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Stenotic Lesions and the Maximum Diameter of Coronary Artery
Aneurysms in Kawasaki Disease
Etsuko Tsuda, MD, PhD, Nobuyuki Tsujii, MD, and Yohsuke Hayama, MD
Objectives To determine the prevalence of subsequent stenotic lesions based on the maximum diameter of the
largest coronary artery aneurysm in patients with Kawasaki disease and the threshold value of coronary artery di-
ameter associated with risk of developing stenotic lesion.
Study design There were 214 patients (160 males) who had at least 1 aneurysm in a selective coronary an-
giogram (CAG) done <100 days after the onset of Kawasaki disease were studied. We measured the maximal coro-
nary artery aneurysm diameter in 3 major branches in the initial CAGs. Branches were classified into 3 groups
according to their maximal coronary artery aneurysm diameter: large, ≥8.0 mm; medium, ≥6.0 mm but <8.0 mm;
and small, <6.0 mm. Subsequent CAGs were performed in the late follow-up period. We investigated the stenotic
lesion in the follow-up CAGs, and evaluated the prevalence of stenotic lesion in each group based on body surface
area (BSA) by the Kaplan-Meier method. Localized stenosis of ≥25% and complete occlusion were included as
stenotic lesion in this study. We also determined the cutoff point for stenotic lesion.
Results The median interval from the initial CAGs to the latest CAG was 8 years, with a maximum of 32 years.
For a BSA of <0.50 m2, the 20-year prevalence of large and medium stenotic lesions was 78% (n =62; 95% CI,
63-89) and 81% (n =40; 95% CI, 63-89), respectively. For a BSA of ≥0.50 m2, large and medium stenotic lesions
were 82% (n =75; 95% CI, 67-91) and 40% (n =56; 95% CI, 20-64), respectively (P<.0001).
Conclusion The cutoff points of the coronary artery diameter within the first 100 days after the onset of Kawa-
saki disease leading to a stenotic lesion in the late period, were a diameter of ≥6.1 mm with a BSA of <0.50 m2
and a diameter of ≥8.0 mm with a BSA of ≥0.50 m2. Those cutoff points would have corresponded with a Zscore
of at least 10 on 2-dimensional echocardiography. Careful follow-up and antithrombotic therapy should be pro-
vided to patients who meet these criteria. (J Pediatr 2018;194:165-70).
See editorial, p 8
Kawasaki disease (KD), first described in 1967, is an acute febrile disease that can lead to coronary artery aneurysm (CAA).
The appearance of CAA affects the outcome in patients after KD. To prevent CAA, various treatments have been used
over the last 50 years. Steroids were tried in 1970, and aspirin was used from the late 1970s to the early 1980s. Since
the mid-1980s, intravenous immunoglobulin has remarkably decreased the prevalence of CAA. Unfortunately, there is no de-
finitive treatment for intravenous immunoglobulin–resistant cases.
The prevalence of a large aneurysm (≥8.0 mm) has decreased to <0.5% in a recent national survey of Japan.1The CAA changes
morphologically in the late period after acute KD. Most small CAA regress, whereas large CAA may persist, or evolve into ste-
notic lesion, which may cause a cardiac event. In 2005, we reported that dilatation of >6.0 mm produces a high probability of
irreversible change in the coronary arterial wall, leading to subsequent stenotic lesions.2Because >10 years have passed since
those studies, we investigated the prevalence of stenotic lesions based not only on the degree of maximal CAA diameter in the
coronary angiograms (CAG) obtained immediately after KD, but also the impact of body surface area (BSA) at the initial CAG,
to clarify the maximal CAA diameter leading to a stenotic lesion.
2DE 2-dimensional echocardiography
AUC Area under the curve
BSA Body surface area
CAA Coronary artery aneurysm
CAG Coronary angiogram
CAL Coronary artery lesion
KD Kawasaki disease
LAD Left anterior descending artery
LCX Left circumflex
RCA Right coronary artery
From the Department of Pediatric Cardiology, National
Cerebral and Cardiovascular Center, Osaka, Japan
The authors declare no conflicts of interest.
0022-3476/$ - see front matter. © 2017 Elsevier Inc. All rights
reserved.
https://doi.org10.1016/j.jpeds.2017.09.077
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ARTICLES
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Methods
The diagnosis of CAA has recently been facilitated by the ap-
plication of noninvasive methods such as 2-dimensional
echocardiography (2DE), computed tomography angiogra-
phy, and magnetic resonance angiography. However, until the
1990s, selective CAG by cardiac catheterization was the only
method for the precise diagnosis of coronary artery lesion
(CAL). There were 579 patients with CALs who had previ-
ously undergone CAG between 1978 and 2011 in our insti-
tution. We reviewed 214 patients (160 males and 54 females)
(Table I;availableatwww.jpeds.com) who had had ≥1 CAA
caused by KD in the initial CAG performed <100 days from
the onset of KD and had undergone follow up CAGs ≥2times.
The number of patients per decade of the initial CAG was 16
patients in 1978-1979; 113 patients in 1980-1989; 55 patients
in 1990-99; and 30 patients in 2000-2011 . For this study, the
final diagnosis of KD and CAA was based on diagnostic guide-
lines prepared by the Japanese Circulation Society.3,4 The age
at acute KD episode ranged from 2 months to 13 years (median,
23 months). Initial CAG was performed from 20 to 99 days
(median, 59), and BSA at the initial CAG was 0.31-1.63 m2
(median, 0.52). The treatment of acute KD is shown in Tab le I .
In our institution, aspirin, 1-2 mg/kg, as an antiplatelet agent
was usually administered to patients with CAL. In addition,
warfarin was added in patients with large aneurysms
(≥8.0 mm). If the CAA had regressed in the follow-up CAG,
medication was stopped. Treatment in the late period con-
sisted of antiplatelet agents in 213 patients (99%) and warfa-
rin in 47 patients (22%). The duration of medication ranged
from 1 month to 38 years (median, 10 years).
We retrospectively investigated the prevalence of stenotic
lesion in the follow-up CAG, based on the degree of the
maximal CAA diameter at each branch and BSA in the initial
CAG. The ethical committee of our institution approved this
retrospective study.
Two hu n d re d t h ir te e n pa t ie n ts u n de r we n t a se c on d C AG af t e r
an interval of 1 year. Only 1 patient without a second CAG
had died, and his CAGs had been done immediately after his
death. Subsequent follow-up CAGs were performed at 3- to
5-year intervals depending on the previous findings until the
middle of the 2000s. If the coronary aneurysm regressed, sub-
sequent CAGs were not performed. However,such patients were
followed in the outpatient clinic by noninvasive imaging, in-
cluding 2DE and computed tomography angiography. Further,
treadmill testing and radioisotope myocardial perfusion scan-
ning were performed depending on CALs. If progression of
CAL was suspected on noninvasive imaging, CAG was con-
sidered at that time.
The maximum diameters of all aneurysms were measured
in the initial CAGs, and their locations were noted. Right coro-
nary artery (RCA) diameters were measured in the left ante-
rior oblique 60° view, and the left anterior descending artery
(LAD) and the left circumflex (LCX) diameters were mea-
sured in the right anterior oblique 30° or right anterior oblique
30° with caudal angulation of 30°. The diameters of the LCX
were also measured in the left anterior oblique 60° view with
30° cranial angulation. We described the measurement of coro-
nary arteries and the intraobserver and interobserver accu-
racy in a previous publication.4,5 The diagnosis of CAA was
determined by 2 pediatric cardiologists. Two different pedi-
atric cardiologists had measured the maximal CAA diameter
at each branch in the initial CAG. We divided the major
branches into 3 groups determined by the maximal CAA di-
ameter in each branch (large, ≥8.0 mm; medium, ≥6.0 mm but
<8.0 mm; and small, <6.0 mm).
Stenotic lesions included localized stenosis of ≥25% and com-
plete occlusion. The percentage of localized stenosis is defined
as the degree of stenosis for near normal coronary arteries. Seg-
mental stenosis implies the development of multiple new small
vessels, which are speculated to occur after thrombotic occlu-
sion of an aneurysm.6In this study, segmental stenosis was in-
cluded in complete occlusion. If acute myocardial infarction
occurred and the occluded branch was diagnosed on electro-
cardiogram or on CAG after the episode, it was considered a
symptomatic complete occlusion. In contrast, complete oc-
clusion first found in the follow-up CAGs are considered as-
ymptomatic complete occlusion.We investigated the prevalence
of stenotic lesion (localized stenosis of ≥25%, asymptomatic
complete occlusion, symptomatic complete occlusion, the
branch that had undergone coronary artery revascularization
for stenotic lesion) in respective groups from the medical
records and the follow-up CAGs. Coronary artery
revascularization entailed coronary artery bypass grafting or
percutaneous coronary intervention.
We cons i d er e d t he fi r s t ap p ea r an c e o f ste n o t ic l e si o n a n ev e n t,
and evaluated its prevalence overall and in the 3 major branches
by the Kaplan-Meier method. Second, we analyzed the preva-
lence of stenotic lesions in the 3 groups based on the maximal
CAA diameter. Further, normal coronary arteries diameter in
children differed by body size. However, there was no normal
value for children in CAGs. Because we could not base our
analysis on the ZCAGs score, we divided them into 2 groups
based on BSA. BSA was calculated using the Haycock formula.
One group had a BSA of <0.50 m2,andtheothergrouphad
aBSAof≥0.50 m2.Third,wedeterminedtheprevalenceofste-
notic lesions in the groups based on the maximal CAA diam-
eter in each branch and BSA in the initial CAGs. Fourth, we
determined the cutoff points, which were the threshold value
of coronary artery diameter in the initial CAG at risk of de-
veloping stenotic lesion in the late period.
Japanese normal values of coronary artery diameters by 2DE
were reported, including Zscore corrected by BSA.7Finally,
we speculated about the prevalence of stenotic lesion in the
values corresponding with the Zscore measured by 2DE. Fur-
thermore, the cutoff points corresponding with the Zscore mea-
sured by 2DE leading to a stenotic lesion in the late period were
calculated.
Statistical Analyses
Statistical analysis was performed using JMP 10 (SAS
Institute Inc, Cary, North Carolina). Measurements are
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166 Tsuda, Tsujii, and Hayama
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expressed as mean ±SD. The prevalence of stenotic lesions
was analyzed by the Kaplan-Meier method with 95% CI, and
differences were assessed by the log-rank test. The cutoff
points of the original coronary artery diameter at risk of
developing stenotic lesion were analyzed using a receiver
operator characteristic curve. P<.05 was considered
significant.
Results
The mean number of CAGs studies was 4 ±2 with a median
interval from the onset of KD to the latest CAG being 8 years,
and a maximum interval of 32 years. The follow-up period
ranged from 2.5 months to 38 years (median, 17 years). Cardiac
events occurred in 44 patients (21%). Death, myocardial in-
farction, and coronary artery revascularization occurred in 5,
20, and 36 patients, respectively.
The total number of ≥1CAAwas392branches.Thenumber
of respective groups in the initial CAGs were: large, 137;
medium, 96; and small, 159. The total number of BSA of
<0.50 m2was 178 branches and of BSA of ≥0.50 m2was 214
branches. The number in the respective groups were 62 large,
40 medium, and 76 small in BSA of <0.50 m2,andforaBSA
of ≥0.50 m2,75large,56medium,and83small.Stenoticlesions
occurred in 123 branches (31%) (Figures 1 and 2). Local-
ized stenosis of ≥25%, coronary artery revascularization, as-
ymptomatic complete occlusion, and symptomatic complete
occlusion were 37 (9%), 26 (7%), 35 (9%), and 25 (6%), re-
spectively. Of the patients who underwent coronary artery
revascularization, 20 had bypass grafting and 6 percutaneous
coronary intervention.
Figure 1. Coronary artery angiograms (CAGs). (Upper) Initial CAGs. A 4-month-old boy had acute KD. The initial CAG was
done 71 days after the onset of KD. He was included in the group with a BSA of <0.50. (Left) The maximum diameter at the
segment 1 of the RCA was 6.5 mm. The Zscore corresponding with the Zscore measured by 2DE was 10.4. (Right)Themaximum
diameter at the segment 6 of the LAD was 7.5 mm. That of Zscore corresponding by 2DE measurement was 11.5. (Lower)
CAGs 15 years after KD. The patients had undergone CAG at 15 years of age because of myocardial ischemia by 99mTc myo-
cardial perfusion imaging. (Left) The aneurysm at the proximal segment of the RCA was detected. (Right) The localized ste-
nosis at the proximal segment of the LAD.
Figure 2. The relation between the maximum diameter of each
branch and the interval from the onset of KD. The number of
stenotic lesions was increased with increasing of the maximum
diameter, and it was increased with years from the onset of
acute KD.
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The number of each stenotic lesion in the respective groups
is shown in Figure 3 (available at www.jpeds.com). In the RCA,
the number of stenotic lesion in a BSA of <0.50 m2was 30
(41%) and in a BSA of ≥0.50 m238 (40%). In the LAD, those
in BSA of <0.50 m2accounted for 22 (34%) and BSA of
≥0.50 m2for 24 (30%). For the LCX, those in BSA of <0.50 m2
and BSA of ≥0.50 m2were 7 (18%) and 2 (5%), respectively.
Stenotic lesions in the small subgroup occurred in 2 branches
of the LAD and 1 branch of the LCX. The smallest coronary
artery diameter was 4.8 mm, equivalent to 8.5 calculated as a
Zscore. The number of asymptomatic complete occlusions in
the RCA was significantly higher than that in the LAD
(P<.001). In contrast, the prevalence of coronary artery
revascularization in the LAD was significantly higher than in
the RCA (P<.0001).
The 10-, 20-, and 30-year prevalences of stenotic lesions in
all branches with CAA were 31% (95% CI, 26-37), 53% (95%
CI, 40-60), and 58% (95% CI, 45-70), respectively (Figure 4,
A; available at www.jpeds.com). The 20-year prevalence of ste-
notic lesions in the RCA, LAD, and LCX were 62% (n =169;
95% CI, 50-72), 61% (n =144; 95% CI, 46-74), and 15%
(n =79; 95% CI, 8-27), respectively (Figure 4, B; available at
www.jpeds.com). The prevalence of total stenotic lesions in the
LCX was significantly lower than in the RCA and the LAD
(P<.0001).
The 20-year prevalence of large, medium, and small was 81%
(n =137; 95% CI, 71-88), 59% (n =96; 95% CI, 44-74), and
3% (n =159; 95% CI, 1-8), respectively (P<.0001) (Figure 5,
A). The 20-year prevalence in large, medium, and small of BSA
of <0.50 was 78% (n =62; 95% CI, 63-89), 81% (n =40; 95%
CI, 58-93), and 2% (n =76; 95% CI, 1-10), respectively
(P<.0001) (Figure 5, B). The 20-year prevalence in large,
medium, and small of BSA of ≥0.50 was 82% (n =75; 95% CI,
67-91), 40% (n =56; 95% CI, 20-64), and 5% (n =83; 95%
CI, 1-18), respectively (P<.0001).
The 20-year prevalence of stenotic lesion in the (Z≥10)
group and the (Z>5 and Z≤10) group were 84% (n =169;
95% CI, 70-92) and 29% (n =169; 95% CI, 18-44), respec-
tively (P<.0001) (Figure 5,C).Astenoticlesionwasnotfound
in the group with a Zscore of <5. Further, the 20-year preva-
lence of stenotic lesions in the (Z≥12.5) group, the (Z>10
and Z≤12.5) group, and the (Z>7.5 and Z≤10) group was
81% (n =91; 95% CI, 70-89), 73% (n =80; 95% CI, 58-85),
and 34% (n =95; 95% CI, 23-49), respectively (Figure 5, D).
The 20-year prevalence of stenotic lesions in the (Z>5 and
Z≤7.5) group was 21% (n =72; 95% CI, 5-60).
Figure 5. Prevalence of stenotic lesions. A, Prevalence of stenotic lesions based on the maximum diameter of each branch.
B, Prevalence of stenotic lesions based on the maximum diameter of each branch and BSA. C, Prevalence of stenotic lesions
based on the Zscore of the maximum diameter of each branch. D, Prevalence of stenotic lesions based on Zscore on the
maximum diameter of each branch.
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The cutoff point for the coronary artery diameter for ste-
notic lesions in total branches was 7.0 mm (area under the
curve [AUC], 0.884; P<.0001; n =392) (Table II). That of Z
score corresponding with a Zscore measured by 2DE was
10.4 (AUC, 0.858; P<.0001; n =392). Those in BSA of <0.50
and BSA of ≥0.50 were 6.1 mm (AUC,0.878; P<.0001; n =178)
and 8.0 mm (AUC, 0.892; P<.0001; n =214), respectively.
The sensitivity, specificity, positive predictive value, and
negative predictive value for each cutoff point are shown in
Table II.
The cutoff point of the coronary artery diameter in the RCA
was 7.1 mm (AUC, 0.893; P<.0001; n =169) (Ta bl e I I). That
of the Zscore corresponding to the Zscore measured by 2DE
was 11.1 (AUC, 0.842; P<.0001; n =169). The cutoff point
of the coronary artery diameter in the LAD was 7.1 mm (AUC,
0.862; P<.0001; n =144). The Zscore corresponding to the
Zscore measured by 2DE was 10.6 (AUC, 0.848; P<.0001;
n=144). The cutoff point of the coronary artery diameter in
the LCX was 6.1 mm (AUC, 0.897; P=.0004; n =79). That of
Zscore corresponding to Zscore measured by 2DE was 8.2
(AUC, 0.833; P=.0003; n =79).
In BSA of <0.50, the cutoff point of the coronary artery di-
ameter in the RCA, the LAD and the LCX were 7.0 mm (AUC,
0.909; P<.0001; n =73), 6.3 mm (AUC, 0.815; P<.0001;
n=65), and 6.1 mm (AUC, 0.893; P=.0004; n =40), respec-
tively. In BSA of ≥0.50, the cutoff point of the coronary artery
diameter in the RCA and the LAD were 8.0 mm (AUC, 0.880;
P<.0001; n =96) and 8.3 mm (AUC, 0.896; P<.0001; n =79),
respectively. They had high negative predictive values, whereas
the positive predictive values were modest, especially in the
group with a BSA of <0.50.
Discussion
Recently, normal Japanese values for coronary artery diam-
eters measured by 2DE were reported, and the Zscore cor-
rected by BSA was included.7There is a correlation between
the values measured by CAG and those by 2DE for the coro-
nary arteries, although there are some limitations in the
methods.5,8 Overestimation of the coronary artery diameter by
2DE might be more likely than those in CAG. The cutoff value
of 6 mm the subgroup with a BSA pf <0.50 m2seems to be
equivalent to the cutoff value of 8 mm in the subgroup with
aBSAof>0.50 m2. Those cutoff points seem to be equiva-
lent to 10 of Zscore, if calculated from the Zscore by 2DE
measurements. If antithrombotic therapy and optimal coro-
nary artery revascularization were performed, their progno-
sis would improve.9-11
At 20 years after the onset of KD, stenotic lesions occurred
in 40% in the subgroup with a BSA of ≥0.50 m2and a
maximum coronary artery diameter of between 6 and 8 mm.
In essence, this study also indicated that coronary dilatation
exceeding 6.0 mm carries a high probability of subsequent ste-
notic lesion.2However, stenotic lesions also occurred in the
<6.0 mm group with a BSA of <0.50 m2,althoughthenumber
was very small. Those stenotic lesions were found in the LAD.
In contrast, there was no stenotic lesion in the group <4.0 mm
Table II. Cutoff points of the coronary artery diameter for stenotic lesions
Diameter
(mm) AUC Pn
Sensitivity
(%)
Specificity
(%)
PPV
(%)
NPV
(%) PA Zscore AUC P
Sensitivity
(%)
Specificity
(%)
PPV
(%)
NPV
(%) PA
Total 7.0 0.884 <.0001 392 89 72 59 94 78.3 10.4 0.858 <.0001 80 90 65 89 79.6
BSA <0.50 m26.1 0.878 <.0001 178 97 68 61 98 77.7
BSA ≥0.50 m28.0 0.892 <.0001 214 80 85 69 87 84.6
Branches
RCA 7.1 0.893 <.0001 169 93 68 66 93 78.1 11.1 0.841 <.0001 85 72 67 88 76.3
LAD 7.1 0.862 <.0001 144 83 74 62 90 77.1 10.6 0.848 <.0001 77 81 67 88 79.9
LCX 6.1 0.897 .0011 79 89 77 33 98 78.5 8.2 0.833 .001 89 73 30 98 74.7
BSA <0.50 m2
RCA 7.0 0.909 <.0001 73 97 70 69 97 80.8
LAD 6.3 0.815 <.0001 65 91 67 60 93 75.3
LCX 6.1 0.893 .0003 40 100 70 54 100 81.6
BSA ≥0.50 m2
RCA 8.0 0.880 <.0001 96 82 81 74 87 81.3
LAD 8.3 0.896 <.0001 79 80 89 77 91 86.7
NPV, negative predictive value; PA, predictive accuracy; PPV, positive predictive value.
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and in the branches of Zscore <5 calculated from the Zscore
by 2DE. The use of the Zscore is suitable for risk stratifica-
tion. However, our risk stratification by raw coronary artery
diameter using BSA is very easy in the outpatient clinic. Further,
the predictive accuracy of cutoff points in raw coronary artery
diameter was not necessarily inferior to the Zscore risk strati-
fication calculated by 2DE measurements.
The prevalence of coronary artery revascularization to pre-
serve myocardial perfusion of the whole heart was as high in
the LAD. In contrast, the prevalence of asymptomatic com-
plete occlusion was significantly higher in the RCA. The preva-
lence of stenotic lesion in the LCX was also significantly lower
than those of the RCA and the LAD, although the prevalence
of CAA in the LCX was significantly lower than those of the
RCA and the LAD.12 Although the cutoff values for stenotic
lesions were almost the same in the 3 major branches, it dif-
fered in its characteristics and the prevalence of each stenotic
lesion, and these differences might depend on the anatomic
characteristics of each branch. The bifurcation of the left coro-
nary artery is a high-risk site for CAA. The outcome of CAA
in the LAD and the LCX sometimes depends on the degree
of the maximal diameter of CAA at the bifurcation of the left
coronary artery. Even if the maximal CAA diameter is smaller
than the cutoff values in the LAD and the LCX, stenotic lesion
might occur in the patients with CAA more than cutoff values
at the bifurcation of the left coronary artery.5Further inves-
tigations of the complications of CAA at the bifurcation of the
left coronary artery are necessary.
Thrombotic occlusion is likely to occur within 1-2 years after
KD. In contrast, most localized stenosis caused by intima medial
thickening gradually progress over the years.2,10,13 Acute coro-
nary syndrome occurs in young adult patients with CAA, in
addition to well-recognized coronary risk factors such as
smoking, hyperlipidemia, and obesity.14 Coronary artery cal-
cification acts as a marker, which indicates that irreversible
change in the coronary artery wall has occurred with aging,
even if the maximum diameter of CAA is <6.0 mm.15 Ste-
notic lesions caused by atherosclerosis can occur in adults with
ahistoryofKD.Therefore,stenoticlesionsmightoccurinsmall
CAA immediately after acute KD with aging. The clinical course
of coronary arteries extending over 50 years remains to be seen.
The percentage of localized stenosis is defined as the degree
of stenosis for near normal coronary arteries. However, the mea-
surement of stenosis is subject to error and to be certain which
coronary artery segments are normal in dimension is diffi-
cult in some cases, because of multiple large aneurysms. The
appearance of stenotic lesion in most of our cases depended
on the timing of elective CAGs owing to the retrospective nature
of this study. This study included patients who underwent CAG
from 1978 to the present. Further, we selected the 214 pa-
tients who had undergone CAG <100 days after the acute phase
of KD. Usually, most aneurysms, except giant aneurysms, are
likely to regress some months after acute KD. We cannot exclude
the possibility of selection bias in our study sample. The treat-
ment in the acute phase and subsequent examination for CAL
have improved remarkably for many years. The patients in the
modern era should be studied as a separate group in the future.
The results of this study indicate that coronary artery dila-
tation of >6.0 mm results in a high probability of subse-
quent stenotic lesion. A CAA of ≥4.0 mm but <6.0 mm in the
LAD rarely leads to a stenotic lesion. Careful follow-up and
antithrombotic therapy should be provided to patients with
high-risk lesions. ■
We th a n k P rofe s s o r Pet e r O l le y and Dr Sets u k o Olley for t h e i r k ind En g l i s h
language consultation.We thank Dr Tetsuro Kamiya, Dr Atsuko Suzuki,
and Dr Kohji Kimura for the previous management and examination
with the patients after KD in this study.
Submitted for publication May 10, 2017; last revision received Sep 19, 2017;
accepted Sep 27, 2017
Reprint requests: Etsuko Tsuda, MD, PhD, 5-7-1 Fujishirodai, Suita, Osaka,
Japan. E-mail: etsuda@ncvc.go.jp
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Figure 3. The number of stenotic lesions in each branch based on the maximum diameter of coronary artery. CR, coronary
artery revascularization; PCI, percutaneous coronary intervention.
Figure 4. Prevalence of stenotic lesions. A, Prevalence of stenotic lesion in all branches with CAA. B, Prevalence of stenotic
lesion in each branch.
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Stenotic Lesions and the Maximum Diameter of Coronary Artery Aneurysms in Kawasaki Disease
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Table I. Patient characteristics
n
Patient 214
Male 160 (75%)
KD typical 201 (94%)
Age at KD (mo)
Median 23
Range 2 months-13 years
Acute treatment
Aspirin 66 (31%)
Aspirin and IVIG 63 (29%)
Aspirin and steroid 20 (27%)
Steroid 14 (7%)
Aspirin, IVIG, steroid 13 (6%)
IVIG 12 (6%)
Aspirin, IVIG, others 9 (3%)
IVIG and steroid 2 (1%)
None 4 (2%)
Unknown 11 (5%)
Treatment in the late period
Antiplatelet 213 (99%)
Coumadin 47 (22%)
Interval of medication (y)
Median 10
Range 1 month-38
Initial CAG (d)
Median 59
Range 20-99
Interval from the initial CAG to latest CAG (y)
Median 8
Range 6 days-32 years
Follow-up (y)
Median 17
Range 0.21-38.00
IVIG, Intravenous immunoglobulin.
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