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Coronary thrombosis and myocardial ischemia in Kawasaki disease: a case report

BMC Cardiovascular Disorders volume 24, Article number: 473 (2024) Cite this article

Abstract

Background

Coronary artery thrombosis and myocardial ischemia caused by giant coronary aneurysms are the main causes of death in children with Kawasaki disease. The use of thrombolytic therapy in children with Kawasaki disease who have coronary thrombosis is a controversial topic, especially with respect to the timing of treatment.

Case presentation

In this article, we report a case of a child aged two years and nine months with Kawasaki disease whose coronary arteries had no involvement in the acute phase. However, by only one week after discharge, the patient returned because we found giant coronary aneurysms complicated by thrombosis via echocardiography. Despite aggressive thrombolytic therapy, the child developed myocardial ischemia during thrombolytic therapy. Fortunately, because of timely treatment, the child’s thrombus has dissolved, and the myocardial ischemia has resolved.

Conclusions

This case suggests that for patients at high risk of coronary artery aneurysms, echocardiography may need to be reviewed earlier. Low-molecular-weight heparin should be added to antagonize the early procoagulant effects of warfarin when warfarin therapy is initiated. In the case of first-detected coronary thrombosis, aggressive thrombolytic therapy may be justified, particularly during the acute and subacute phases of the disease course.

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Background

Patients with giant coronary aneurysms due to Kawasaki disease (KD) are at high risk of thrombosis [1]. Coronary artery thrombosis may lead to myocardial ischemia which is the main cause of sudden death in children after KD [2]. The use of thrombolytic therapy in children with KD who have coronary thrombosis is a controversial topic, especially regarding the timing of treatment for nonmyocardial ischemia. Herein, we report a case of a child with KD without a coronary aneurysm in the acute phase. However, echocardiography revealed a giant coronary aneurysm complicated by thrombosis one week after discharge from the hospital. Thrombolytic therapy was administered to the child, despite the initial absence of myocardial ischemia. Despite the aggressive thrombolytic therapy, the child developed a thrombus elsewhere and suffered from myocardial ischemia. Thankfully, the child’s symptoms of myocardial ischemia were relieved after receiving timely thrombolytic therapy, which resolved the thrombus.

Case presentation

A male toddler, aged two years and nine months, was admitted to the hospital with a fever lasting four days, scattered red skin rashes for two days, and conjunctival hyperemia for one day. Antibiotics were given at the local hospital but did not improve symptoms. Physical examination at admission revealed a high fever, tachycardia, conjunctival hyperemia in both eyes, red skin rash on the face and trunk, strawberry tongue, cervical lymphadenopathy in the right neck, and redness at the site of Bacille Calmette–Guèrin inoculation. The subject weighed 12.5 kg and was 97 centimeters tall. Laboratory examination revealed the following: white blood cells, 16.37 × 109/L; neutrophils, 80.6%; lymphocytes, 12.8%; monocytes, 5.6%; hemoglobin, 127 g/L; platelets, 292 × 109/L; C-reactive protein (CRP), 97.13 mg/L; serum sodium, 128 mmol/L; erythrocyte sedimentation rate, 89 mm/h; alanine aminotransferase, 221 U/L; aspartate aminotransferase, 140 U/L; direct bilirubin, 10.7 µmol/L; triglycerides, 2.72 mmol/L; D-dimer, 4.81 mg/L; fibrinogen, 5.69 g/L; brain natriuretic peptide (BNP), 1569 pg/ml; and procalcitonin, 2.92 ng/ml. The electrocardiogram (ECG) at admission revealed sinus tachycardia, with a normal ST segment (see Additional file 1 A). The timeline of treatment is shown in Fig. 1. A diagnosis of KD was made. Once admitted, the patient was given intravenous immunoglobulin (IVIG) at a dose of 25 g [2 g/kg] and oral aspirin (200 mg [16 mg/kg] every 8 h) but still had a persistent fever 36 h after the administration of IVIG. A re-check of liver function after three days revealed an albumin level of 31.4 g/L and alanine aminotransferase level of 72 U/L. Considering IVIG resistance, methylprednisolone at a dose of 25 mg [2 mg/kg] was given intravenously every 12 h. After three days of intravenous methylprednisolone, the body temperature returned to normal. Methylprednisolone at a dose of 4 mg every 8 h as well as a small dose of oral aspirin (50 mg per day) were given. A routine blood test before discharge revealed white blood cells (16.52 × 109/L), neutrophils (53.1%), lymphocytes (31.9%), monocytes (14.3%), hemoglobin (115 g/L), platelets (626 × 109/L), and CRP (4.32 mg/L).

Fig. 1
figure 1

Timeline of treatment. IVIG: intravenous immunoglobulin. TTE: transthoracic echocardiography. ECG: electrocardiograph. LAD: left anterior descending artery

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On the fourth day after admission, ultrasonography (Fig. 2A) revealed that the patient’s coronary arteries had no involvement as follows: left coronary artery (LCA), 2.4 mm (Z = 0.97); left anterior descending artery (LAD), 2.2 mm (Z = 1.83); circumflex artery, 1.5 mm (Z=-0.02); and right coronary artery (RCA), 2.2 mm (Z = 1.09). The patient was discharged after 7 days of treatment. After being discharged, he continued to take methylprednisolone tablets of 12 mg per day in 3 divided doses and oral aspirin (50 mg [4 mg/kg] daily). At the same time, the methylprednisolone dose was weaned 4 mg every 3 days.

Fig. 2
figure 2

Changes in transthoracic echocardiography (TTE). A The coronary artery had no involvement on the 8th day after onset. B TTE image showing giant aneurysms in the left coronary artery (LCA), left anterior descending artery (LAD) and right coronary artery (RCA). C TTE revealed a 16.8 mm×8.2 mm thrombosis in the LAD. D TTE revealed thrombosis in the LAD artery and new thrombosis in the RCA. E TTE revealed that the thrombosis in the LAD artery decreased and that there was no thrombus in the RCA. F There was no obvious thrombus in the left or right coronary arteries on echocardiography

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After one week, the patient visited the outpatient clinic, and a follow-up echocardiogram revealed left and right coronary artery aneurysm-like expansion (Fig. 2B). The child exhibited no symptoms and was scheduled for a follow-up echocardiogram in accordance with the agreed-upon plan with the parents during the discharge process. The LCA exhibited a tumor-like enlargement measuring 7.5 mm in inner diameter (Z = 14.67). Similarly, the LAD demonstrated a tumor-like expansion, with the widest part measuring 12.0 mm in inner diameter (Z = 30.22). The RCA also presented a tumor-like expansion, featuring an inner diameter of 3.2 mm at its opening and reaching 10.0 mm at its widest point (Z = 22.31). ECG at readmission revealed sinus rhythm, occasional ventricular premature beats, and a normal ST segment (see Additional file 1B). Owing to giant coronary aneurysms, the child was readmitted to the hospital and treated with oral warfarin 0.5 mg daily, aspirin 50 mg daily, and metoprolol 6.25 mg every 12 h. However, two days later, echocardiography (Fig. 2C) revealed a 16.8 mm×8.2 mm thrombosis in the LAD. The child did not exhibit prolonged uncontrollable crying, irritability, dyspnea, syncope, or excessive sweating. The patient’s heart rate fluctuated between 112 and 128 beats per minute. At that time, the prothrombin time (PT) was 11.7 s, the international normalized ratio (INR) was 0.97, and the activated partial thromboplastin time (APTT) was 30.8 s. Due to thrombosis, 4400 IU/kg urokinase was given intravenously, and then, 4400 IU/kg/h urokinase was pumped for thrombolysis. Warfarin was discontinued and replaced with low-molecular-weight heparin (1250 U every 12 h) administered subcutaneously, while aspirin was continued orally. After thrombolysis, platelet counts were measured on the 1st, 2nd, 6th, and 11th days, and fibrinogen concentrations were measured daily during the thrombolysis period. On the 6th day after admission, the patient was diagnosed with myocardial ischemia, as we detected abnormal elevations in high-sensitivity troponin T (0.689 ng/mL) and creatine kinase MB (19.40 ng/mL), along with an abnormal ECG. ECG revealed occasional premature ventricular beats, deep q waves in V1 precordial leads, and mild changes in the ST segment (ST depression across leads III and AVF) (Fig. 3). On the seventh day, the coagulation panel was checked for PT 71.5 s, INR 6.07, and APTT 59.5 s, and there was obvious bleeding at the femoral vein cannulation site. The administration of urokinase and subcutaneous injection of low-molecular-weight heparin were stopped, whereas warfarin (introduced two days prior) and aspirin were continued orally. The femoral vein cannulation was removed, and vitamin K1 (10 mg) was administered intramuscularly. Additionally, a fresh plasma transfusion (130 mL), a human fibrinogen infusion (0.5 g daily), and sedation therapy were administered. Two days later, when the coagulation function improved, urokinase was given once again (4400 IU/kg/h, 3 h/time, two times every day). Echocardiography (Fig. 2D) on the 10th day after admission revealed that the thrombosis in the LAD was still present, and a new thrombus was found in the RCA. Two weeks after the application of urokinase, the thrombus in the LAD decreased, and the thrombus in the RCA had disappeared (Fig. 2E). Additionally, the ECG (see Additional file 1 C), hypersensitivity troponin T, and creatine kinase MB results returned to normal, leading to the discontinuation of urokinase. The final diagnosis was KD complicated by giant aneurysms, coronary artery thrombosis, and myocardial ischemia. The patient was discharged again after 23 days of treatment. The patient continued taking warfarin at a dose of 1 mg daily and aspirin at a dose of 50 mg daily to prevent the reformation and expansion of coronary thrombosis after discharge. At the second discharge, the PT was 29.4 s, the INR was 2.47, and the APTT was 46.0 s. After a two-week period of outpatient monitoring and follow-up, echocardiography revealed that the thrombus in the LAD decreased in size. After one month, no obvious thrombus was found in the dilated left or right coronary artery on echocardiography (Fig. 2F). After discharge, the child was treated with continuous warfarin and aspirin over a four-year period. Warfarin was discontinued for a period of one week because of the occurrence of tongue bleeding with hematoma. The dosage of warfarin was subsequently adjusted in accordance with the child’s weight and the results of the INR monitoring (1–1.5 mg, daily). Furthermore, metoprolol was administered orally. After three years, echocardiography revealed a large tumor-like expansion of the left and right coronary arteries and the left anterior descending branch. The inner diameter of the left coronary artery was 3.5 mm (Z = 2.61), and the inner diameter of the left anterior descending branch was approximately 13.1 mm (Z = 29.81). The inner diameter of the circumflex branch was 2.5 mm (Z = 1.59). The inner diameter of the right coronary artery was 2.5 mm (Z = 0.8) at the beginning and approximately 11.6 mm (Z = 22.43) at dilation. There was no obvious thrombus in the left or right coronary arteries. A contrast-enhanced computed tomography (CT) scan (Fig. 4) after four years revealed that the distal diameter of the LCA was approximately 5.1 mm (Z = 6.08), whereas the luminal diameter of the LAD was significantly dilated to approximately 10.7 mm (Z = 22.60). The proximal segment of the RCA was dilated with a diameter of approximately 5.7 mm (Z = 7.91). Calcifications were present in the LAD and RCA vessel walls.

Fig. 3
figure 3

Electrocardiography (ECG) demonstrated occasional ventricular premature beats, deep q waves in V1 precordial leads, and mild changes in the ST segment (ST depression across leads III and AVF)

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Fig. 4
figure 4

Contrast-enhanced computed tomography scan four years after the onset of Kawasaki disease

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Discussion and conclusions

KD is an acute fever and rash disease that mainly occurs in infants under five years of age [3]. KD is currently the most common cause of acquired cardiovascular disease in pediatric patients in China. Coronary aneurysms due to KD may cause sudden death [2]. The aneurysm forms approximately 12 days after the onset of KD [4]. Treatments to prevent the development of coronary artery lesions (CALs) should be given within 10 days after the onset of KD [4].

To detect CALs, echocardiography should be performed both within one to two weeks and four to six weeks after treatment [5, 6]. For patients with coronary artery dilatation (Z > 2.5), echocardiography is needed at least twice a week until coronary dilation stops progressing. In this case, echocardiography did not indicate coronary artery dilation in the acute phase, so we sent the child home for a regular outpatient follow-up visit one week later. At that time, echocardiography revealed that giant coronary aneurysms were present. In high-risk children with CALs, even if the initial echocardiogram does not reveal any dilation, it is recommended that it be repeated at an earlier stage, ideally within a week and during the first 10–14 days. In addition, patients who have been treated with steroids may exhibit occult inflammation, necessitating more frequent echocardiograms.

There are two points to note in the evaluation of giant coronary aneurysms caused by KD. First, the use of echocardiography alone is clinically problematic in the acute, subacute, and remote phases of a cardiovascular event. According to the recommendations of the JCS/JSCS 2020 guidelines [4], for giant aneurysms or coronary stenotic lesions, coronary imaging modalities (CT, magnetic resonance imaging, and coronary angiography) should be considered during the convalescent phase, one year later, and then every 1–5 years. Another issue that requires consideration is the presence of systemic aneurysms. Patient with KD complicated with multiple coronary aneurysms and coronary thrombosis, may have systemic arterial involvement, such as subclavian or abdominal arterial aneurysms. The report by Filiz Ekici et al [7]. described a 4-month-old patient with KD who suffered from multiple giant coronary thrombi and myocardial ischemia due to the presence of “superlarge” aneurysms in the coronary arteries. In addition to coronary aneurysms, angiography revealed multiple giant aneurysms and stenoses in the subclavian artery, celiac artery, and iliac artery. For children with multiple coronary aneurysms, especially giant coronary artery aneurysms, vascular ultrasound, contrast-enhanced CT, magnetic resonance imaging, or angiography may be needed to confirm the presence of systemic aneurysms. Therefore, a second method for morphologic assessment of the coronary artery and other high-risk arteries, should have been performed much earlier in patients with giant aneurysms. This patient was particularly resistant to IVIG and had multiple large aneurysms.

Many scoring systems, such as the Kobayashi score, are used to predict IVIG resistance and CALs [8]. Based on the Kobayashi score, the day of illness at initial treatment, age in months, percentage of white blood cells representing neutrophils, platelet count, and serum aspartate aminotransferase, sodium, and C-reactive protein levels are used to assess the risk score for IVIG resistance. According to the Kobayashi scoring system, the child’s IVIG resistance score was 9, and the probability of developing IVIG resistance was 87.5%. In addition, owing to the heterogeneity of KD, different racial groups have shown different predictive results when the same scoring system is used. We also summarized our own scoring system according to our hospital data [9]. In both the Kobayashi scoring system and our own system, this child was at high risk of IVIG resistance. For high-risk IVIG-resistant children, early use of corticosteroids is advocated. Jessica Green et al [10]. analyzed pooled data from eight studies on corticosteroid therapy for KD and reported that, compared with not using corticosteroids in the acute phase of KD in children, the use of corticosteroids can reduce the incidence of coronary aneurysm, shorten the time for CRP and ESR normalization, shorten the hospital stay, and shorten the duration of clinical symptoms such as fever and rash. Compared with unused corticosteroids, first-line corticosteroid therapy is more effective in reducing coronary artery abnormalities, but this effect is not significant in the second-line treatment subgroup. The recommended dosage and duration of treatment are as follows: prednisone [1–2 mg/(kg-d), taken orally in the morning as a single dose, with a total daily dose of < 60 mg/d] or methylprednisolone [1–2 mg/(kg-d), intravenous infusion, 1–2 times daily]. Once body temperature and CRP levels return to normal, the treatment should switch to oral prednisone [1–2 mg/(kg-d), taken orally in the morning as a single dose] and tapering of the dose should begin, gradually reducing and stopping treatment within 15 days [11].

Furthermore, for children with high-risk IVIG resistance and CALs, some researchers suggest more aggressive treatment with cytokine inhibitors (for example, infliximab) as initial therapy. In a retrospective study, the combination of IVIG and infliximab as initial therapy was more effective than IVIG therapy alone in reducing the need for further treatment for children with KD who initially presented with CALs [12]. A systematic review and meta-analysis [13] demonstrated that the combined infliximab group exhibited a significantly greater treatment response than the IVIG alone group did, particularly in high-risk patients. In addition, the incorporation of infliximab demonstrated favorable effects on the Z scores of the LAD and RCA, irrespective of whether it was employed as an initial treatment or an additional treatment. Moreover, infliximab had significant effects on treatment response in the Asian cohort compared with IVIG treatment. Furthermore, the beneficial effects of infliximab did not increase the risk of adverse events.

For patients with KD resistant to IVIG, a second dose of IVIG, intravenous methylprednisolone, or infliximab is recommended [4, 5]. According to a network meta-analysis published in 2023 [14], the use of infliximab in patients with IVIG resistance appears to be more effective in treating acute disease. Infliximab, methylprednisolone, and a second IVIG infusion did not significantly affect the risk of developing a coronary artery aneurysm. In this case, methylprednisolone was administered at a dose of 4 mg/(kg-d) divided into two intravenous infusions and gradually tapered as the CRP level normalized. Infliximab is primarily employed as a rescue treatment for KD that is unresponsive to IVIG or IVIG combination therapy in cases of severe KD [5]. Following treatment with IVIG and methylprednisolone, the patient’s temperature returned to normal, there was no further fever, and CRP levels returned to baseline. Consequently, despite the discovery of a giant coronary aneurysm on day 19 of the disease course, the decision was made not to utilize infliximab as a step-up therapy.

Masaru Miura [15] reported that large aneurysms, male sex, and resistance to IVIG were associated with coronary events. For children with KD who suffer from giant coronary aneurysms, myocardial ischemia caused by newly developed thrombi at the narrow entrance or exit of the coronary aneurysm is the leading cause of death [2]. Patients with giant coronary aneurysms (Z-score ≥ 10 or diameter ≥ 8 mm) have the highest risk of thrombotic occlusion [4]. Current guidelines mostly recommend the addition of anticoagulation agents, such as warfarin, for giant coronary aneurysms [4, 5, 16]. However, a web-based global survey of physicians [1] revealed significant differences in antithrombotic therapy for patients with coronary aneurysms after KD. Surprisingly, 26% of the physicians did not recommend anticoagulation for patients with giant coronary aneurysms. This may be related to the fact that some of the respondents were noncardiovascular or rheumatology physicians and had less experience in the diagnosis and treatment of KD [1]. Warfarin has a slow onset of action, typically taking several days to reach rapid anticoagulant therapy levels [17]. In the early stages of warfarin treatment, a paradoxical procoagulant effect can be observed. One study revealed that the risk of ischemic stroke may temporarily increase after the initiation of warfarin therapy [18]. Regrettably, in this instance, the child developed coronary thrombosis two days after receiving oral warfarin. At that time, the INR was still below 1.5. In contrast, low-molecular-weight heparin has several advantages. These include more predictable pharmacokinetics, rapid achievement of therapeutic levels of anticoagulation, and minimal monitoring [19]. To reduce the risk of thrombosis in newly detected giant coronary aneurysms, oral warfarin with concomitant low-molecular-weight heparin administration was given in our center. Low-molecular-weight heparin could be discontinued after INR values of 1. 5–2.5 were achieved. For patients at increased risk of thrombosis with giant aneurysms and a recent history of coronary artery thrombosis, “triple therapy” with aspirin, a second antiplatelet agent (such as clopidrogel), and anticoagulation with warfarin or low-molecular-weight heparin may be considered. Many studies of “triple therapy” in adults have shown that shorter treatment durations may reduce the risk of bleeding events without increasing the overall risk of major adverse cardiac events. However, long-term use may not reduce cardiovascular mortality but may increase the risk of adverse bleeding [20]. A single-center observational study [21] revealed that the overall bleeding risk in KD patients receiving “triple therapy” was low. We recommend short-term “triple therapy” for children with an extremely high risk of coronary thrombosis, such as those with multivessel coronary artery involvement, absolute coronary artery diameter ≥ 8 mm, thrombocytosis, and increased adhesiveness.

In retrospect, if we had initially treated a child with high-risk IVIG resistance or coronary artery aneurysm scores by administering glucocorticoids or even infliximab in addition to IVIG and aspirin, the incidence or degree of coronary artery aneurysm in this patient may have decreased. Second, performing echocardiographic evaluation earlier after discharge may have facilitated earlier detection of coronary artery aneurysms in this child. Subsequently, more aggressive treatment of the aneurysm according to established anticoagulation recommendations may have reduced the incidence of coronary thrombosis and improved the coronary prognosis. In addition, once a large coronary artery aneurysm is identified, the administration of oral warfarin with concomitant use of low-molecular-weight heparin until the INR reaches therapeutic levels to achieve anticoagulation goals and counteract the early procoagulant effect of warfarin may reduce the likelihood of thrombosis.

Acute myocardial infarction and death caused by thrombi are the most common within one to two years after the onset of KD [22]. Vascular occlusion in KD is thought to be caused by a mixed effect of vascular endothelial dysfunction, coronary blood flow obstruction, and abnormal coagulation of the fibrinogen lytic system [4, 23]. The diagnosis and severity are judged by abnormal changes in ST-T on electrocardiography, echocardiographic focal myocardial dyskinesia, elevated myocardial injury markers, and elevated BNP or NT-proBNP [4]. Our patient had ST-segment depression, changes in the deep q wave in the V1 precordial leads, and increases in troponin T and CK-MB, suggesting that he was suffering from myocardial ischemia.

Thrombolytic therapy, including alteplase, is recommended for adult patients with ischemia who develop significant symptoms within a short period of time. The timing of thrombosis can be clearly assessed, and the guidelines suggest administering therapy within 12 h of the onset of myocardial infarction [24]. However, thrombus formation in pediatric patients with KD occurs in dilated coronary arteries, and thrombi develop slowly. Therefore, complete blood occlusion is unlikely to occur within a short period of time. Consequently, clinical symptoms may not be as pronounced as they are in adult ischemic patients [25]. As a result, there is limited clinical experience with thrombolytic therapy in children with KD, particularly for treating asymptomatic coronary thrombosis after childhood KD [26, 27].

Urokinase, tissue plasminogen activator (t-PA) or modified t-PA are commonly used for thrombolysis treatment [4]. Urokinase has low tissue affinity and can activate the fibrinolytic system. In contrast, t-PA has high tissue affinity, and the modified t-PA has a longer biological half-life. Therefore, the latter two drugs can reduce the total dose and allow for rapid infusion in a single administration [4]. Our practical experience indicates that the thrombolytic effect of urokinase is highly effective. However, it is essential to be aware of the potential risk of bleeding. Previous studies [28] have documented the use of intravenous urokinase, heparin, and oral warfarin in the treatment of coronary thrombosis, with complete dissolution of thrombi observed in 9 out of 10 patients within 5–10 days. One patient discontinued treatment because of bleeding. Alteplase, a type of t-PA, was only approved for use in our hospital three years prior. The patient had undergone thrombolytic therapy five years prior. At that time, we used urokinase for first-line thrombolysis. Moreover, the fragmentation of the clot with microembolization to the distal coronary vascular bed is an unavoidable consequence of lysis. Therefore, anticoagulants such as intravenous heparin should be administered concurrently with thrombolysis to help prevent thrombosis and support thrombolytic therapy. On the 22nd day of the disease course, echocardiography revealed thrombosis in the left anterior descending artery. Although there were no signs of myocardial ischemia in this child at that time, we believed that it was important for the child to receive thrombolytic therapy, given that the first coronary thrombosis was detected within 1 month of the course of KD. The patient’s parents were informed of the necessity for thrombolysis and its possible side effects. The parents expressed their understanding and agreed to add the thrombolytic drug urokinase. Despite aggressive thrombolytic therapy, the child developed another thrombus in the right coronary artery and developed myocardial ischemia on day 26 of the course of the disease. After 18 days of thrombolysis with urokinase, there was a significant reduction in left coronary thrombosis and complete resolution of the right coronary thrombosis. On the 56th day of the disease course, echocardiography revealed that there was no thrombosis in either the left or right coronary arteries. Although there was a transient abnormality of coagulation function and blood oozing from the venous catheter during treatment, we adjusted the dose of urokinase without serious visceral hemorrhage or other complications, indicating that the use of urokinase thrombolysis for coronary thrombosis is safe and effective.

In summary, coronary artery aneurysm formation caused by CALs following KD is the most important hazard in acute and long-term KD. Giant coronary aneurysms may be combined with coronary thrombosis and even cause myocardial ischemia. For patients with a high risk of CALs, even if the coronary arteries are not dilated in the acute phase, echocardiography may still need to be reviewed earlier. To reduce the risk of thrombosis, low-molecular-weight heparin should be added to antagonize the early procoagulant effects of warfarin when warfarin therapy is initiated. Aggressive anticoagulation is recommended for newly detected giant coronary aneurysms. In the case of first-detected coronary thrombosis, aggressive thrombolytic therapy may be justified, particularly during the acute and subacute phases of the disease course.

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Abbreviations

KD:

Kawasaki disease

BNP:

Brain natriuretic peptide

CRP:

C-reactive protein

IVIG:

Intravenous immunoglobulin

LCA:

Left coronary artery

LAD:

Left anterior descending artery

RCA:

Right coronary artery

CAL:

Coronary artery lesions

PT:

Prothrombin time

INR:

International normalized ratio

APTT:

Activated partial thromboplastin time

CT:

Computed tomography

TTE:

Transthoracic echocardiography

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Acknowledgements

The authors thank the patient and his family for their participation in this study. The authors also thank Zhufei Xu (Dept. Pulmonology, Children’s Hospital, Zhejiang University School of Medicine) for close reading of the manuscript.

Funding

This work is supported, in part (interpretation of data and writing of the manuscript), by grants from The National Natural Science Foundation of China (No. 81970434).

Author information

Author notes

  1. Lichao Gao and Chunhong Xie contributed equally to this work.

Authors and Affiliations

  1. Department of Cardiology, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, 57 Zhugan Lane, 310003, Hangzhou, Zhejiang, P. R. China

    Lichao Gao, Chunhong Xie, Qing Zhang, Songling Fu, Jian Hu, Yiying Zhang & Fangqi Gong

  2. Department of IT Center, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, P. R. China

    Xiaofeng Wang

Authors
  1. Lichao Gao
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Contributions

L.G. and C.X. designed the case report, collected the data, drafted the initial manuscript, and revised the manuscript; Q.Z., X.W., S.F., J.H. and Y.Z. collected the data and revised the manuscript; F.G. conceptualized and designed the study and reviewed and revised the manuscript; and all the authors approved the final manuscript as submitted and agreed to be accountable for all aspects of the work.

Corresponding author

Correspondence to Fangqi Gong.

Ethics declarations

Ethics approval and consent to participate

The study was approved by the medical ethics committee of the Children’s Hospital of Zhejiang University School of Medicine (2021-IRB-217). The parents provided informed consent for this report.

Consent for publication

Written informed consent was obtained from the patient’s parents for all the manuscripts that included images and details. The authors have deidentified patient-specific information.

Competing interests

The authors declare no competing interests.

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Gao, L., Xie, C., Zhang, Q. et al. Coronary thrombosis and myocardial ischemia in Kawasaki disease: a case report. BMC Cardiovasc Disord 24, 473 (2024). https://doi.org/10.1186/s12872-024-04148-8

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Keywords

BMC Cardiovascular Disorders

ISSN: 1471-2261

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