Clinical Characteristics, Treatment, and Outcomes of Children with Severe Mycoplasma Pneumonia Complicated with Cardiac Thrombosis: A retrospective study

Clinical Characteristics, Treatment, and Outcomes of Children with Severe Mycoplasma Pneumonia Complicated with Cardiac Thrombosis: A retrospective study | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Clinical Characteristics, Treatment, and Outcomes of Children with Severe Mycoplasma Pneumonia Complicated with Cardiac Thrombosis: A retrospective study juan yang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8614234/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 10 You are reading this latest preprint version Abstract Objective: To explore the clinical characteristics, treatment, and outcomes of children with severe mycoplasma pneumonia (SMPP) complicated with cardiac thrombosis. Methods: Clinical data of 16 children with SMPP complicated with cardiac thrombosis, who were treated at three medical centers in China from July 2018 to April 2025, were retrospectively analyzed. Results: Among the 16 children, 11 were males and 5 were females, with an age of onset of 8.03 ± 2.17 years. All 16 children presented with fever and cough, while additional symptoms included dyspnea in 8 cases, chest pain in 7 cases, hemoptysis in 3 cases, and chest tightness in 1 case. A total of 15 children underwent testing for the Mycoplasma pneumoniae drug resistance genes 2063A>G and 2064A>G, of which 14 tested positive. The plasma D‑dimer levels of 16 children were 9.18 (6.57, 15.91) mg/L, all of which were higher than normal. Among the 16 children, 5 had decreased activity of anticoagulant proteins (protein C, protein S, antithrombin Ⅲ), and 8 tested positive for antiphospholipid antibodies. Chest CT scans of all 16 children showed pulmonary consolidation and (or) atelectasis, with pleural effusion present in 12 cases. In the 16 children, thrombosis was detected at 14.0(11.25, 17.25) days after the onset of illness. The locations of cardiac thrombosis included the right ventricle in 10 cases, the right atrium in 5 cases, and the left atrium in 1 case.Additionally, 11 cases had pulmonary vascular embolism, comprising 10 cases of pulmonary artery thrombosis and 1 case of pulmonary vein thrombosis. After anticoagulant treatment, cardiac thrombi disappeared in 11children. Five children who did not show improvement with anticoagulation underwent surgical thrombectomy. In the follow‑up of 16 children, lung imaging basically returned to normal, with no major hemorrhagic events or other adverse events. Conclusion: An early and thorough cardiac ultrasound examination should be performed in children with SMPP who present with chest pain, hemoptysis, significantly elevated D-dimer levels, pulmonary consolidation, atelectasis, and pericardial effusion. SMPP complicated by cardiac thrombosis, prognosis is good following anticoagulation or surgical treatment. Mycoplasma pneumonia Cardiac thrombosis Pulmonary vein thrombosis Pulmonary embolism children Introduction Mycoplasma pneumoniae (MP) is an important pathogen responsible for community-acquired pneumonia in children. In addition to causing typical pulmonary inflammation, it can lead to various pulmonary and extrapulmonary complications that affect the physical and mental health of the affected children [ 1 ] . Severe mycoplasma pneumonia (SMPP) can result in thrombosis in different body parts, with complex and varied clinical manifestations. Although cases of cardiac thrombosis are rare, potential hazards associated with this complication should not be overlooked. Cardiac thrombosis can lead to valve incompetence, chordae tendineae rupture, hemodynamic instability, heart failure, and arrhythmias. Dislodgement of a thrombus can result in outflow tract obstruction, causing coronary artery occlusion, heart failure, pulmonary embolism, stroke, and other serious complications, which significantly affects treatment outcomes and prognosis and has long-term effects on the quality of life of the child. However, the demographic characteristics, clinical features, risk factors, and prognosis of children with SMPP complicated with cardiac thrombosis remain unclear. Consequently, the present multicenter clinical sought to enhance clinicians’ awareness of this rare but serious complication, improve diagnostic and therapeutic levels, and provide references for the management and treatment of pediatric MP infections. Methods Study Subjects A retrospective analysis was conducted on the clinical data of 16 children diagnosed with SMPP combined with cardiac thrombus in the Department of Pediatrics at Shandong First Medical University Affiliated Provincial Hospital from July 2018 to April 2025. Inclusion criteria: (1) Patients aged 0–14 years; (2) those diagnosed with SMPP based on the “Expert Consensus on the Diagnosis and Treatment of Mycoplasma Pneumonia in Children” [ 2 ] ; (3) imaging findings indicating intracardiac thrombus: echocardiography showing hypoechoic or isoechoic/mixed echogenic masses within heart chambers; chest computed tomography angiography (CTA) indicating filling defects within cardiac cavities; and (4) those without underlying diseases related to hematologic, rheumatologic, or cardiovascular system. The study was approved by the Ethics Committee of Shandong First Medical University Affiliated Provincial Hospital (SWYX: No. 2024-067). The requirement for informed consent was waived because of the retrospective nature of the study. Statistical Methods All statistical analyses were conducted using SPSS 25.0 software. Categorical data were expressed as counts (percentages) and compared using the chi-square test and Fisher’s exact test. Non-normally distributed continuous data were expressed as the median (interquartile range) and analyzed using the Mann-Whitney U test. P < 0.05 was considered statistically significant. Results Basic Information of Patients Sixteen children were included in the analysis, of whom 11 were males and 5 were females, with an age of onset of 8.03 ± 2.17 years. None of the patients had a history of underlying diseases related to hematologic, rheumatologic, or cardiovascular system before admission. Neither parent had a history of venous thromboembolism. The duration of the illness prior to admission for the children was 11.69 ± 3.80 days, and cardiac thrombus formation was detected on day 14.0 (11.25, 17.25) of the disease course. Clinical Manifestations and Physical Examination All 16 children exhibited fever and cough, with a duration of fever of 10.81 ± 2.77 days and a peak temperature of 39.5 (39.1, 40.4) °C.Other symptoms included dyspnea in 8 cases, chest pain in 7 cases, hemoptysis in 3 cases, and chest tightness in 1 case. Physical examinations revealed moist rales in 13 cases, tachycardia in 11 cases, and decreased localized breath sounds in the lungs in 8 cases, with no significant murmurs detected upon cardiac auscultation. All 16 children had blood pressure within the normal range, while 3 cases exhibited peripheral oxygen saturation below 0.95. Inflammatory Indicators and Pathogen Detection All 16 children presented elevated infection markers, with a leukocyte count of 13.54 (8.5, 24.92) × 10^9/L, a neutrophil percentage of 74.40 (64.7, 89.3)%, C-reactive protein level of 33.58 (18.42, 230 mg/L), and lactate dehydrogenase level of 527.50 (312, 1510) U/L. Two children exhibited mild anemia, while the hemoglobin levels of the remaining children were within the normal range. Among 15 children tested, 14 were positive for mycoplasma resistance genes 2063A > G and 2064A > G. All 16 children underwent testing for Epstein-Barr virus (EBV), sputum culture, and common respiratory viruses. Among them, 5 cases tested positive for EBV, 4 cases for rhinovirus, and 2 cases for respiratory syncytial virus. Sputum cultures identified Haemophilus influenzae, Streptococcus pneumoniae, and Staphylococcus aureus, with each pathogen positive in 1 case. Coagulation Function Tests and Thrombophilia-related Tests The plasma D-dimer levels in the 16 children were measured at 9.18 (6.57, 15.91) mg/L (reference value: 0–0.5 mg/L), with 15 cases exceeding 5.0 mg/L. Fibrinogen levels and platelet counts were within the normal range. Among the 16 children, 5 had decreased activity of anticoagulant proteins (protein C, protein S, antithrombin Ⅲ), and 8 tested positive for antiphospholipid antibodies. Five cases underwent thrombophilia gene testing, and no relevant gene mutations were found. Autoimmune Disease Testing Among the 16 children, 8 tested positive for antiphospholipid antibodies. Specifically, 6 cases were positive for lupus anticoagulant, 5 for anticardiolipin antibodies, and 3 for anti-β2 glycoprotein I antibodies. Notably, 3 cases were positive for both lupus anticoagulant and anticardiolipin antibodies. Additionally, 5 cases tested positive for antinuclear antibodies. No abnormalities were detected in the tests for anti-double-stranded DNA antibodies, anti-Smith antibodies, anti-SSA antibodies, or anti-SSB antibodies. Myocardial Injury Markers and Liver Function Tests All 16 children underwent testing for myocardial injury markers. Three cases showed elevated creatine kinase isoenzyme levels, and four cases demonstrated increased B-type natriuretic peptide levels, while the troponin T results were within normal ranges. Liver function tests indicated elevated alanine aminotransferase levels in 8 cases and decreased albumin levels in 9 cases, whereas bilirubin levels and prothrombin time remained normal. Imaging Examination Chest CT scans of all 16 children revealed pulmonary consolidation and/or atelectasis, with 12 cases presenting associated pleural effusion. Echocardiograms indicated that cardiac function was within normal ranges, with left ventricular ejection fractions between 62% and 66%. Pericardial effusion was noted in 8 cases, segmental myocardial injury in 3 cases, pulmonary hypertension in 2 cases, and left ventricular diameter enlargement in 1 case. The time of thrombus formation was identified as being on day 14.0 (11.25, 17.25) of the disease course, with thrombus locations comprising 10 cases in the right ventricle, 5 cases in the right atrium, and 1 case in the left atrium. All 16 children underwent pulmonary artery CTA, revealing that 10 out of the 15 cases with right heart thrombus also had concurrent pulmonary embolism. One child with a left atrial thrombus exhibited an adjacent thrombus in the right lower pulmonary vein. Additionally, all 16 children received brain MRI angiography and venography, as well as ultrasound examinations of the limb arteries and veins and large systemic vessels, which showed 1 case of lower limb venous thrombosis, while no other thrombus formation was observed in the remaining cases. Treatment Antibacterial Treatment All children received azithromycin as part of the antibacterial treatment protocol. After further examinations, 15 cases tested positive for mycoplasma resistance genes 2063A > G and 2064A > G, of which 8 cases with disease progression and poor treatment response were switched to levofloxacin. In light of the presence of bacterial infection and suboptimal treatment responses, 4 cases of children with mixed bacterial infections were simultaneously treated with cephalosporins for antimicrobial therapy. Additionally, 5 children with concurrent Epstein-Barr virus (EBV) infection were administered ganciclovir for antiviral treatment. Bronchoscopy Examination Twelve children underwent bronchoscopy. Among them, 4 children showed significant atelectasis on chest X-ray despite the resolution of cardiac thrombus following anticoagulant therapy; thus, bronchoscopy and alveolar lavage were performed after evaluating their condition. Two children underwent bronchoscopy due to atelectasis following cardiac thrombectomy. Furthermore, 6 children had already undergone bronchoscopy prior to the detection of cardiac thrombus. Bronchoscopy in all 12 children revealed bronchial mucosal congestion and edema, with 8 cases exhibiting plastic bronchitis. Anticoagulation Therapy All 16 children were hemodynamically stable and were immediately given anticoagulation therapy upon detection of thrombus. The initial anticoagulant used was low molecular weight heparin or unfractionated heparin. Ten children switched to warfarin treatment after 3 to 5 days of low molecular weight heparin therapy, with an initial dose of 0.1 to 0.2 mg/(kg·dose), taken once daily, and the dosage was adjusted based on the International Normalized Ratio (INR) to maintain it between 2 and 3. Four children received a combination of low molecular weight heparin and urokinase thrombolysis treatment (4,400 U/(kg·dose), continuous intravenous infusion for 2 hours, once daily for 10 days). Two children were treated solely with low molecular weight heparin or unfractionated heparin. Seven children had poor adherence to oral warfarin or subcutaneous heparin and were switched to oral rivaroxaban therapy after three weeks. After anticoagulation therapy, 11 children had their cardiac thrombus resolved, with 8 of them showing resolution within three weeks of treatment. The remaining 3 children had their thrombus resolved at 2.5, 5.0, and 6.0 months, respectively. Among the 11 children who successfully received anticoagulation therapy, 7 had combined pulmonary embolism, and during follow-up, all pulmonary thrombi disappeared with lung imaging returning to normal. No major bleeding or other adverse reactions occurred during the anticoagulation treatment. Surgical treatment Five children underwent surgical intervention after 2 to 3 weeks of anticoagulation therapy showed no reduction in cardiac thrombus, following an evaluation by the cardiac surgery team. Among these, 3 children who had pulmonary embolism continued oral rivaroxaban for anticoagulation therapy postoperatively, and follow-up CT pulmonary angiography at 3 to 5 months showed complete resolution of pulmonary thrombi. The other 2 children, who did not have pulmonary embolism, did not receive further anticoagulation treatment after surgery and were followed up in the outpatient clinic for 3 months. In the subsequent follow-up of all 5 children, lung imaging returned to normal. Discussion The incidence of pediatric MPP has gradually increased in recent years, especially in northern China, with a growing number of refractory and severe cases [ 1 ] . MP infection is primarily characterized by respiratory symptoms and can lead to multisystem complications. Although cardiac thrombosis associated with MPP is rare, its potential risks should not be overlooked. Therefore, clinicians should maintain a high level of vigilance for thrombosis in MPP patients. Thrombosis is a common type of occupying lesion in the heart. In adults, thrombus formation is often associated with traditional risk factors such as atherosclerosis and venous thromboembolism; it commonly occurs in the context of blood flow stasis within the heart chambers due to conditions such as myocardial infarction, heart failure, atrial fibrillation, and mitral stenosis [ 3 ] . Previous studies have suggested that cardiac thrombosis occurring in the left atrium and left ventricle is often associated with a history of rheumatic disease, cardiomyopathy, and impaired regional wall motion [ 3 , 4 ] . Right heart thrombosis is often caused by the migration of thrombosis from the venous system of the lower limbs or is related to blood stasis, central venous catheterization, and other factors [ 5 ] .This study found that among 16 children with severe mycoplasma pneumonia, all had no underlying diseases. Fifteen cases involved the formation of right heart thrombus, primarily located near the right ventricle and tricuspid valve, while only one case involved left heart thrombus, and one case was associated with lower limb venous thrombus formation. The possibility of primary cardiac thrombus formation attributable to Mycoplasma pneumonia infection is considered. The mechanism by which MP induces thrombosis remains unclear. Existing literature indicates that MP infection may activate the coagulation system through various pathways, leading to coagulopathy and promoting thrombus formation. MP can trigger inflammatory responses, disrupt vascular endothelium integrity, and disturb the balance between coagulation and anticoagulation, resulting in a hypercoagulable state and thrombosis, which may cause local thrombotic occlusion [ 6 ][ 7 ] . Children often experience high fever, dehydration, and hemodynamic changes during infection, which further increases the risk of thrombosis. The liver also plays an important role in maintaining the body’s coagulation balance. When an inflammatory response occurs, the function of liver cells may be compromised, decreasing the synthesis of anticoagulant factors such as AT-III, protein C, and protein S and increasing consumption of these factors. This results in enhanced coagulation activities, promoting the formation of thrombi [ 7 ] . Among the 16 children, 5 cases exhibited decreased anticoagulant protein activity (including Protein C, Protein S, and Antithrombin III), and another 8 cases tested positive for antiphospholipid antibodies. Liver function tests showed elevated alanine aminotransferase levels in 8 patients, decreased albumin levels in 9 patients, and reduced anticoagulant protein activity in 5 patients. All tested indicators returned to normal during follow-up after anti-infection treatment. These results are consistent with our previous experiences in treating children with pulmonary embolism following mycoplasma infection, indicating that the decrease in the activity of these anticoagulant factors is closely related to mycoplasma infection. Previous studies and case reports have confirmed that patients with thrombosis secondary to MP infection exhibit positive antiphospholipid antibodies, β2 glycoprotein I antibodies, and lupus anticoagulants. These antiphospholipid antibodies interact with phospholipids, phospholipid-protein complexes, and phospholipid-binding proteins, thereby damaging endothelial cells, promoting platelet aggregation and activation, and increasing the risk of thrombus formation. The aforementioned antibodies typically become negative after 3–6 months [ 8 ][ 9 ] . Liu et al [ 10 ] found that among children with MP infection and thrombosis, the positivity rates for anticardiolipin antibody (ACL)-immunoglobulin M (IgM), anti-beta 2 glycoprotein 1 (β2GP1)-IgM, and lupus anticoagulants were 60.0%, 64.0%, and 42.1%, respectively. In this study, 8 cases tested positive for antiphospholipid antibodies, including 6 cases positive for lupus anticoagulant, 5 cases positive for anticardiolipin antibodies, and 3 cases positive for anti-β2 glycoprotein antibodies. During follow-up at 3 to 6 months, all but 1 case was diagnosed with antiphospholipid syndrome, and the remaining children had all their test indicators return to normal. This further corroborates the association between immune dysfunction caused by Mycoplasma pneumonia infection and thrombus formation. Unlike in adults, cardiac thrombosis and pulmonary embolism in children often present atypically in clinical manifestations. However, although symptoms or signs are frequently present after reviewing the medical history after diagnosis, they are often overlooked. In the current study, all cases exhibited fever and cough, with other symptoms occurring in the following order: chest pain, shortness of breath, hemoptysis, and chest tightness. Notably, 33.3% of the children had only fever and cough as symptoms. Therefore, when children with SMPP exhibit symptoms of chest pain or hemoptysis, there should be a heightened awareness of the potential for cardiac thrombosis, and proactive measures should be taken to conduct thrombosis-related examinations to reduce the risk of missed diagnoses. In laboratory tests, changes in D-dimer levels are of significant diagnostic value for assessing thrombosis, as they reflect intravascular thrombus formation and the subsequent fibrinolytic process. D-dimer can serve as an independent predictor of embolic risk; however, it has high sensitivity but low specificity. Therefore, clinicians should consider other factors in their comprehensive assessment [ 11 ] . Research shows that the plasma fibrinogen and D-dimer levels are significantly higher in children with MPP than in healthy children, whereas PT and activated partial thromboplastin time (APTT) are shortened [ 12 ] . Liu et al [ 10 ] found that among children with MPP and thrombosis, 58.1% (25/43) had D-dimer levels greater than 5.0 mg/L. In our study, the D-dimer levels of 16 children were found to be above the normal range, with 15 cases exceeding 5.0 mg/L, indicating a hypercoagulable state in these patients. It is recommended to promptly conduct echocardiography and pulmonary artery CTA for patients with D-dimer levels greater than 5.0 mg/L. Echocardiography is an important evaluation tool for investigating cardiac thrombosis, allowing for real-time observation of heart and main pulmonary artery thrombi and their effects on cardiac function. Fresh thrombi appear as hypoechoic structures on ultrasound, whereas organized thrombi present as heterogeneous hyperechoic structures [ 13 ] . In addition, cardiac thrombi may exhibit some echogenic characteristics similar to cardiac myxomas, such as having echogenic boundaries and a stalk that can gently move with the blood flow, with some appearing nearly round and attached to the cardiac septum. This can easily lead to misdiagnosis as myxomas. If the lesion decreases or disappears following thrombolytic or anticoagulant treatment, it can be confirmed as a thrombus [ 14 ] . When echocardiography shows right heart dilation, widening of the pulmonary artery, weakened ventricular wall motion, tricuspid regurgitation, and pulmonary hypertension, it can indirectly suggest pulmonary embolism. Additionally, echocardiography can clarify myocardial motion, cardiac ejection fraction, and the presence or absence of pulmonary hypertension. CTA, through CT imaging of the heart, pulmonary arteries, and even the systemic vasculature, can demonstrate the presence and location of thrombi, which appear as low-density filling defects on contrast-enhanced CT. Although CTA is very effective in differentiating between cardiac thrombosis and pulmonary embolism, caution must be exercised regarding radiation exposure and reliance on contrast agents; appropriate follow-up tools should be selected based on the child’s clinical characteristics. Furthermore, there is considerable variability in the timing of cardiac thrombus formation associated with MP infection. In the 16 children, thrombosis was detected at 14.0(11.25, 17.25) days after the onset of illness. Notably, two children who initially underwent echocardiography showed no evidence of thrombus but were later found to have thrombi due to a slow decline in D-dimer levels following repeat echocardiography. This highlights the importance of dynamic monitoring of the disease. The occurrence of massive ventricular thrombi one day after percutaneous cardiopulmonary support treatment has been reported in some patients with ventricular fibrillation [ 15 ] . Therefore, it is recommended that clinicians perform echocardiography on high-risk patients 1–2 weeks after fever onset to check for the presence of thrombus formation. Furthermore, coagulation tests and echocardiography may be repeated depending on the patient’s condition. Currently, there is no consensus regarding the treatment of cardiac thrombosis in children with MPP, because the formation of cardiac thrombi has been linked to the development of pathogen infection. Therefore, effective management of cardiac thrombus necessitates addressing the underlying condition. This typically involves treatment with anti-mycoplasma agents and anti-inflammatory medications. Current therapeutic options for cardiac thrombus include anticoagulant therapy, thrombolytic therapy, and surgical thrombectomy. In anticoagulant therapy, the application of heparin derivatives should be administered after assessment of the complete blood counts, coagulation profiles, and checking for any active bleeding. Moreover, APTT should be closely monitored during treatment [ 16 ] . Heparin can be applied alone or in combination with vitamin K antagonists administered 12–48 hours after initiation of heparin treatment. The commonly used oral anticoagulant is warfarin, which is prescribed for at least 3 months. During this period, the International Normalized Ratio (INR) should be monitored, and kept within a range of 2–3 [ 16 ] . Rivaroxaban, as a highly selective factor Xa inhibitor, has a wide therapeutic window, does not accumulate after multiple doses, has minimal drug and food interactions, and does not require monitoring of coagulation function. Research into the application of rivaroxaban in the treatment of deep vein thrombosis in children has revealed that the rivaroxaban treatment decreases the thrombus burden and carries a lower risk of recurrence and bleeding compared with standard anticoagulants [ 17 ] . Experience with thrombolytic therapy for intracardiac thrombi in pediatric cases is still limited. In the study by Emine Zengin et al., it is suggested that systemic thrombolysis can effectively save the lives of children under closely monitored conditions. Due to the smaller vascular diameter in children, intra-vascular thrombolysis is often limited; however, intravenous thrombolysis is feasible [ 18 ] . Y. Fu et al. [ 19 ] treated two patients with pulmonary embolism and cardiac thrombus formation with urokinase, and the results were good, with no complications observed. The most commonly utilized thrombolytic agents, rt-PA and urokinase, primarily rely on treatment guidelines established for adults. However, specific recommendations for drug dosing and treatment duration in pediatric populations are currently lacking. Considering that rtPA has a short half-life, surgical intervention may be considered if thrombolysis is ineffective [ 20 ] . However, thrombolytic therapy may increase the potential for dissolution of intracardiac thrombi, enhancing the risk of embolism to the systemic and pulmonary circulation, pulmonary embolism and organ embolism. For patients who have failed conservative treatment or have contraindications, as well as those with larger thrombus volumes and a higher risk of dislodgment, surgical thrombectomy is recommended.In this study, 4 patients received a combined treatment of urokinase and low molecular weight heparin for thrombolysis, achieving satisfactory results, with cardiac thrombus resolution within 14 days. In five cases where anticoagulant treatment did not reduce the thrombus, surgical thrombectomy was performed, three of which were complicated by pulmonary embolism. These patients continued rivaroxaban anticoagulation therapy, and at the three-month follow-up, it was observed that the pulmonary artery thrombi had completely disappeared. Together with previous reports, most children with cardiac thrombi and pulmonary embolism who received appropriate anticoagulant treatment achieve good prognosis. However, caution should be observed regarding the potential for new pulmonary embolism due to thrombus lysis during treatment. Summary In summary, during the course of MPP, the occurrence of clinical symptoms such as dyspnea, chest pain, and hemoptysis, along with elevated D-dimer levels, should raise suspicion for the development of cardiac thrombus, prompting timely echocardiographic evaluation. Children with MPP who present with cardiac thrombosis generally have a good prognosis with aggressive anticoagulation or surgical treatment. Ethical Approval and Consent to participate This retrospective study was approved by the Ethics Committee of the Affiliated Provincial Hospital of Shandong First Medical University (Approval No.: SWYX: NO.2024-067). Declarations Consent for publication The need for written informed consent was waived by the same ethics committee due to the retrospective nature of the study and the use of anonymized data. Competing interests The authors declare no conflicts of interest. Funding Not applicable Author Contribution Yang Juan was responsible for the data collection and manuscript preparation of this paper. Acknowledgements The authors would like to express sincere gratitude to the Department of Pediatric Respiratory Medicine, Affiliated Provincial Hospital of Shandong First Medical University, for providing clinical resources and research support for this study. Data Availability The analyzed data sets generated during the present study are available from the corresponding author on reasonable request. References Gao LW, Yin J, Hu YH, et al. The epidemiology of paediatric Mycoplasma pneumoniae pneumonia in North China: 2006 to 2016. Epidemiol Infect. 2019;147:e192. Respiratory Branch of Chinese Pediatric Society of Chinese Medical Association;Editorial Board of Chinese Journal of Applied Clinical Pediatrics Less. Expert consensus on diagnosis and treatment of mycoplasma pneumoniae pneumonia in children(2015). Chin J Appl Clin Pediatr. 2015;30(17):1304–8. Tam E, Graglia S. How to recognise an LV thrombus when you see one: a review of cardiac point-of-care ultrasound. 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Advances in the Research on Anticardiolipin Antibody. J Immunol Res. 2019. 2019: 8380214. Liu J, He R, Wu R, et al. Mycoplasma pneumoniae pneumonia associated thrombosis at Beijing Children's hospital. BMC Infect Dis. 2020;20(1):51. Weitz JI, Fredenburgh JC, Eikelboom JW. A Test in Context: D-Dimer. J Am Coll Cardiol. 2017;70(19):2411–20. Li T, Yu H, Hou W, Li Z, Han C, Wang L. Evaluation of variation in coagulation among children with Mycoplasma pneumoniae pneumonia: a case-control study. J Int Med Res. 2017;45(6):2110–8. Lee JM, Cha MJ, Nam GB, et al. Incidence and predictors of left atrial thrombus in patients with atrial fibrillation under anticoagulation therapy. Clin Res Cardiol. 2024;113(8):1242–50. Oktaviono YH, Saputra P, Arnindita JN, et al. Clinical characteristics and surgical outcomes of cardiac myxoma: A meta-analysis of worldwide experience. Eur J Surg Oncol. 2024;50(2):107940. Okamura A, Miake J, Miyagi M, Yamamoto K. 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Iatrogenic Right Atrial Thrombus Complicated by Pulmonary Embolism: Management and Outcomes. Curr Cardiol Rev. 2021;17(4):e230421188336. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 24 Feb, 2026 Reviewers agreed at journal 22 Feb, 2026 Reviewers agreed at journal 20 Feb, 2026 Reviewers agreed at journal 17 Feb, 2026 Reviewers agreed at journal 15 Feb, 2026 Reviewers invited by journal 13 Feb, 2026 Editor invited by journal 20 Jan, 2026 Editor assigned by journal 20 Jan, 2026 Submission checks completed at journal 20 Jan, 2026 First submitted to journal 15 Jan, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8614234","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":592779609,"identity":"d749f188-de6a-42f6-bc25-d6ca86346cbb","order_by":0,"name":"juan yang","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA+klEQVRIiWNgGAWjYLACCRDBzHzwwYcKCTl+4rWwsyUbzjhjYSzZQLRV/Dxm0rxtFYkbCGkxOH728AvLNrs8BmYGA2neeRKMGxiYHz66gU/Lmbw0C8m25GKglgTDudskmM0Z2IyNc/BpOZBjZiDZxpzYwMxwIOHtNgk2ywYeNmm8Ws6/AWmpB2phbDjAO0eCx+AAIS03cowfSLYdBmphZmzkbZCQIKhF8sYbMwaJc8eBWtiYGWcckzCQbCbgF77zOcafJcqqExv4z3//8aGmrr6fvfnhY3xaFA4wsEmDotL+AEyIGY9yEJBvYGD++IGAolEwCkbBKBjhAAC6g0mZvpaXWQAAAABJRU5ErkJggg==","orcid":"","institution":"Shandong Provincial Hospital","correspondingAuthor":true,"prefix":"","firstName":"juan","middleName":"","lastName":"yang","suffix":""}],"badges":[],"createdAt":"2026-01-16 01:23:13","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8614234/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8614234/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":102964498,"identity":"2cd8eee8-b66a-41e9-afcc-ad09bbeac190","added_by":"auto","created_at":"2026-02-19 04:22:31","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":602155,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8614234/v1/0a9d5f91-1a19-4b22-9ac9-1c4833e56ee3.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Clinical Characteristics, Treatment, and Outcomes of Children with Severe Mycoplasma Pneumonia Complicated with Cardiac Thrombosis: A retrospective study","fulltext":[{"header":"Introduction","content":"\u003cp\u003e \u003cem\u003eMycoplasma pneumoniae\u003c/em\u003e (MP) is an important pathogen responsible for community-acquired pneumonia in children. In addition to causing typical pulmonary inflammation, it can lead to various pulmonary and extrapulmonary complications that affect the physical and mental health of the affected children \u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/sup\u003e. Severe mycoplasma pneumonia (SMPP) can result in thrombosis in different body parts, with complex and varied clinical manifestations. Although cases of cardiac thrombosis are rare, potential hazards associated with this complication should not be overlooked. Cardiac thrombosis can lead to valve incompetence, chordae tendineae rupture, hemodynamic instability, heart failure, and arrhythmias. Dislodgement of a thrombus can result in outflow tract obstruction, causing coronary artery occlusion, heart failure, pulmonary embolism, stroke, and other serious complications, which significantly affects treatment outcomes and prognosis and has long-term effects on the quality of life of the child. However, the demographic characteristics, clinical features, risk factors, and prognosis of children with SMPP complicated with cardiac thrombosis remain unclear. Consequently, the present multicenter clinical sought to enhance clinicians\u0026rsquo; awareness of this rare but serious complication, improve diagnostic and therapeutic levels, and provide references for the management and treatment of pediatric MP infections.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy Subjects\u003c/h2\u003e \u003cp\u003eA retrospective analysis was conducted on the clinical data of 16 children diagnosed with SMPP combined with cardiac thrombus in the Department of Pediatrics at Shandong First Medical University Affiliated Provincial Hospital from July 2018 to April 2025. Inclusion criteria: (1) Patients aged 0\u0026ndash;14 years; (2) those diagnosed with SMPP based on the \u0026ldquo;Expert Consensus on the Diagnosis and Treatment of Mycoplasma Pneumonia in Children\u0026rdquo; \u003csup\u003e[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]\u003c/sup\u003e; (3) imaging findings indicating intracardiac thrombus: echocardiography showing hypoechoic or isoechoic/mixed echogenic masses within heart chambers; chest computed tomography angiography (CTA) indicating filling defects within cardiac cavities; and (4) those without underlying diseases related to hematologic, rheumatologic, or cardiovascular system. The study was approved by the Ethics Committee of Shandong First Medical University Affiliated Provincial Hospital (SWYX: No. 2024-067). The requirement for informed consent was waived because of the retrospective nature of the study.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eStatistical Methods\u003c/h3\u003e\n\u003cp\u003eAll statistical analyses were conducted using SPSS 25.0 software. Categorical data were expressed as counts (percentages) and compared using the chi-square test and Fisher\u0026rsquo;s exact test. Non-normally distributed continuous data were expressed as the median (interquartile range) and analyzed using the Mann-Whitney U test. P\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant.\u003c/p\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003eBasic Information of Patients\u003c/h2\u003e \u003cp\u003eSixteen children were included in the analysis, of whom 11 were males and 5 were females, with an age of onset of 8.03\u0026thinsp;\u0026plusmn;\u0026thinsp;2.17 years. None of the patients had a history of underlying diseases related to hematologic, rheumatologic, or cardiovascular system before admission. Neither parent had a history of venous thromboembolism. The duration of the illness prior to admission for the children was 11.69\u0026thinsp;\u0026plusmn;\u0026thinsp;3.80 days, and cardiac thrombus formation was detected on day 14.0 (11.25, 17.25) of the disease course.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eClinical Manifestations and Physical Examination\u003c/h3\u003e\n\u003cp\u003eAll 16 children exhibited fever and cough, with a duration of fever of 10.81\u0026thinsp;\u0026plusmn;\u0026thinsp;2.77 days and a peak temperature of 39.5 (39.1, 40.4) \u0026deg;C.Other symptoms included dyspnea in 8 cases, chest pain in 7 cases, hemoptysis in 3 cases, and chest tightness in 1 case. Physical examinations revealed moist rales in 13 cases, tachycardia in 11 cases, and decreased localized breath sounds in the lungs in 8 cases, with no significant murmurs detected upon cardiac auscultation. All 16 children had blood pressure within the normal range, while 3 cases exhibited peripheral oxygen saturation below 0.95.\u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eInflammatory Indicators and Pathogen Detection\u003c/h2\u003e \u003cp\u003eAll 16 children presented elevated infection markers, with a leukocyte count of 13.54 (8.5, 24.92) \u0026times; 10^9/L, a neutrophil percentage of 74.40 (64.7, 89.3)%, C-reactive protein level of 33.58 (18.42, 230 mg/L), and lactate dehydrogenase level of 527.50 (312, 1510) U/L. Two children exhibited mild anemia, while the hemoglobin levels of the remaining children were within the normal range. Among 15 children tested, 14 were positive for mycoplasma resistance genes 2063A\u0026thinsp;\u0026gt;\u0026thinsp;G and 2064A\u0026thinsp;\u0026gt;\u0026thinsp;G. All 16 children underwent testing for Epstein-Barr virus (EBV), sputum culture, and common respiratory viruses. Among them, 5 cases tested positive for EBV, 4 cases for rhinovirus, and 2 cases for respiratory syncytial virus. Sputum cultures identified Haemophilus influenzae, Streptococcus pneumoniae, and Staphylococcus aureus, with each pathogen positive in 1 case.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eCoagulation Function Tests and Thrombophilia-related Tests\u003c/h3\u003e\n\u003cp\u003eThe plasma D-dimer levels in the 16 children were measured at 9.18 (6.57, 15.91) mg/L (reference value: 0\u0026ndash;0.5 mg/L), with 15 cases exceeding 5.0 mg/L. Fibrinogen levels and platelet counts were within the normal range. Among the 16 children, 5 had decreased activity of anticoagulant proteins (protein C, protein S, antithrombin Ⅲ), and 8 tested positive for antiphospholipid antibodies. Five cases underwent thrombophilia gene testing, and no relevant gene mutations were found.\u003c/p\u003e\n\u003ch3\u003eAutoimmune Disease Testing\u003c/h3\u003e\n\u003cp\u003eAmong the 16 children, 8 tested positive for antiphospholipid antibodies. Specifically, 6 cases were positive for lupus anticoagulant, 5 for anticardiolipin antibodies, and 3 for anti-β2 glycoprotein I antibodies. Notably, 3 cases were positive for both lupus anticoagulant and anticardiolipin antibodies. Additionally, 5 cases tested positive for antinuclear antibodies. No abnormalities were detected in the tests for anti-double-stranded DNA antibodies, anti-Smith antibodies, anti-SSA antibodies, or anti-SSB antibodies.\u003c/p\u003e \u003cdiv id=\"Sec11\" class=\"Section2\"\u003e \u003ch2\u003eMyocardial Injury Markers and Liver Function Tests\u003c/h2\u003e \u003cp\u003eAll 16 children underwent testing for myocardial injury markers. Three cases showed elevated creatine kinase isoenzyme levels, and four cases demonstrated increased B-type natriuretic peptide levels, while the troponin T results were within normal ranges. Liver function tests indicated elevated alanine aminotransferase levels in 8 cases and decreased albumin levels in 9 cases, whereas bilirubin levels and prothrombin time remained normal.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec12\" class=\"Section2\"\u003e \u003ch2\u003eImaging Examination\u003c/h2\u003e \u003cp\u003eChest CT scans of all 16 children revealed pulmonary consolidation and/or atelectasis, with 12 cases presenting associated pleural effusion. Echocardiograms indicated that cardiac function was within normal ranges, with left ventricular ejection fractions between 62% and 66%. Pericardial effusion was noted in 8 cases, segmental myocardial injury in 3 cases, pulmonary hypertension in 2 cases, and left ventricular diameter enlargement in 1 case. The time of thrombus formation was identified as being on day 14.0 (11.25, 17.25) of the disease course, with thrombus locations comprising 10 cases in the right ventricle, 5 cases in the right atrium, and 1 case in the left atrium.\u003c/p\u003e \u003cp\u003eAll 16 children underwent pulmonary artery CTA, revealing that 10 out of the 15 cases with right heart thrombus also had concurrent pulmonary embolism. One child with a left atrial thrombus exhibited an adjacent thrombus in the right lower pulmonary vein. Additionally, all 16 children received brain MRI angiography and venography, as well as ultrasound examinations of the limb arteries and veins and large systemic vessels, which showed 1 case of lower limb venous thrombosis, while no other thrombus formation was observed in the remaining cases.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec13\" class=\"Section2\"\u003e \u003ch2\u003eTreatment\u003c/h2\u003e \u003cdiv id=\"Sec14\" class=\"Section3\"\u003e \u003ch2\u003eAntibacterial Treatment\u003c/h2\u003e \u003cp\u003eAll children received azithromycin as part of the antibacterial treatment protocol. After further examinations, 15 cases tested positive for mycoplasma resistance genes 2063A\u0026thinsp;\u0026gt;\u0026thinsp;G and 2064A\u0026thinsp;\u0026gt;\u0026thinsp;G, of which 8 cases with disease progression and poor treatment response were switched to levofloxacin. In light of the presence of bacterial infection and suboptimal treatment responses, 4 cases of children with mixed bacterial infections were simultaneously treated with cephalosporins for antimicrobial therapy. Additionally, 5 children with concurrent Epstein-Barr virus (EBV) infection were administered ganciclovir for antiviral treatment.\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv id=\"Sec15\" class=\"Section2\"\u003e \u003ch2\u003eBronchoscopy Examination\u003c/h2\u003e \u003cp\u003eTwelve children underwent bronchoscopy. Among them, 4 children showed significant atelectasis on chest X-ray despite the resolution of cardiac thrombus following anticoagulant therapy; thus, bronchoscopy and alveolar lavage were performed after evaluating their condition. Two children underwent bronchoscopy due to atelectasis following cardiac thrombectomy. Furthermore, 6 children had already undergone bronchoscopy prior to the detection of cardiac thrombus. Bronchoscopy in all 12 children revealed bronchial mucosal congestion and edema, with 8 cases exhibiting plastic bronchitis.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec16\" class=\"Section2\"\u003e \u003ch2\u003eAnticoagulation Therapy\u003c/h2\u003e \u003cp\u003eAll 16 children were hemodynamically stable and were immediately given anticoagulation therapy upon detection of thrombus. The initial anticoagulant used was low molecular weight heparin or unfractionated heparin. Ten children switched to warfarin treatment after 3 to 5 days of low molecular weight heparin therapy, with an initial dose of 0.1 to 0.2 mg/(kg\u0026middot;dose), taken once daily, and the dosage was adjusted based on the International Normalized Ratio (INR) to maintain it between 2 and 3. Four children received a combination of low molecular weight heparin and urokinase thrombolysis treatment (4,400 U/(kg\u0026middot;dose), continuous intravenous infusion for 2 hours, once daily for 10 days). Two children were treated solely with low molecular weight heparin or unfractionated heparin. Seven children had poor adherence to oral warfarin or subcutaneous heparin and were switched to oral rivaroxaban therapy after three weeks.\u003c/p\u003e \u003cp\u003eAfter anticoagulation therapy, 11 children had their cardiac thrombus resolved, with 8 of them showing resolution within three weeks of treatment. The remaining 3 children had their thrombus resolved at 2.5, 5.0, and 6.0 months, respectively. Among the 11 children who successfully received anticoagulation therapy, 7 had combined pulmonary embolism, and during follow-up, all pulmonary thrombi disappeared with lung imaging returning to normal. No major bleeding or other adverse reactions occurred during the anticoagulation treatment.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec17\" class=\"Section2\"\u003e \u003ch2\u003eSurgical treatment\u003c/h2\u003e \u003cp\u003eFive children underwent surgical intervention after 2 to 3 weeks of anticoagulation therapy showed no reduction in cardiac thrombus, following an evaluation by the cardiac surgery team. Among these, 3 children who had pulmonary embolism continued oral rivaroxaban for anticoagulation therapy postoperatively, and follow-up CT pulmonary angiography at 3 to 5 months showed complete resolution of pulmonary thrombi. The other 2 children, who did not have pulmonary embolism, did not receive further anticoagulation treatment after surgery and were followed up in the outpatient clinic for 3 months. In the subsequent follow-up of all 5 children, lung imaging returned to normal.\u003c/p\u003e \u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003eThe incidence of pediatric MPP has gradually increased in recent years, especially in northern China, with a growing number of refractory and severe cases \u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/sup\u003e. MP infection is primarily characterized by respiratory symptoms and can lead to multisystem complications. Although cardiac thrombosis associated with MPP is rare, its potential risks should not be overlooked. Therefore, clinicians should maintain a high level of vigilance for thrombosis in MPP patients.\u003c/p\u003e \u003cp\u003eThrombosis is a common type of occupying lesion in the heart. In adults, thrombus formation is often associated with traditional risk factors such as atherosclerosis and venous thromboembolism; it commonly occurs in the context of blood flow stasis within the heart chambers due to conditions such as myocardial infarction, heart failure, atrial fibrillation, and mitral stenosis \u003csup\u003e[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/sup\u003e. Previous studies have suggested that cardiac thrombosis occurring in the left atrium and left ventricle is often associated with a history of rheumatic disease, cardiomyopathy, and impaired regional wall motion \u003csup\u003e[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]\u003c/sup\u003e. Right heart thrombosis is often caused by the migration of thrombosis from the venous system of the lower limbs or is related to blood stasis, central venous catheterization, and other factors \u003csup\u003e[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]\u003c/sup\u003e.This study found that among 16 children with severe mycoplasma pneumonia, all had no underlying diseases. Fifteen cases involved the formation of right heart thrombus, primarily located near the right ventricle and tricuspid valve, while only one case involved left heart thrombus, and one case was associated with lower limb venous thrombus formation. The possibility of primary cardiac thrombus formation attributable to Mycoplasma pneumonia infection is considered.\u003c/p\u003e \u003cp\u003eThe mechanism by which MP induces thrombosis remains unclear. Existing literature indicates that MP infection may activate the coagulation system through various pathways, leading to coagulopathy and promoting thrombus formation. MP can trigger inflammatory responses, disrupt vascular endothelium integrity, and disturb the balance between coagulation and anticoagulation, resulting in a hypercoagulable state and thrombosis, which may cause local thrombotic occlusion \u003csup\u003e[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e][\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]\u003c/sup\u003e. Children often experience high fever, dehydration, and hemodynamic changes during infection, which further increases the risk of thrombosis. The liver also plays an important role in maintaining the body\u0026rsquo;s coagulation balance. When an inflammatory response occurs, the function of liver cells may be compromised, decreasing the synthesis of anticoagulant factors such as AT-III, protein C, and protein S and increasing consumption of these factors. This results in enhanced coagulation activities, promoting the formation of thrombi \u003csup\u003e[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]\u003c/sup\u003e. Among the 16 children, 5 cases exhibited decreased anticoagulant protein activity (including Protein C, Protein S, and Antithrombin III), and another 8 cases tested positive for antiphospholipid antibodies. Liver function tests showed elevated alanine aminotransferase levels in 8 patients, decreased albumin levels in 9 patients, and reduced anticoagulant protein activity in 5 patients. All tested indicators returned to normal during follow-up after anti-infection treatment. These results are consistent with our previous experiences in treating children with pulmonary embolism following mycoplasma infection, indicating that the decrease in the activity of these anticoagulant factors is closely related to mycoplasma infection.\u003c/p\u003e \u003cp\u003ePrevious studies and case reports have confirmed that patients with thrombosis secondary to MP infection exhibit positive antiphospholipid antibodies, β2 glycoprotein I antibodies, and lupus anticoagulants. These antiphospholipid antibodies interact with phospholipids, phospholipid-protein complexes, and phospholipid-binding proteins, thereby damaging endothelial cells, promoting platelet aggregation and activation, and increasing the risk of thrombus formation. The aforementioned antibodies typically become negative after 3\u0026ndash;6 months \u003csup\u003e[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e][\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]\u003c/sup\u003e. Liu et al \u003csup\u003e[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]\u003c/sup\u003e found that among children with MP infection and thrombosis, the positivity rates for anticardiolipin antibody (ACL)-immunoglobulin M (IgM), anti-beta 2 glycoprotein 1 (β2GP1)-IgM, and lupus anticoagulants were 60.0%, 64.0%, and 42.1%, respectively. In this study, 8 cases tested positive for antiphospholipid antibodies, including 6 cases positive for lupus anticoagulant, 5 cases positive for anticardiolipin antibodies, and 3 cases positive for anti-β2 glycoprotein antibodies. During follow-up at 3 to 6 months, all but 1 case was diagnosed with antiphospholipid syndrome, and the remaining children had all their test indicators return to normal. This further corroborates the association between immune dysfunction caused by Mycoplasma pneumonia infection and thrombus formation.\u003c/p\u003e \u003cp\u003eUnlike in adults, cardiac thrombosis and pulmonary embolism in children often present atypically in clinical manifestations. However, although symptoms or signs are frequently present after reviewing the medical history after diagnosis, they are often overlooked. In the current study, all cases exhibited fever and cough, with other symptoms occurring in the following order: chest pain, shortness of breath, hemoptysis, and chest tightness. Notably, 33.3% of the children had only fever and cough as symptoms. Therefore, when children with SMPP exhibit symptoms of chest pain or hemoptysis, there should be a heightened awareness of the potential for cardiac thrombosis, and proactive measures should be taken to conduct thrombosis-related examinations to reduce the risk of missed diagnoses.\u003c/p\u003e \u003cp\u003eIn laboratory tests, changes in D-dimer levels are of significant diagnostic value for assessing thrombosis, as they reflect intravascular thrombus formation and the subsequent fibrinolytic process. D-dimer can serve as an independent predictor of embolic risk; however, it has high sensitivity but low specificity. Therefore, clinicians should consider other factors in their comprehensive assessment \u003csup\u003e[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]\u003c/sup\u003e. Research shows that the plasma fibrinogen and D-dimer levels are significantly higher in children with MPP than in healthy children, whereas PT and activated partial thromboplastin time (APTT) are shortened \u003csup\u003e[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]\u003c/sup\u003e. Liu et al \u003csup\u003e[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]\u003c/sup\u003e found that among children with MPP and thrombosis, 58.1% (25/43) had D-dimer levels greater than 5.0 mg/L. In our study, the D-dimer levels of 16 children were found to be above the normal range, with 15 cases exceeding 5.0 mg/L, indicating a hypercoagulable state in these patients. It is recommended to promptly conduct echocardiography and pulmonary artery CTA for patients with D-dimer levels greater than 5.0 mg/L.\u003c/p\u003e \u003cp\u003eEchocardiography is an important evaluation tool for investigating cardiac thrombosis, allowing for real-time observation of heart and main pulmonary artery thrombi and their effects on cardiac function. Fresh thrombi appear as hypoechoic structures on ultrasound, whereas organized thrombi present as heterogeneous hyperechoic structures \u003csup\u003e[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/sup\u003e. In addition, cardiac thrombi may exhibit some echogenic characteristics similar to cardiac myxomas, such as having echogenic boundaries and a stalk that can gently move with the blood flow, with some appearing nearly round and attached to the cardiac septum. This can easily lead to misdiagnosis as myxomas. If the lesion decreases or disappears following thrombolytic or anticoagulant treatment, it can be confirmed as a thrombus \u003csup\u003e[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]\u003c/sup\u003e. When echocardiography shows right heart dilation, widening of the pulmonary artery, weakened ventricular wall motion, tricuspid regurgitation, and pulmonary hypertension, it can indirectly suggest pulmonary embolism. Additionally, echocardiography can clarify myocardial motion, cardiac ejection fraction, and the presence or absence of pulmonary hypertension. CTA, through CT imaging of the heart, pulmonary arteries, and even the systemic vasculature, can demonstrate the presence and location of thrombi, which appear as low-density filling defects on contrast-enhanced CT. Although CTA is very effective in differentiating between cardiac thrombosis and pulmonary embolism, caution must be exercised regarding radiation exposure and reliance on contrast agents; appropriate follow-up tools should be selected based on the child\u0026rsquo;s clinical characteristics. Furthermore, there is considerable variability in the timing of cardiac thrombus formation associated with MP infection. In the 16 children, thrombosis was detected at 14.0(11.25, 17.25) days after the onset of illness. Notably, two children who initially underwent echocardiography showed no evidence of thrombus but were later found to have thrombi due to a slow decline in D-dimer levels following repeat echocardiography. This highlights the importance of dynamic monitoring of the disease. The occurrence of massive ventricular thrombi one day after percutaneous cardiopulmonary support treatment has been reported in some patients with ventricular fibrillation \u003csup\u003e[\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]\u003c/sup\u003e. Therefore, it is recommended that clinicians perform echocardiography on high-risk patients 1\u0026ndash;2 weeks after fever onset to check for the presence of thrombus formation. Furthermore, coagulation tests and echocardiography may be repeated depending on the patient\u0026rsquo;s condition.\u003c/p\u003e \u003cp\u003eCurrently, there is no consensus regarding the treatment of cardiac thrombosis in children with MPP, because the formation of cardiac thrombi has been linked to the development of pathogen infection. Therefore, effective management of cardiac thrombus necessitates addressing the underlying condition. This typically involves treatment with anti-mycoplasma agents and anti-inflammatory medications. Current therapeutic options for cardiac thrombus include anticoagulant therapy, thrombolytic therapy, and surgical thrombectomy. In anticoagulant therapy, the application of heparin derivatives should be administered after assessment of the complete blood counts, coagulation profiles, and checking for any active bleeding. Moreover, APTT should be closely monitored during treatment \u003csup\u003e[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]\u003c/sup\u003e. Heparin can be applied alone or in combination with vitamin K antagonists administered 12\u0026ndash;48 hours after initiation of heparin treatment. The commonly used oral anticoagulant is warfarin, which is prescribed for at least 3 months. During this period, the International Normalized Ratio (INR) should be monitored, and kept within a range of 2\u0026ndash;3\u003csup\u003e[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]\u003c/sup\u003e. Rivaroxaban, as a highly selective factor Xa inhibitor, has a wide therapeutic window, does not accumulate after multiple doses, has minimal drug and food interactions, and does not require monitoring of coagulation function. Research into the application of rivaroxaban in the treatment of deep vein thrombosis in children has revealed that the rivaroxaban treatment decreases the thrombus burden and carries a lower risk of recurrence and bleeding compared with standard anticoagulants \u003csup\u003e[\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]\u003c/sup\u003e. Experience with thrombolytic therapy for intracardiac thrombi in pediatric cases is still limited. In the study by Emine Zengin et al., it is suggested that systemic thrombolysis can effectively save the lives of children under closely monitored conditions. Due to the smaller vascular diameter in children, intra-vascular thrombolysis is often limited; however, intravenous thrombolysis is feasible\u003csup\u003e[\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]\u003c/sup\u003e. Y. Fu et al. \u003csup\u003e[\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]\u003c/sup\u003e treated two patients with pulmonary embolism and cardiac thrombus formation with urokinase, and the results were good, with no complications observed. The most commonly utilized thrombolytic agents, rt-PA and urokinase, primarily rely on treatment guidelines established for adults. However, specific recommendations for drug dosing and treatment duration in pediatric populations are currently lacking. Considering that rtPA has a short half-life, surgical intervention may be considered if thrombolysis is ineffective\u003csup\u003e[\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]\u003c/sup\u003e. However, thrombolytic therapy may increase the potential for dissolution of intracardiac thrombi, enhancing the risk of embolism to the systemic and pulmonary circulation, pulmonary embolism and organ embolism. For patients who have failed conservative treatment or have contraindications, as well as those with larger thrombus volumes and a higher risk of dislodgment, surgical thrombectomy is recommended.In this study, 4 patients received a combined treatment of urokinase and low molecular weight heparin for thrombolysis, achieving satisfactory results, with cardiac thrombus resolution within 14 days. In five cases where anticoagulant treatment did not reduce the thrombus, surgical thrombectomy was performed, three of which were complicated by pulmonary embolism. These patients continued rivaroxaban anticoagulation therapy, and at the three-month follow-up, it was observed that the pulmonary artery thrombi had completely disappeared. Together with previous reports, most children with cardiac thrombi and pulmonary embolism who received appropriate anticoagulant treatment achieve good prognosis. However, caution should be observed regarding the potential for new pulmonary embolism due to thrombus lysis during treatment.\u003c/p\u003e \u003cdiv id=\"Sec19\" class=\"Section2\"\u003e \u003ch2\u003eSummary\u003c/h2\u003e \u003cp\u003eIn summary, during the course of MPP, the occurrence of clinical symptoms such as dyspnea, chest pain, and hemoptysis, along with elevated D-dimer levels, should raise suspicion for the development of cardiac thrombus, prompting timely echocardiographic evaluation. Children with MPP who present with cardiac thrombosis generally have a good prognosis with aggressive anticoagulation or surgical treatment.\u003c/p\u003e \u003cp\u003e \u003cstrong\u003eEthical Approval and Consent to participate\u003c/strong\u003e \u003cp\u003eThis retrospective study was approved by the Ethics Committee of the Affiliated Provincial Hospital of Shandong First Medical University (Approval No.: SWYX: NO.2024-067).\u003c/p\u003e \u003c/p\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003ch2\u003eConsent for publication\u003c/h2\u003e \u003cp\u003eThe need for written informed consent was waived by the same ethics committee due to the retrospective nature of the study and the use of anonymized data.\u003c/p\u003e \u003c/p\u003e\u003cp\u003e \u003ch2\u003eCompeting interests\u003c/h2\u003e \u003cp\u003eThe authors declare no conflicts of interest.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eNot applicable\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eYang Juan was responsible for the data collection and manuscript preparation of this paper.\u003c/p\u003e\u003ch2\u003eAcknowledgements\u003c/h2\u003e \u003cp\u003eThe authors would like to express sincere gratitude to the Department of Pediatric Respiratory Medicine, Affiliated Provincial Hospital of Shandong First Medical University, for providing clinical resources and research support for this study.\u003c/p\u003e\u003ch2\u003eData Availability\u003c/h2\u003e\u003cp\u003eThe analyzed data sets generated during the present study are available from the corresponding author on reasonable request.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eGao LW, Yin J, Hu YH, et al. The epidemiology of paediatric Mycoplasma pneumoniae pneumonia in North China: 2006 to 2016. Epidemiol Infect. 2019;147:e192.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRespiratory Branch of Chinese Pediatric Society of Chinese Medical Association;Editorial Board of Chinese Journal of Applied Clinical Pediatrics\u0026ensp;Less. Expert consensus on diagnosis and treatment of mycoplasma pneumoniae pneumonia in children(2015). Chin J Appl Clin Pediatr. 2015;30(17):1304\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTam E, Graglia S. How to recognise an LV thrombus when you see one: a review of cardiac point-of-care ultrasound. Emerg Med J. 2022;39(11):867\u0026ndash;70.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChang P, Xiao J, Hu Z, Kwan AC, Fan Z. Imaging of left heart intracardiac thrombus: clinical needs, current imaging, and emerging cardiac magnetic resonance techniques. Ther Adv Cardiovasc Dis. 2022;16:17539447221107737.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAl Badri A, Kliger C, Weiss D, et al. Right Atrial Vacuum-Assisted Thrombectomy: Single-Center Experience. J Invasive Cardiol. 2016;28(5):196\u0026ndash;201.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNarita M. Pathogenesis of extrapulmonary manifestations of Mycoplasma pneumoniae infection with special reference to pneumonia. J Infect Chemother. 2010;16(3):162\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNarita M. Classification of Extrapulmonary Manifestations Due to Mycoplasma pneumoniae Infection on the Basis of Possible Pathogenesis. Front Microbiol. 2016;7:23.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJo\u0026atilde;o MD, Costa JV, Santos GC, Leite RD, Guimar\u0026atilde;es S. Retinal vein and artery occlusion as the first manifestation of primary antiphospholipid syndrome in a pediatric patient. Arq Bras Oftalmol. 2022;87(2):0431.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang D, Lv W, Zhang S, Zhang J. Advances in the Research on Anticardiolipin Antibody. J Immunol Res. 2019. 2019: 8380214.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu J, He R, Wu R, et al. Mycoplasma pneumoniae pneumonia associated thrombosis at Beijing Children's hospital. BMC Infect Dis. 2020;20(1):51.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWeitz JI, Fredenburgh JC, Eikelboom JW. A Test in Context: D-Dimer. J Am Coll Cardiol. 2017;70(19):2411\u0026ndash;20.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLi T, Yu H, Hou W, Li Z, Han C, Wang L. Evaluation of variation in coagulation among children with Mycoplasma pneumoniae pneumonia: a case-control study. J Int Med Res. 2017;45(6):2110\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLee JM, Cha MJ, Nam GB, et al. Incidence and predictors of left atrial thrombus in patients with atrial fibrillation under anticoagulation therapy. Clin Res Cardiol. 2024;113(8):1242\u0026ndash;50.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOktaviono YH, Saputra P, Arnindita JN, et al. Clinical characteristics and surgical outcomes of cardiac myxoma: A meta-analysis of worldwide experience. Eur J Surg Oncol. 2024;50(2):107940.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOkamura A, Miake J, Miyagi M, Yamamoto K. Ultra-Rapid and Massive Thrombus Formation in Cardiac Chambers. Intern Med. 2015. 54(15): 1947.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMonagle P, Cuello CA, Augustine C, et al. American Society of Hematology 2018 Guidelines for management of venous thromboembolism: treatment of pediatric venous thromboembolism. Blood Adv. 2018;2(22):3292\u0026ndash;316.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMale C, Lensing A, Palumbo JS, et al. Rivaroxaban compared with standard anticoagulants for the treatment of acute venous thromboembolism in children: a randomised, controlled, phase 3 trial. Lancet Haematol. 2020;7(1):e18\u0026ndash;27.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZengin E, Sarper N, Yazal Erdem A, et al. Thrombolysis with Systemic Recombinant Tissue Plasminogen Activator in Children: A Multicenter Retrospective Study. Turk J Haematol. 2021;38(4):294\u0026ndash;305.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFu Y, Zhang TQ, Dong CJ, Xu YS, Dong HQ, Ning J. Clinical characteristics of 14 pediatric mycoplasma pneumoniae pneumonia associated thrombosis: a retrospective study. BMC Cardiovasc Disord. 2023;23(1):1.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBattisha A, Madoukh B, Sawalha K, Patel B. Iatrogenic Right Atrial Thrombus Complicated by Pulmonary Embolism: Management and Outcomes. Curr Cardiol Rev. 2021;17(4):e230421188336.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-pulmonary-medicine","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"pulm","sideBox":"Learn more about [BMC Pulmonary Medicine](http://bmcpulmmed.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/pulm/default.aspx","title":"BMC Pulmonary Medicine","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Mycoplasma pneumonia, Cardiac thrombosis, Pulmonary vein thrombosis, Pulmonary embolism, children","lastPublishedDoi":"10.21203/rs.3.rs-8614234/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8614234/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eObjective:\u003c/strong\u003e To explore the clinical characteristics, treatment, and outcomes of children with severe mycoplasma pneumonia (SMPP) complicated with cardiac thrombosis.\u003cbr\u003e\n \u003cstrong\u003eMethods:\u003c/strong\u003e Clinical data of 16 children with SMPP complicated with cardiac thrombosis, who were treated at three medical centers in China from July 2018 to April 2025, were retrospectively analyzed.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults: \u003c/strong\u003eAmong the 16 children, 11 were males and 5 were females, with an age of onset of 8.03 ± 2.17 years. All 16 children presented with fever and cough, while additional symptoms included dyspnea in 8 cases, chest pain in 7 cases, hemoptysis in 3 cases, and chest tightness in 1 case. A total of 15 children underwent testing for the Mycoplasma pneumoniae drug resistance genes 2063A\u0026gt;G and 2064A\u0026gt;G, of which 14 tested positive. The plasma D‑dimer levels of 16 children were 9.18 (6.57, 15.91) mg/L, all of which were higher than normal. Among the 16 children, 5 had decreased activity of anticoagulant proteins (protein C, protein S, antithrombin Ⅲ), and 8 tested positive for antiphospholipid antibodies. Chest CT scans of all 16 children showed pulmonary consolidation and (or) atelectasis, with pleural effusion present in 12 cases. In the 16 children, thrombosis was detected at 14.0(11.25, 17.25) days after the onset of illness. The locations of cardiac thrombosis included the right ventricle in 10 cases, the right atrium in 5 cases, and the left atrium in 1 case.Additionally, 11 cases had pulmonary vascular embolism, comprising 10 cases of pulmonary artery thrombosis and 1 case of pulmonary vein thrombosis. After anticoagulant treatment, cardiac thrombi disappeared in 11children. Five children who did not show improvement with anticoagulation underwent surgical thrombectomy. In the follow‑up of 16 children, lung imaging basically returned to normal, with no major hemorrhagic events or other adverse events.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion:\u003c/strong\u003e An early and thorough cardiac ultrasound examination should be performed in children with SMPP who present with chest pain, hemoptysis, significantly elevated D-dimer levels, pulmonary consolidation, atelectasis, and pericardial effusion. SMPP complicated by\u003c/p\u003e\n\u003cp\u003ecardiac thrombosis, prognosis is good following anticoagulation or surgical treatment.\u003c/p\u003e","manuscriptTitle":"Clinical Characteristics, Treatment, and Outcomes of Children with Severe Mycoplasma Pneumonia Complicated with Cardiac Thrombosis: A retrospective study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-18 14:28:25","doi":"10.21203/rs.3.rs-8614234/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2026-02-24T07:48:48+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"140913654082983677242101973442421485236","date":"2026-02-22T18:30:42+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"324790644197541784338343302717823020792","date":"2026-02-20T16:11:30+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"148878119382481016877047757143294078064","date":"2026-02-17T13:41:56+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"242258891072366203788261789293215327370","date":"2026-02-15T07:33:08+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-02-13T06:43:49+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-01-20T17:27:12+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-20T14:13:43+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-20T14:08:06+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Pulmonary Medicine","date":"2026-01-16T01:10:34+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-pulmonary-medicine","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"pulm","sideBox":"Learn more about [BMC Pulmonary Medicine](http://bmcpulmmed.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/pulm/default.aspx","title":"BMC Pulmonary Medicine","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"06652c02-a034-4da9-9787-133475ebbaad","owner":[],"postedDate":"February 18th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-02-18T14:28:25+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-18 14:28:25","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8614234","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8614234","identity":"rs-8614234","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}