version
9.4, Cary, NC) for all analyses.
P values <.05 were considered
statistically significant.
Results
A total of 1483 subjects were
identified and screened for eligibility.
Of them, 270 were excluded for
the following reasons: 33 did
not receive IVIg or ASA, 20 had
missing information on initial ASA
treatment, 152 received IVIg after
10 days of fever, 42 had missing
echocardiography results, 19 had
structural heart defects, and 4
already had KD in the past. The 1213
remaining subjects were included in
the final analysis. Among them, 848
were admitted in institutions where
high-dose ASA is routinely prescribed
in acute KD. The remaining
365 subjects were admitted in
institutions where low-dose ASA is
routinely prescribed in acute KD.
able 1 presents the characteristics
T able 2 presents the proportion
of the study population. In the
high-dose ASA group, 794 subjects
(93.6%) received an ASA dose 10
mg/kg per day. Of them, all but 2
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patients received an ASA dose 70
mg/kg per day. In the low-dose ASA
group, 341 subjects (93.4%) received
an ASA dose <10 mg/kg per day. In
the low-dose ASA group, there were
4 subjects (1.1%) who received an
ASA dose between 11 and 70 mg/
kg per day and 20 subjects (5.5%)
who received an ASA dose 70 mg/
kg per day. Treatment groups were
similar for age, sex, and number of
days of fever before first dose of
IVIg. There were more patients with
complete Kawasaki (4 criteria) in
the low-dose ASA group (76.2% vs
69.0%). Subjects in the low-dose ASA
group were slightly more likely to
require a second IVIg course (27.4%
vs 24.4%), less likely to receive oral
steroid treatment (2.5% vs 4.0%),
and more likely to receive infliximab
(0.8% vs 0.2%), but these differences
did not reach statistical significance.
IVIg brand varied considerably
between institutions (see details in
Table 1). We observed a higher mean
C-reactive protein concentration in
the low-dose ASA group. Significant
P values for differences between
groups were also observed for
hemoglobin, white cell count, and
albumin, although the differences
were small.
Our primary outcome, any CA
abnormalities, was observed in
255 subjects (21.0%). Of these,
there were 98 subjects (8.1%)
with transient small CA dilatations
(z score 2.5 but <5) at diagnosis
that did not persist at the 6-week
follow-up: 62 subjects (7.3%) in the
high-dose ASA group and 36 subjects
(9.9%) in the low-dose ASA group.
Excluding these transient dilatations,
we found 157 subjects (12.9%) with
persistent CA abnormalities. Of these,
there were 5.5% with medium or
large CA aneurysms and 2.3% with
giant CA aneurysm.
T
of subjects with CA abnormalities
according to treatment groups as
well as the unadjusted and adjusted
risk differences. The risk of any CA
3
TABLE 1 Population Characteristics (95% CI: 5.3% to 1.5%). Accordingly,
Characteristic Mean SD, or Percentage our hypothesis of a noninferior effect
All Subjects, High-dose ASA Group, Low-dose ASA Group, of low ASA dose was confirmed
N = 1213 N = 848 (69.9%) N = 365 (30.1%) for the primary outcome (any CA
Age, y 3.4 2.3 3.4 2.4 3.2 2.2
abnormalities) and for persistent
Aged <1y at diagnosis 14.4 13.8 15.9 CA abnormalities. Given that a z
Male sex 59.2 59.4 58.4 score >2.5 that is only observed for
Complete Kawasaki (4 71.2 69.0 76.2* the left main CA can be considered
criteria) a normal anatomic variation, we
Subjects receiving ASA dose 32.6 6.4 93.4
<10 mg/kg per d
also analyzed CA dilatations without
No. days of fever at first IVIg 6.2 1.7 6.2 1.7 6.2 1.8 isolated mild dilatation of the left
treatment main CA with a z score >2.5 but <5.
Fever duration, d 7.8 3.5 7.8 3.8 7.9 2.6 Excluding these, we found that 19.5%
IVIg brand
and 18.9% of subjects had abnormal
Iveegam 18.2 26.1 0a
Gammagard 13.4 16.0 7.4 CA in the high- and low-dose ASA
Gamunex 28.7 18.0 53.4 groups, respectively. The unadjusted
Privigen 10.6 9.2 14.0 risk difference was 0.5% (95% CI:
Other/unknown 29.0 30.7 25.2 5.4% to 4.3%) and the adjusted risk
Other treatments
difference was 2.0% (95% CI: 6.4%
2 doses of IVIg 25.3 24.4 27.4
3 doses of IVIg 1.8 2.5 0.3 to 2.4%).
Steroids 9.9 9.7 10.7
Steroids (parenteral) 6.4 5.7 8.2 For medium or larger CA aneurysms
Steroids (enteral) 3.5 4.0 2.5 (CA z score 5.0), the adjusted
Infliximab 0.4 0.2 0.8
risk difference was statistically
Cyclosporine 0 0 0
Hemoglobin, g/L 112.0 13.1 113.8 11.6 109.4 14.6* significant, favoring the low-dose
White cell count, 109 L1 14.0 6.6 13.6 6.0 14.7 7.6* ASA group: 4.0% (95% CI: 7.4%
Platelet counts, 109 L1 369.8 158.3 370.3 161.7 368.9 149.5 to 0.5%), P value = .024. There was
Erythrocyte sedimentation 59.7 28.4 60.8 30.8 57.8 24.0 no significant risk difference between
rate, mm/h
groups for giant CA aneurysm
C-reactive protein, mg/L 86.4 75.3 78.6 75.0 100.6 73.8*
Albumin, g/L 35.3 7.3 36.4 6.1 33.3 8.7* (adjusted risk difference: 1.9%
All laboratory values are at baseline, before IVIg treatment.
[95% CI: 4.4% to 0.5%]).
a Overall table probability P < .05 for IVIg brand. Individual IVIg brands were not tested.
* P value <.05 (high- versus low-dose group).
Some subjects treated in an
institution routinely prescribing
abnormalities was similar in the high-dose ASA group was close to low-dose ASA actually received
high-dose and low-dose ASA groups zero: adjusted risk difference of 0.3% high-dose ASA (24 subjects or 6.6%
(unadjusted risk difference of 1.7% (95% CI: 4.5% to 5.0%). When of the low-dose ASA group). Also,
[95% CI: 3.4% to 6.7%]). After only persistent CA aneurysms were 54 subjects (6.4% of high-dose
adjustment for confounders, the risk considered, there was no significant ASA group) received low-dose
difference for any CA abnormalities risk difference between groups: ASA in the institutions routinely
in the low-dose compared with the adjusted risk difference of 1.9% prescribing high-dose ASA. When risk

TABLE 2 Primary and Secondary Outcomes (Intent-to-Treat Analysis)

Outcomes All Subjects, ASA High ASA Low Dose, Unadjusted Risk Difference Adjusteda Risk Difference and
n (%) Dose, n (%) n (%) and [95% CI] (Low Dose [95% CI] (Low Dose Versus High
Versus High Dose) Dose)
Any CA abnormalities (z score 2.5) 255/1213 174/848 81/365 (22.2) 1.7% [3.4% to 6.7%] 0.3% [4.5% to 5.0%]
(21.0) (20.5)
Persistent CA abnormalities (z score 2.5) 157/1213 112/848 45/365 (12.3) 0.9% [5.0% to 3.2%] 1.9% [5.3% to 1.5%]
(12.9) (13.2)
Any CA abnormalities excluding small isolated 234/1213 165/848 69/365 (18.9) 0.5% [5.4% to 4.3%] 2.0% [6.4% to 2.4%]
dilatation of the left main CA (19.3) (19.5)
Medium or larger CA aneurysm (z score 5) 66/1213 (5.4) 51/848 (6.0) 15/365 (4.1) 1.9% [4.5% to 0.7%] 4.0% [7.4% to 0.5%]
Giant CA aneurysm (z score 10 or diameter 28/1213 (2.3) 22/848 (2.6) 6/365 (1.6) 1.0% [2.6% to 0.7%] 1.9% [4.4% to 0.5%]
>8 mm)
a Adjusted for type of Kawasaki (complete versus incomplete), sex, need for retreatment (any treatment after the first IVIg), and young age (<12 mo of age at diagnosis).

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4 Dallaire et al
differences were computed by using
the actual ASA dose received, the
results were similar, with an overall
slight decrease in risk differences
compared with the intent-to-treat
analysis. For any CA abnormalities,
the adjusted risk difference was
0.7% (95% CI 5.2% to 3.8%). The
adjusted risk difference of persistent
CA abnormalities was 2.1% (95% CI
5.3% to 1.1%).
The risk of requiring further
treatment after the first dose of IVIg
was similar between groups (24.4%
and 27.4% in the high- and low-
dose ASA group, respectively). After
adjusting for the type of Kawasaki
(complete versus incomplete),
sex, and age at diagnosis, the risk
difference of requiring retreatment
was small and not statistically
significant: adjusted risk difference
of 2.9% (95% CI: 2.5% to 8.4%).
Fever duration was similar
between high-dose and low-dose
ASA groups: 7.8 3.8 days and
7.9 2.6 days, respectively, with
an adjusted absolute difference of
0.18 days that was not statistically
significant (95% CI: 0.25 days to
0.61 days).
Discussion
The results of our study suggest that
using low-dose ASA concomitantly
with IVIg in acute KD is not inferior
to high-dose ASA in preventing
CA abnormalities. We also did not
observe a significant effect of ASA
dose on treatment resistance or on
fever duration.
Before the IVIg era, ASA was used
for its anti-inflammatory and
antithrombotic effects. Although it
has been the mainstay treatment of
KD, studies performed at that time
showed little effect of ASA on the
incidence of CA aneurysms.21,22
It is
only when IVIg was introduced as
part of standard KD management that
a significant change in the risk of CA
complications was seen.35
In these
PEDIATRICS Volume 139, number 6, June 2017
trials, IVIg was used concomitantly
with high-dose ASA. As a
consequence, high-dose ASA (80100
mg/kg per day) remained central
in the treatment recommendations
of acute KD in North America.1
However, the Japanese guidelines
suggest lower doses of ASA (3050
mg/kg per day) for the treatment of
acute KD as compared with the North
American recommendations.23 In
2013, Ogata reported that there were
no differences in CA aneurysm rates
between 5 institutions in the United
States and Japan despite differences
in ASA dose used in acute KD.24
The appropriate dose of ASA to be
used with IVIg in the treatment
of acute KD has been the subject
of debate.13,14
To our knowledge,
no prospective study has shown
that ASA, at any dose, reduces the
incidence of CA aneurysm. There
have been 3 meta-analyses that all
concluded that there is no evidence
that high-dose ASA decreases the risk
of CA abnormalities compared with
low-dose ASA.1012
More recently, Kuo et al9 compared
patients receiving moderate and
high-dose ASA (>30 mg/kg per
day) during treatment of acute KD
to patients receiving no ASA. They
found no significant difference in the
risk of CA lesions (17.0% vs 15.4%).
In 2016, Kim et al15 studied a large
sample of 8456 children from a
retrospective survey of 116 hospitals
in South Korea. They reported that
compared with low-dose ASA (35
mg/kg per day), medium or higher
dose ASA (>30 mg/kg per day)
during treatment of acute KD was
associated with a higher risk of CA
abnormalities after adjustment for
confounders. In both studies, the
reasons for using low-dose ASA in
settings where higher doses are
routinely used was not stated. An
important indication bias cannot
be ruled out if low-dose ASA was
prescribed to milder cases or to
patients with a lower risk for the
development of CA aneurysms.
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In usual circumstances, comparing
treatment efficacy in retrospective
studies is prone to indication bias.
Different clinical characteristics
at presentation may influence
treatment as well as outcome,
thus potentially confounding the
association between the two. A
strength of our study lies in the fact
that the participating institutions in
Canada have been routinely using
different ASA doses in the treatment
of acute KD, thus potentially
minimizing this bias. Subjects
included in this study mostly
received a given ASA dose according
to where they lived, irrespective of
their clinical characteristics. That
being said, a small proportion of
subjects in the low-dose group did
receive high-dose ASA, possibly
because of some physicians
preference and/or a more severe
disease at presentation. We elected
to use a design analogous to an
intent-to-treat protocol to reduce
the indication bias that would be
introduced if sicker patients were
being prescribed higher doses of
ASA. Nevertheless, when subjects
were assigned to a treatment group
according to the actual dose of ASA
prescribed, the risk difference of CA
abnormalities between treatment
groups was similar to that of the
intent-to-treat analysis.
Our study has limitations. Possible
variations in unmeasured population
characteristics between institutions
may have introduced a bias. In
particular, ethnic background,
differential use of rescue therapy,
and variation in CA imaging and
measurements may have influenced
the association between treatment
and outcome. We did not collect
information on adverse effects of
ASA.
Conclusions
In conjunction with IVIg, our data
suggest that using low-dose ASA
5
during acute KD is not inferior to Acknowledgments
high-dose ASA to reduce the risk of
Abbreviations
CA abnormalities. Given that ASA at Frederic Dallaire is supported in ASA:acetylsalicylic acid
any dose has never been shown to part by the Fonds de recherche CA:coronary artery
reduce the risk of CA abnormalities, du Qubec Sant. We thank the CI:confidence interval
our study suggests that ASA at a dose Fondation En Coeur for the initial IVIg:intravenous immunoglobulin
superior to 3 to 5 mg/kg per day may support of the Registre Qubcois de KD:Kawasaki disease
not be indicated in acute KD. la Maladie de Kawasaki.

study design, coordinated and supervised the study at 1 of the 4 sites, and critically reviewed the manuscript; Dr Scuccimarri helped to conceptualize the study,
contributed to the study design, reviewed and contributed to the data collection instruments, coordinated and supervised data collection at 1 of the 4 sites, and
critically reviewed the manuscript; and all authors approved the final manuscript as submitted.
DOI: https://doi.org/10.1542/peds.2017-0098
Accepted for publication Mar 20, 2017
Address correspondence to Frederic Dallaire, MD, PhD, Division of Pediatric Cardiology, Department of Pediatrics, Faculty of Medicine and Health Sciences,
University of Sherbrooke, 3001, 12e Ave Nord, Sherbrooke, QC J1H 5N4, Canada. E-mail: frederic.a.dallaire@usherbrooke.ca
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).
Copyright 2017 by the American Academy of Pediatrics
FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.
FUNDING: No external funding.
POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

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7
 Aspirin Dose and Prevention of Coronary Abnormalities in Kawasaki Disease
Frederic Dallaire, Zoe Fortier-Morissette, Samuel Blais, Anita Dhanrajani, Dania
Basodan, Claudia Renaud, Mathew Mathew, Astrid M. De Souza, Audrey Dionne,
Joel Blanchard, Harrison Saulnier, Kimberley Kaspy, Soha Rached-d'Astous, Nagib
Dahdah, Brian W. McCrindle, Derek G. Human and Rosie Scuccimarri
Pediatrics 2017;139;; originally published online May 2, 2017;
DOI: 10.1542/peds.2017-0098
Updated Information & including high resolution figures, can be found at:
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PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

publication, it has been published continuously since 1948. PEDIATRICS is owned, published,
and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk
Grove Village, Illinois, 60007. Copyright 2017 by the American Academy of Pediatrics. All
rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.

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 Aspirin Dose and Prevention of Coronary Abnormalities in Kawasaki Disease
Frederic Dallaire, Zoe Fortier-Morissette, Samuel Blais, Anita Dhanrajani, Dania
Basodan, Claudia Renaud, Mathew Mathew, Astrid M. De Souza, Audrey Dionne,
Joel Blanchard, Harrison Saulnier, Kimberley Kaspy, Soha Rached-d'Astous, Nagib
Dahdah, Brian W. McCrindle, Derek G. Human and Rosie Scuccimarri
Pediatrics 2017;139;; originally published online May 2, 2017;
DOI: 10.1542/peds.2017-0098

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
/content/139/6/e20170098.full.html

PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

publication, it has been published continuously since 1948. PEDIATRICS is owned,
published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point
Boulevard, Elk Grove Village, Illinois, 60007. Copyright 2017 by the American Academy
of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.

Downloaded from by guest on June 1, 2017