Abstract
Background
In the current guidelines, the management algorithm for patients with Kawasaki disease (KD) without coronary artery (CA) aneurysms primarily depends on the clinical experience of pediatricians. It is necessary to conduct a comprehensive evaluation of these patients to provide a higher level of evidence for their management. Therefore, our study aimed to assess patients with KD using multidimensional data and investigate their prognosis.
Methods
A total of 455 patients with KD were retrospectively recruited and divided into a non-CA involvement group (n=313) and a CA dilation-only group (n=142), with 16.1% (50/311) and 15.5% (22/142), respectively, undergoing cardiac magnetic resonance (CMR) examinations during recovery. Data regarding inflammatory markers, electrocardiography, and echocardiography were compared between the two groups both in the acute phase and during the recovery period. Kaplan-Meier analysis was performed to estimate the cumulative probability of the endpoints including coronary events, cardiac death, heart failure, and new-onset malignant arrhythmias.
Results
Baseline inflammatory markers, including white blood cell count (WBC) and C-reactive protein (CRP), were not significantly different between patients with KD and non-CA involvement and those with dilation only (median WBC: 14.1×109/L vs. 13.9×109/L, P=0.57; median CRP: 87.4 vs. 85.6 mg/L, P=0.73). In terms of echocardiography assessment at baseline, there were no significant differences between the non-CA involvement group and the dilation-only group in terms of left ventricular ejection fraction (67.8%±13.6% vs. 68.1%±10.3%; P=0.13) or fractional shortening (37.6%±5.3% vs. 35.4%±6.6%; P=0.25). For CMR assessment at recovery, the myocardial systolic function of patients with KD but non-CA involvement was not significantly different from that of patients with CA dilation only in terms of global radial strain (38.3%±18.7% vs. 39.9%±20.5%; P=0.20), global circumferential strain (–18.7%±6.8% vs. –18.3%±7.2%; P=0.38), and global longitudinal strain (–13.2%±3.7% vs. −13.4%±4.1%; P=0.17). The global native T1 value of patients with non-CA involvement was 1,296.5±74.1 msec, while that of patients with CA dilation only was 1,313.3±80.5 msec (P=0.21); there was also no significant difference in global T2 values between the two groups of patients (38.2±4.1 vs. 38.1±3.5 msec; P=0.53). Finally, at a median follow-up of 4.2 years, there was a favorable prognosis in both two groups of patients, with no patients reaching the endpoints.
Conclusions
Comprehensive assessment revealed no significant differences between patients with KD and CA dilation only and those with non-CA involvement, and thus these patients should be treated according to the same medium-long-term management algorithm.
Keywords: Kawasaki disease (KD), dilation only, coronary artery (CA), echocardiography, cardiac magnetic resonance (CMR)
Introduction
Kawasaki disease (KD) is an acute vasculitis occurring primarily in young children and is associated with lesions in the coronary artery (CA) (1). According to research, the proportion of patients with KD and coronary artery aneurysms (CAAs) after intravenous immunoglobulin (IVIG) treatment is about 5–25% (1-4). Severe CAA formation can cause subsequent thrombosis and/or stenosis (5). Therefore, patients with KD and CAAs have garnered heightened attention from pediatricians. Several studies have shown that patients with small CAAs have near universal normalization of the CA internal lumen diameter size over follow-up and a near-zero risk of adverse cardiac events (5-7). However, patients with KD but non-CAA dilation have not been extensively examined, particularly during the recovery period. Moreover, in the current guidelines, the management algorithm for patients with KD and non-CA involvement and those with dilation only is primarily based on the clinical experience of pediatricians (8,9), and related cohort studies that would provide high-level evidence for their management are lacking.
Echocardiography is the primary imaging modality for cardiac assessment in the follow-up of patients with KD due to its noninvasiveness, high sensitivity, and high specificity in the detection of abnormalities of the proximal CA segments (10); however, it is limited in its inability to evaluate myocardial tissue. Cardiac magnetic resonance (CMR) is the imaging tool of choice for in vivo myocardial tissue characterization in KD due to its unique advantages (11). Specifically, CMR allows for the assessment of ventricular morphology, contractile function, and blood flow (12) during the same session, and tissue characteristics can be integrated into a comprehensive “all-in-one” imaging examination. A few studies have examined cardiac dysfunction and myocardial damage in patients with KD without CA dilation (13,14), but no studies have specifically evaluated patients with CA dilation only using CMR.
Therefore, we conducted a comprehensive evaluation of patients with KD with non-CA involvement and of those with dilation only combining clinic, echocardiography, CMR, and follow-up findings from patients with KD admitted to West China Second University Hospital. The overall aim was to generate high level of evidence to inform the management of this patient population. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2772/rc).
Methods
This study was conducted in accordance with the declaration of Helsinki and its subsequent amendments and was approved by the Institutional Review Board (IRB) of West China Second University Hospital (approval No. 2023095). The requirement for individual consent was waived due to the retrospective nature of the analysis.
Participants
From January 2012 to December 2023, 482 patients diagnosed with KD at West China Second University Hospital and who satisfied the inclusion criteria were retrospectively included in this study. Structured questionnaires with precoded questions including basic demographic information, manifestations, treatment conditions, laboratory data, electrocardiography results, echocardiography data, and follow-up outcomes were used for data collection.
In this study, the inclusion criteria were (I) patients aged ≤18 years old; (II) patients diagnosed with KD according to the 2004 and 2017 American Heart Association (AHA) recommendations for KD (9,15); (III) a standardized treatment regimen administered within 10 days from fever onset (9) at West China Second University Hospital; (IV) blood sampling analysis conducted before initial IVIG infusion; (V) echocardiography examinations administered at baseline and at 2 weeks and 1 month from onset; (VI) maximal Z-scores of coronary arteries <2.5 at baseline; and (VII) absence of inflammatory diseases, immune diseases, hematological diseases, metabolic diseases, other heart diseases, and cancer, liver, and kidney diseases. Patients with incomplete follow-up data were excluded.
Laboratory analysis
Blood samples were collected from all participants before initial IVIG treatment. Inflammatory factor levels were retrieved from medical records, including the data of white blood cell count (WBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) level, percentage of lymphocytes (L%) and neutrophils (N%), plasma cardiac troponin I (cTnI) level, and creatine kinase MB (CK-MB) level. After IVIG treatment, blood sampling analysis was conducted again in patients with KD.
Electrocardiography
The electrocardiogram typically reflects the arrhythmia situation, including sinus node and atrioventricular node functional abnormalities, with a prolonged PR interval and nonspecific ST and T-wave changes or low voltage being present if there is myocardial or pericardial involvement. Cardiac arrhythmia was identified with a 12-lead electrocardiogram.
Echocardiography
The echocardiography examinations were performed at baseline and 2 weeks and 1 month from onset. Patients with KD who received echocardiography examinations at 2 months, 6 months, 1 year, and 2 years from onset were also recorded. Measurements of left ventricular (LV) dimensions, LV fractional shortening (LVFS), CA segment diameters, and LV ejection fraction (LVEF) were assessed. The Z-scores of CAs were computed according to the internal diameters of the CAs, sex, height, and weight of patients with KD (16). The severity of valvular regurgitation was qualitatively analyzed via color Doppler imaging, with notation made if there was at least mild mitral regurgitation (MR), tricuspid regurgitation (TR), aortic regurgitation (AR), or pulmonary regurgitation. Pericardial effusion was considered present if its maximal dimension was at least 1 mm in any imaging plane. Patients with a Z-score from 2 to <2.5 were placed in the CA dilation-only group, while those with a Z-score <2.0 were placed in the non-CA involvement group.
CMR
The data of patients with KD who underwent CMR during the recovery period were analyzed. CMR scanning was performed with a Skyra 3.0-T scanner (Siemens Healthineers, Erlangen, Germany) with an 18-channel coil. The CMR scanning protocol included cine images, native T1 mapping and T2 mapping images, and late gadolinium enhancement (LGE) images (Figure 1). Image analysis was performed with commercially available software (cvi42 v.5.17.2, Circle Cardiovascular Imaging, Calgary, Canada). The cardiac diameters and volume parameters were measured on the cine images. Myocardial systolic function was measured using three-dimensional strain tissue tracking based on cine diameters. The native T1 and T2 values of the myocardium were automatically computed in the characterization module of the cvi software after the endocardial and epicardial borders of the myocardium were outlined.
Figure 1.
An example of CMR scanning protocol in an 8-year-old patient with KD. (A) Short-axis cine image. (B) LGE image. (C) T1 mapping image. (D) T2 mapping image. CMR, cardiac magnetic resonance; KD, Kawasaki disease; LGE, late gadolinium enhancement.
Clinical follow-up
Clinical follow-up was performed through the medical record system and telephone interviews. The primary endpoint was the occurrence of at least one of the following events: (I) coronary events including CA thrombosis, obstruction, stenosis, procedural events, and acute ischemic events (17); (II) cardiac death, defined as death from all cardiac causes, including sudden cardiac death (SCD), heart failure, and aborted SCD (18); (III) heart failure; and (IV) new-onset malignant arrhythmias. The secondary endpoint included the following: (I) mild reduced cardiac function (19); (II) persistent mild atrioventricular block (AVB) or other kinds of arrhythmias; and (III) residual cardiovascular symptoms such as chest tightness and palpitations.
Statistical analysis
Data analyses were performed with SPSS version 27.0 (IBM Corp., Armonk, NY, USA) and GraphPad Prism version 9.5 (Dotmatics, Boston, MA, USA). Normally distributed continuous variables are presented as the mean ± standard deviation and continuous variables that were not normally distributed as the median and IQR; meanwhile, categorical variables are expressed as frequencies and percentages. The Chi-squared test and paired sample t-test were performed to compare demographic characteristics, laboratory data, echocardiography data, and CMR parameters between the KD groups. The proportions of patients with primary and secondary endpoints were assessed, and Kaplan-Meier analysis was used to estimate the cumulative probability of endpoints during the follow-up. A P value <0.05 was considered to indicate statistical significance.
Results
As shown in Figure S1, a total of 482 patients were diagnosed with KD on admission. After 27 patients were excluded for incomplete follow-up data, 455 patients with KD were included in our study and divided into the non-CA involvement group (n=313; 180 males; age 2.2±1.3 years) and CA dilation-only group (n=142; 86 males; age 2.1±1.1 years). Among the patients, 6.2% (28/455) had an onset age of <1 year. There were 50 patients with KD who underwent CMR examinations during the recovery people in the non-CA involvement group, and there were 22 of these patients in the CA dilation-only group. The basic vital signs and onset data of patients with KD at baseline are shown in Table 1.
Table 1. Baseline clinical data of the subgroups of patients with KD.
| Parameter | No involvement (n=313) | Dilation only (n=142) | P value |
|---|---|---|---|
| Demographic data | |||
| Age (years) | 2.2±1.3 | 2.1±1.1 | 0.76 |
| Male gender | 180 (57.5) | 86 (60.6) | 0.54 |
| Basic vital signs | |||
| DBP (mmHg) | 80.3±16.7 | 77.4±11.7 | 0.81 |
| SBP (mmHg) | 52.8±13.9 | 55.7±15.2 | 0.63 |
| HR (bpm) | 109.8±30.4 | 112.6±26.4 | 0.89 |
| Onset data | |||
| Incomplete KD | 87 (27.8) | 36 (25.4) | 0.59 |
| Oral changes | 273 (87.2) | 127 (89.4) | 0.50 |
| Conjunctivitis | 270 (86.3) | 125 (88.0) | 0.61 |
| Rash | 216 (69.0) | 99 (69.7) | 0.88 |
| Extremity changes | 154 (49.2) | 74 (52.1) | 0.57 |
| Cervical lymphadenopathy | 131 (41.9) | 48 (33.8) | 0.10 |
| Treatment | |||
| IVIG | 313 (100.0) | 142 (100.0) | 0.99 |
| Aspirin | 170 (54.3) | 74 (52.1) | 0.24 |
| Warfarin | 0 (0.0) | 0 (0.0) | 0.99 |
| Glucocorticoids | 22 (7.0) | 11 (7.7) | 0.57 |
Normally distributed continuous variables are expressed as the mean ± standard deviation, and categorical variables are expressed as frequencies and percentages. DBP, diastolic blood pressure; HR, heart rate; IVIG, intravenous immunoglobulin; KD, Kawasaki disease; SBP, systolic blood pressure.
Laboratory analysis
In our study population, all the patients underwent laboratory analysis before IVIG treatment, and in a mean 5.6 days after IVIG treatment, 247 in the non-CA involvement group and 88 in the CA dilation-only group underwent the same laboratory analysis. The laboratory parameters were not significantly different between the two groups of patients with KD both before and after IVIG treatment (all P values >0.05; Table S1). Before IVIG treatment, the majority of patients in the non-CA involvement group and CA dilation–only group had elevated WBC (median 14.1×109/L vs. 13.9×109/L; P=0.57), CRP (median 87.4 vs. 85.6 mg/L; P=0.73), and ESR (median 66.5 vs. 59.8 mm/h; P=0.15). After standardized treatment, the laboratory parameters of patients with KD returned to normal levels, with several patients showing mild abnormalities.
Electrocardiographic abnormalities
In our study, only 5.9% (27/455) of the patients with KD showed abnormalities on electrocardiography. After treatment, this proportion decreased to 2.2% (10/455). As it shown in Table S2, no significant differences in ST-T changes, prolonged PR, ventricular premature beat, or pre-excitation syndrome were observed between the two groups regardless of treatment (all P value >0.05).
Echocardiographic changes
The echocardiography results at baseline, 1 month, and 1 year were compared between patients with KD and without CA involvement and those with CA dilation only (Table 2). At baseline, the non-CA involvement group and CA dilation-only group were not significantly different in terms of LVEF (67.8%±13.6% vs. 68.1%±10.3%; P=0.13) and FS (37.6%±5.3% vs. 35.4%±6.6%; P=0.25). The proportion of patients with KD with echocardiography abnormalities is detailed in Table 2. The ratio of systolic dysfunction (LVEF% <55%), valvular regurgitation, and pericardial effusion in patients with CA dilation only were not significantly different from that in patients with non-CA involvement (all P values >0.05). At 1 month, the majority of the echocardiographic abnormalities in the two groups of patients had recovered. There was also no difference in echocardiography results between the two groups of patients with KD (all P values >0.05). There were 97 patients with KD and non-CA involvement and 28 with CA dilation only who received echocardiography examinations at 1 year from onset, with the echocardiography results of the two groups of patients being similar at 1-year follow-up (all P values >0.05).
Table 2. Echocardiography follow-up in the subgroups of patients with KD.
| Parameter | Baseline | 1-month follow-up | 1-year follow-up | |||||
|---|---|---|---|---|---|---|---|---|
| No involvement (n=313) | Dilation only (n=142) | No involvement (n=313) | Dilation only (n=142) | No involvement (n=97) | Dilation only (n=28) | |||
| LVEF (%) | 67.8±13.6 | 68.1±10.3 | 66.3±13.4 | 64.2±11.4 | 64.7±12.5 | 68.1±14.5 | ||
| FS (%) | 37.6±5.3 | 35.4±6.6 | 38.4±5.8 | 37.3±6.2 | 37.1±7.2 | 39.0±5.9 | ||
| LVEF <55% | 27 (8.6) | 4 (2.8) | 0 (0.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | ||
| CA dilation | 0 (0.0) | 142 (100.0) | 0 (0.0) | 15 (10.6) | 0 (0.0) | 2 (7.1) | ||
| Valvular regurgitation | 73 (23.3) | 31 (21.8) | 10 (3.2) | 2 (1.4) | 3 (3.1) | 0 (0.0) | ||
| MR | 40 (12.8) | 21 (14.8) | 5 (1.6) | 2 (1.4) | 2 (2.1) | 0 (0.0) | ||
| TR | 40 (12.8) | 17 (12.0) | 5 (1.6) | 0 (0.0) | 1 (1.0) | 0 (0.0) | ||
| AR | 25 (8.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | ||
| Pulmonary regurgitation | 10 (3.2) | 0 (0.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | ||
| Pericardial effusion | 25 (8.0) | 7 (4.9) | 0 (0.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | ||
Normally distributed continuous variables are expressed as the mean ± standard deviation, and categorical variables are expressed as frequencies and percentages. AR, aortic regurgitation; CA, coronary artery; FS, fractional shortening; KD, Kawasaki disease; LVEF, left ventricular ejection fraction; MR, mitral regurgitation; TR, tricuspid regurgitation.
CMR parameters
There were 50 patients with KD with non-CA involvement and 22 patients with CA dilation only who underwent CMR examinations. Table 3 shows the baseline CMR parameters of the two groups of patients with KD. For cardiac function, the myocardial systolic function of patients with KD with non-CA involvement was not different from that of patients with CA dilation only in terms of GRS (38.3%±18.7% vs. 39.9%±20.5%; P=0.20), GCS (–18.7%±6.8% vs. –18.3%±7.2%; P=0.38), and GLS (–13.2%±3.7% vs. –13.4%±4.1%; P=0.17). To assess myocardial characteristics, the native T1 value of myocardium in patients with non-CA involvement was 1,296.5±74.1 msec, while that in patients with CA dilation only was 1,313.3±80.5 msec (Figure 2A) (P=0.21); there was no significant difference in global T2 values between the two groups of patients with KD (38.2±4.1 vs. 38.1±3.5 msec; P=0.53) (Figure 2B), and only 1 patient was LGE positive in each of the non-CA involvement (1/50, 2.0%) group and CA dilation-only (1/22, 4.5%) (P=0.55) groups.
Table 3. Comparison of CMR parameters between subgroups of patients with KD.
| Parameter | No involvement (n=50) | Dilation only (n=22) | P value |
|---|---|---|---|
| Demographic information | |||
| Age (years) | 6.2±4.4 | 6.0±3.9 | 0.77 |
| Male gender | 34 (68.0) | 14 (63.6) | 0.72 |
| BSA (m2) | 0.7±0.2 | 0.8±0.3 | 0.25 |
| HR (beats/min) | 83.4±13.6 | 92.7±12.2 | 0.12 |
| Onset information | |||
| Age onset (years) | 4.3±2.2 | 4.9±3.3 | 0.54 |
| Interval between onset and CMR (days) | 370.4±277.5 | 420.7±329.4 | 0.06 |
| Incomplete KD | 8 (16.0) | 3 (13.6) | 0.47 |
| IVIG resistant | 10 (20.0) | 4 (18.2) | 0.33 |
| CMR parameters | |||
| LVEDV (mL/m2) | 67.7±14.3 | 72.9±10.4 | 0.29 |
| LVESV (mL/m2) | 23.2±7.7 | 22.8±11.4 | 0.63 |
| LVSV (mL/m2) | 44.7±9.2 | 48.5±12.8 | 0.67 |
| LV long axis dimension (mm) | 67.2±14.5 | 67.8±18.4 | 0.89 |
| LV transverse dimension (mm) | 37.4±6.3 | 38.5±4.4 | 0.81 |
| LV septal thickness (mm) | 7.3±2.7 | 6.8±2.3 | 0.47 |
| GRS (%) | 38.3±18.7 | 39.9±20.5 | 0.20 |
| GCS (%) | −18.7±6.8 | −18.3±7.2 | 0.38 |
| GLS (%) | −13.2±3.7 | −13.4±4.1 | 0.17 |
| LGE | 1 (2.0) | 1 (4.5) | 0.55 |
Normally distributed continuous variables are expressed as the mean ± standard deviation, and categorical variables are expressed as frequencies and percentages. BSA, body surface area; CMR, cardiac magnetic resonance; GCS, global circumferential strain; GLS, global longitudinal strain; GRS, global radial strain; HR, heart rate; IVIG, intravenous immunoglobulin; KD, Kawasaki disease; LGE, late gadolinium enhancement; LV, left ventricle; LVEDV, left ventricle end-diastolic volume index; LVESV, left ventricle end-systolic volume index; LVSV, left ventricle stroke volume.
Figure 2.
Comparison of global native T1 value (A) and T2 value (B) between patients with KD with non-CA involvement and those with CA dilation only. CA, coronary artery; KD, Kawasaki disease; ns, no significant differences between patients with KD with non-CA involvement and those with CA dilation only.
Clinical outcomes
Among the two groups of patients with KD, a median of 4.2 [interquartile range (IQR), 1.2–8.6] years of follow-up was conducted, and 45.3% (206/455) of the patients had a follow-up of over 5 years. It was found that none of the patients with non-CA involvement or CA dilation only reached the primary endpoint (P=0.99). As for secondary endpoints, the rates of mild reduced cardiac function, persistent mild AVB, or other kinds of arrhythmias and residual cardiovascular symptoms were 0.0% (0/313) and 0.0% (0/142), 2.9% (9/313) and 2.8% (4/142), and 4.8% (15/313) and 6.3% (9/142) in the non-CA involvement group and CA dilation-only group, respectively. Event-free survival was approximately the same between the two groups (P=0.34; Figure 3).
Figure 3.
Kaplan-Meier analysis of the subgroups of patients with KD. KD, Kawasaki disease.
Discussion
To the best of our knowledge, this study is the first to conduct a comprehensive evaluation of patients with KD with CA dilation only using a follow-up of clinical, echocardiography, and CMR data. Our study identified the characteristics of children with KD and CA dilation only at onset and during recovery, which were similar to those of children and KD but non-CA involvement. The two groups of patients with KD showed abnormal laboratory, electrocardiography, and echocardiography findings at onset, but these recovered after IVIG treatment. There were no significant differences in the clinical, echocardiography, or CMR parameters between the two groups, and they shared a favorable medium-long-term prognosis.
KD is an acute type of vasculitis and occurs primarily in young children, with multisystem involvement being present in the acute phase (9). Our study found the majority of patients with KD showed elevation in WBC, CRP level, and ESR, and a portion of the patients showed abnormalities in N% and L%. The laboratory abnormalities recovered after treatment. The trend in laboratory indicators in our study is consistent with that in Tremoulet et al.’s study (20). We speculate the recovery of elevated laboratory indices was due to IVIG treatment, a conventional therapy for KD, which effectively reduces inflammatory and immune responses and leads to the normalization of multisystem involvement in children after treatment (21,22).
Echocardiography is priorly recommended for the dynamic assessment of cardiovascular injuries in patients with KD. We continuously observed the noncoronary cardiovascular abnormalities of patients with KD with non-CA involvement and those with CA dilation only at baseline, 1 month, and 1 year and found that 23.2% and 21.8%, respectively, had valvular regurgitation at baseline. No significant differences were observed between the two groups. At 1-month follow-up, the majority of noncoronary cardiovascular abnormalities had recovered. Previous studies have indicated that patients with KD may exhibit noncoronary cardiovascular abnormalities on echocardiography examinations during the acute phase (9,23), but the majority recover by the chronic phase (24,25). This is consistent with our findings and attributable to the standard treatment and recovery of myocardial inflammation.
Furthermore, we examined the cardiac morphology and function of patients with KD with CA dilation only and those with non-CA involvement using CMR. We found no differences in morphology or function parameters between the two groups of patients. Compared with echocardiography, CMR is preferable for in vivo myocardial tissue characterization in patients KD. Myocardial T2 maps reflect free tissue water content and can be used to detect myocardial edema (26,27). Native myocardial T1 maps reflect several alterations in myocardial tissue composition, such as edema (28), necrosis, and fibrosis (29,30). Previous pathological studies have reported mild lymphocytic infiltration, hypertrophy, degeneration, disarray, and fibrosis in patients with KD without CA lesions (31,32), which may cause abnormal T1 and T2 values (14). Based on the results of our study, we speculate that the microstructural changes in patients with CA dilation only during recovery are similar to those in patients with KD with non-CA involvement. There was 1 patient in each group that exhibited LGE, and we believe it was caused by the ongoing effects of myocardial inflammation that began in the acute phase (9).
Finally, we analyzed the medium-long-term prognosis of patients with KD with non-CA involvement and of those with CA dilation only. We found no adverse cardiovascular events in either group during a mean follow-up of 4.2 years. A nationwide survey in Japan indicated that the overall prognosis of patients with KD is relatively good (33). Although patients with KD and CAAs appear to have a higher risk of major adverse cardiac events (34) or coronary events (17), those patients with KD and normal CA exhibit normal cardiac findings during the follow-up (35).
Certain limitations to our study should be addressed. First, echocardiography was used to evaluate the CAs, and due to the retrospective study design, there might have been measurement inconsistency in the examinations, leading to grouping error. However, we selected the saved images from the echocardiography department, excluded the incomplete ones, and left those with better image quality. Two researchers measured the diameters of CAs again, and a third was consulted if there was any disagreement. Second, the number of patients who underwent CMR was relatively small, but CMR is not a routine examination for patients with KD. In addition to CMR, patients in our study also underwent electrocardiogram, echocardiography, and laboratory tests, all of which can reflect myocardial tissue to some extent. Therefore, a small number of patients undergoing CMR is somewhat acceptable. Moreover, CMR is unable to assess pathological changes within the CAs. Although the CA diameters of almost all the patients were in the normal range, further studies are required to determine the pathological changes. Third, we employed a single-center design, which inevitably introduced population bias. However, our sample was derived from largest pediatric medical center in Southwest China, and given that our diagnosis and treatment principles are strictly consistent with the most recent international guidelines, our findings may remain applicable regionally; nonetheless, further multicenter studies are warranted. Finally, the median follow-up time of 4.2 years was insufficiently long for long-term follow-up, and a longer observation time is required.
Conclusions
Comprehensive follow-up assessment integrating clinical, echocardiographic, and CMR data indicated no differences between patients with KD and CA dilation only and those with non-CA involvement; therefore, the same medium-long-term management algorithm is suggested for both of these patient groups.
Supplementary
The article’s supplementary files as
Acknowledgments
The authors would like to thank the Information Department of West China Second University Hospital for providing a portion of the clinical data.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the declaration of Helsinki and its subsequent amendments and was approved by the IRB of West China Second University Hospital (No. 2023095). The requirement for individual consent was waived due to the retrospective nature of the analysis.
Footnotes
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2772/rc
Funding: This study was supported by the National Natural Science Foundation of China (Nos. 82120108015, 82471970, 82102020, 82071874, and 81971586) and the Sichuan Science and Technology Program (No. 2020YJ0029).
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2772/coif). The authors have no conflicts of interest to declare.
Data Sharing Statement
Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2772/dss
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