Fulminant myocarditis (FM) is a type of inflammatory cardiomyopathy characterized by sudden onset and severe hemodynamic disturbances. It is the most severe and distinct form of myocarditis, characterized by rapid onset, diverse clinical manifestations, variable course, and rapid progression^[1-4]. If left untreated, patients may die within a few hours to a few days due to malignant arrhythmias, cardiogenic shock, or multi-organ failure^[5]. FM complicated by a thrombus in the left ventricle is a rare but severe complication with a high risk of death. We present a case of FM occurring over three weeks in a middle-aged man, complicated by multiple left ventricular thrombus and severe biventricular dysfunction, who achieved complete functional recovery with multidisciplinary management including mechanical circulatory support (MCS), immunomodulatory therapy, and anticoagulation.

Myocarditis refers to inflammatory injury of the heart muscle induced by factors such as viral infection, autoimmune disease, or drugs/toxins, leading to impaired cardiac function including reduced myocardial contractility and diastolic function, as well as arrhythmias^[1,3,5]. While ordinary acute myocarditis often presents with symptoms like chest tightness and palpitations, FM is characterized by a sudden onset and rapid progression. It can manifest directly as cardiogenic shock and malignant arrhythmias, potentially accompanied by multi-organ dysfunction such as respiratory, hepatic, and renal failure, and carries an extremely high early mortality rate^[11,12]. Therefore, high vigilance is required for such critical cases of FM complicated by cardiogenic shock, emphasizing early recognition, assessment, and resuscitation. Corresponding measures should be promptly implemented if the condition progresses or responds poorly to initial treatment.

Currently, there is no specific diagnostic standard for FM. It is defined as a clinically diagnosed inflammatory heart disease with abrupt onset and hemodynamic compromise, rather than a histological or pathological diagnosis. Comprehensive analysis integrating clinical presentation, laboratory tests, and imaging findings is essential. The 2013 European Society of Cardiology (ESC) position paper^[7] provides diagnostic criteria for clinically suspected myocarditis based on clinical presentation and non-invasive diagnostic techniques, while the 2024 Chinese Society of Cardiology guidelines^[2] on adult FM emphasize very early identification, very early diagnosis, and very early treatment. In this case, the patient met the ESC criteria for clinically suspected myocarditis: a prodromal viral illness, acute onset within 2-4 weeks, rapidly progressive dyspnea, severe left ventricular systolic dysfunction (EF 12%), elevated cardiac biomarkers, and exclusion of acute myocardial infarction by coronary angiography. In this case, the patient's critical condition and the presence of multiple left ventricular thrombi precluded biopsy^[13], and we have acknowledged this as a limitation.

In addition, the cardiac MRI findings—increased left ventricular trabeculations with a non-compacted-to-compacted myocardium ratio > 2.3, possible infero-apical infarction with local aneurysm formation, and multiple left ventricular thrombi—raise important differential diagnostic considerations. LVNC is a cardiomyopathy characterized by excessive trabeculations and a non-compacted-to-compacted ratio > 2.3^[14]. The coexistence of LVNC with acute myocarditis has been described^[15], and whether a pre-existing structural substrate contributed to the acute presentation remains uncertain. However, morphological criteria alone (NC/C > 2.3) are insufficient to establish a diagnosis of pathological LVNC, and a multiparametric approach is required. Nevertheless, from a pathophysiological perspective, the subendocardial structural abnormalities associated with excessive trabeculation, blood stasis within deep recesses, and potential subclinical myocardial dysfunction could theoretically serve as a susceptible substrate for viral myocarditis—for instance, by altering local immune responses or promoting thrombus formation. Therefore, the potential interaction between the LVNC phenotype and acute myocarditis cannot be entirely excluded. In this case, the patient presented with multiple intraventricular thrombi—which, while not uncommon in FM, may have been exacerbated by the deep recesses and blood stasis associated with excessive trabeculation, thereby contributing to disease severity. Continued anticoagulation therapy is warranted to prevent thrombus formation, and close longitudinal follow-up of the patient's myocardial disease status is necessary.

This severe condition demands urgent and specialized intervention. In China, a characteristic comprehensive management strategy has been developed for such critical cases, emphasizing proactive MCS coupled with early initiation of combined immunomodulatory therapy, such as glucocorticoids and IVIG^[2,12,16]. The rationale for this approach is supported by the 2024 Chinese Society of Cardiology guidelines, which recommend a “life support-based comprehensive treatment regimen” with MCS and immunomodulation as the core^[2]. Previous studies have demonstrated that immunomodulatory therapy can suppress myocardial inflammatory responses^[17,18]. In addition, life-support therapy constitutes renal replacement, respiratory support, and circulatory support. Among the various circulatory support modalities. Among the various circulatory support modalities, the IABP and extracorporeal membrane oxygenation (ECMO) are commonly used in clinical practice^[19,20]. In accordance with Chinese guidelines and previous research findings, this case employed a combined therapeutic approach consisting of anti-infection, antiviral, and immunomodulatory treatments, supplemented with circulatory support via IABP. However, in patients with severe left ventricle (LV) dysfunction and LV thrombus, the thromboembolic risk of IABP must be considered, and the choice of IABP versus ECMO depends on the degree of hemodynamic compromise and institutional experience. In this case, the patient's hemodynamics stabilized with IABP alone, and ECMO was not required. Subsequently, the patient's vital signs stabilized, follow-up examinations indicated gradual improvement in cardiac function, and no malignant arrhythmias occurred.

Furthermore, in this case, echocardiography revealed severe left ventricular heart failure accompanied by left ventricular dilation and thrombi. Left ventricular thrombus is a complication of myocarditis and severe left ventricular dysfunction. Embolization of ventricular thrombus can lead to systemic or pulmonary thromboembolism, causing serious consequences like cerebral or pulmonary embolism, which further worsens the condition and increases medical costs. The development of intraventricular thrombi in this patient was primarily attributable to the following factors: influenza B virus triggered a cytokine storm, with IL-6 serving as the central mediator causing endocardial injury and severe biventricular dysfunction (EF 12%); the resulting extremely low intracavitary blood flow velocity created profound apical blood stasis, with abnormal flow vortexes promoting thrombus formation; simultaneously, IL-6 drove a systemic hypercoagulable state via endothelial dysfunction, fibrinolysis inhibition, and platelet activation, as evidenced by a D-dimer level of 5,994 ng/mL. The convergence of these three elements explains the formation of multiple, large left ventricular apical thrombi—the patient's excessive trabeculation phenotype (NC/C > 2.3) may have further amplified thrombogenic risk by providing structural anchor points within deep recesses. Studies suggest that low molecular weight heparin is the most commonly used in-hospital treatment for left ventricular thrombi^[21,22]. Other research suggests that surgical intervention, with left ventriculotomy being the standard method for thrombus removal, may be necessary if there is a risk of systemic embolism or left ventricular outflow tract obstruction^[23]. However, no consensus exists on the optimal heparin regimen. In this case, the patient received low-molecular-weight heparin (5000 IU twice daily) during hospitalization, followed by rivaroxaban after discharge. Echocardiography on day 17 indicated thrombus disappearance. Recent case reports have demonstrated that anticoagulation alone can be effective for thrombus resolution in myocarditis^[15]. The American Heart Association scientific statement on left ventricular thrombus provides guidance on anticoagulation strategies, though optimal regimens remain debated^[24].

This case report has several important limitations. First, the diagnosis of FM was not confirmed by endomyocardial biopsy or by cardiac magnetic resonance meeting the updated Lake Louise criteria. Second, invasive hemodynamic data were not obtained, limiting objective documentation of cardiogenic shock. Third, the viral etiology remains speculative, as respiratory polymerase chain reaction (PCR) and myocardial viral PCR were not performed. Finally, as a single case report, the findings are not generalizable. Despite these limitations, this case demonstrates that significant recovery of cardiac function is possible even in severe myocarditis complicated by multiple left ventricular thrombi, and it underscores the importance of early recognition, multidisciplinary management, and close follow-up.

FM complicated by left ventricular thrombosis is uncommon; however, the reversibility of cardiac dysfunction should not be underestimated, provided that the condition is promptly recognized and addressed through a coordinated, multidisciplinary effort. Key therapeutic elements—early diagnosis, immediate anticoagulation, judicious application of MCS, and immunomodulatory treatment—are paramount. In the present case, the patient achieved complete functional recovery with left ventricular ejection fraction returning to 51% at the 3-month follow-up after discharge, suggesting that even severe cases with multiple left ventricular thrombi can achieve remarkable recovery. This case further serves as a reminder that anticoagulation must be carefully personalized, and that extended follow-up is indispensable.