Revised: September 14, 2025
Accepted: May 8, 2026
Published online: June 26, 2026
Processing time: 308 Days and 15.5 Hours
Myocarditis is an inflammatory disease of the myocardium with a highly variable clinical presentation and is often triggered by viral infections. While corticosteroids have historically been used with caution in viral myocarditis due to con
A previously healthy 27-year-old woman presented with fulminant myocarditis after a paucisymptomatic SARS-CoV-2 infection. The initial episode was characterized by pericardial effusion, rapidly progressing to cardiogenic shock and severe left ventricular dysfunction, requiring veno-arterial extracorporeal membrane oxygenation. Empirical high-dose corticosteroid therapy, remdesivir, and monoclonal anti-SARS-CoV-2 antibodies led to complete recovery of cardiac function. Two years later, the patient developed recurrent myocarditis triggered by H1N1, presenting with chest pain, elevated cardiac biomarkers, and severe reduction in ejection fraction. Cardiac magnetic resonance confirmed acute myocarditis with severe left ventricular dysfunction. High-dose corticosteroids and levosimendan were administered, resulting in progressive improvement without the need for me
This case highlights the diagnostic and therapeutic challenges of recurrent viral myocarditis, as well as the potential role of immunosuppression.
Core Tip: We present the case of a young woman who experienced two episodes of fulminant viral myocarditis following distinct viral infections (severe acute respiratory syndrome coronavirus 2 and influenza A), both of which were successfully treated with high-dose corticosteroids. The case raises key questions about the role of immunosuppressive therapy in managing the immune activation triggered by viral infections in myocarditis. The recurrence in the same patient highlights the importance of investigating possible underlying genetic or autoimmune vulnerabilities. This report provides insights that enhance our understanding of the complex relationship between viral triggers, immune response, and patient susceptibility in cases of myocarditis.
- Citation: Birtolo LI, Ferranti F, Manzi G, Caputo A, Scoccia G, Bruno K, Galea N, Maestrini V, Chimenti C, Severino P, Pugliese F, Badagliacca R, Vizza CD. From COVID-19 to influenza A - recurrent viral myocarditis and successful immunosuppressive therapy: A case report and review of literature. World J Cardiol 2026; 18(6): 113066
- URL: https://www.wjgnet.com/1949-8462/full/v18/i6/113066.htm
- DOI: https://dx.doi.org/10.4330/wjc.113066
Myocarditis is an inflammatory disease of the myocardium characterized by a wide spectrum of clinical manifestations, ranging from asymptomatic cases to fulminant heart failure and sudden cardiac death. The diagnostic process involves integrating clinical presentation, biomarkers (e.g., troponins), cardiac imaging, particularly cardiac magnetic resonance (CMR), and, in select cases, endomyocardial biopsy. CMR has become the cornerstone for non-invasive diagnosis, enabling the detection of myocardial edema and fibrosis, primarily through T2-weighted sequences, T1/T2 mapping, and late gadolinium enhancement (LGE)[1,2].
The pathogenesis of viral myocarditis typically unfolds in three phases: An initial phase of viral invasion, causing direct cardiomyocyte injury; a subsequent immune activation phase characterized by molecular mimicry and T cell-mediated damage; and a chronic phase leading to myocardial fibrosis and remodeling. Innate and adaptive immune responses, particularly involving Th1 and Th17 pathways, are crucial in amplifying myocardial inflammation. Persistent immune activation ultimately leads to ventricular dysfunction and progression toward dilated cardiomyopathy[2,3].
Before the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, acute myocarditis was con
Moreover, influenza A (H1N1) represents an additional established trigger of viral myocarditis. Although it leads to myocardial involvement less frequently than SARS-CoV-2, influenza still plays a relevant role as a viral trigger. In a large United States cohort study, the incidence of myocarditis was 0.24 per 1000 person-years in adults and 0.06 per 1000 person-years in children after influenza, compared with 0.73 and 0.53 per 1000 person-years, respectively, after COVID-19. These findings indicate that, while the overall epidemiological burden is lower than with COVID-19, H1N1 represents an important cause of viral myocarditis[5].
Despite advances in understanding acute myocarditis, uncertainties persist regarding its optimal management. Current guidelines and expert consensus recommend that immunosuppressive therapies, including corticosteroids, should not be routinely used in virus-positive myocarditis because of the potential to promote viral persistence or replication. Instead, their use is generally reserved for specific histological subtypes, such as eosinophilic or giant cell myocarditis, or myocarditis associated with systemic autoimmune disorders. In selected clinical scenarios, particularly fulminant myo
H1N1-related myocarditis raises similar therapeutic questions as SARS-CoV-2 myocarditis. However, the available evidence is much more limited, since most studies have addressed viral myocarditis in general without focusing specifically on H1N1. Evidence on this condition is therefore largely limited to case reports and small case series, often describing fulminant presentations during the H1N1 pandemic, with heterogeneous outcomes following immunosuppressive therapy[11,12].
This case describes a young woman with fulminant myocarditis associated with a SARS-CoV-2 infection requiring mechanical circulatory support. Acute myocarditis during COVID-19 completely recovered, but was followed by a recurrent myocarditis episode during an H1N1 infection, raising questions about therapeutic strategies, genetic predisposition, and long-term management of recurrent viral myocarditis.
A 27-year-old female was admitted to the emergency department in March 2023, complaining of lower abdominal pain associated with nausea and vomiting.
The patient reported a paucisymptomatic SARS-CoV-2 infection in the days prior to admission, managed with analgesics and anti-inflammatory drugs. Upon arrival, she was hemodynamically stable, with a blood pressure of 110/60 mmHg, a heart rate of 110 bpm, and an oxygen saturation of 99% on room air.
The patient had no significant past medical history and was not on any chronic medication.
Her family history was negative for cardiovascular, metabolic, autoimmune, or other hereditary disorders.
Physical examination revealed a regular cardiac rhythm with clear heart sounds, a diffusely tender abdomen with preserved peristalsis, and no signs of peritoneal irritation (negative Murphy’s and Blumberg’s signs). No clinical signs of systemic or pulmonary congestion were observed.
Laboratory tests revealed elevated levels of high-sensitivity Troponin T (0.353-0.358 μg/L, normal values < 0.014 μg/L), an increased white blood cell count (13 × 10³), and an elevated C-reactive protein (CRP) (7.9 mg/dL; normal value ≤ 0.6 mg/dL).
The 12-lead electrocardiogram (ECG) at admission revealed sinus tachycardia and ST-segment elevation in the inferolateral leads, without reciprocal ST-segment depression in the corresponding leads (Figure 1A).
As part of the diagnostic workup for abdominal pain, a contrast-enhanced computed tomography (CT) scan of the chest and abdomen was performed, revealing a pericardial effusion (maximum 2.2 cm) accompanied by signs of peripheral venous congestion. At the pulmonary level, the CT showed bilateral ground-glass opacities and consolidations, during COVID-19 infection (Figure 1B). A transthoracic echocardiogram confirmed the presence of a circumferential pericardial effusion measuring up to 2 cm in the apical region and echocardiographic signs of hemodynamic compromise. Initially, left ventricular systolic function was mildly reduced, with left ventricular ejection fraction (LVEF) of approximately 50%. The patient, hemodynamically stable upon admission, began to develop clinical signs of hemodynamic deterioration progressively.
Given the echocardiographic findings suggestive of cardiac tamponade and the patient’s worsening hypotension (blood pressure of 70/50 mmHg), an emergency pericardiocentesis was performed on the day of admission, successfully draining 250 mL of serous fluid.
On the following day, however, follow-up echocardiograms revealed a further decline in ejection fraction to 10% (Figure 1C), accompanied by progressive hemodynamic deterioration (blood pressure of 70/50 mmHg) and rising lactate levels, reaching 5.3 mmol/L. Due to this worsening condition leading to cardiogenic shock, the patient was transferred to the intensive care unit (ICU) for intubation and inotropic support with noradrenaline, dobutamine and levosimendan (administered as a 24-hour intravenous infusion). Given the rapid hemodynamic deterioration and the insufficient inotropic support, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was promptly started.
Based on the presentation with cardiogenic shock and severe left ventricular dysfunction, there was a strong suspicion of fulminant myocarditis, with SARS-CoV-2 infection considered the most likely underlying cause.
The suspicion of fulminant myocarditis secondary to SARS-CoV-2 infection was very high. However, given the ongoing cardiogenic shock and the impossibility of performing an endomyocardial biopsy due to the VA-ECMO support, which required continuous unfractionated heparin infusion, the patient was empirically treated with high-dose corticosteroid therapy (intravenous methylprednisolone 3 mg/kg/day for 3 days, then 1 mg/kg/day for one month, followed by tapering to 0.33 mg/kg/day, under close monitoring of ventricular function, cardiac biomarkers, and overall clinical status[13]). In addition, considering the previously documented positivity for SARS-CoV-2, monoclonal anti-SARS-CoV-2 antibodies and antiviral therapy with remdesivir were started.
During the ICU stay, further diagnostic investigations were conducted to exclude autoimmune and infectious conditions (through autoantibody testing and bacteriological examinations) or substance abuse (via toxicological screening). However, all these tests yielded negative results. Only a comprehensive viral panel confirmed the already known SARS-CoV-2 positivity.
The chosen treatment, consisting of high-dose corticosteroids and specific antiviral therapy, led to progressive improvement in left ventricular function, with recovery of LVEF up to 60% within 6 days. This was accompanied by stabilization of the hemodynamic profile and overall clinical condition, which enabled weaning from VA-ECMO, ex
The decision to proceed with weaning from VA-ECMO was based on a multiparametric evaluation. The patient ex
Once the patient’s clinical condition improved and hemodynamic stability was achieved, further tests were performed to complete the diagnostic workup. CMR revealed an area of edema in the mid-basal inferior, inferolateral and lateral walls, increased T1 and T2 values in the mid-apical inferior and lateral walls, a non-ischemic LGE pattern with thin meso-/subepicardial striae in the inferior and inferolateral walls consistent with inflammatory sequelae, and a reactive thickening of the pericardial layers without effusion (Figure 1D-I).
The patient was subsequently discharged after one month on bisoprolol 5 mg/day and prednisone 25 mg/day, with scheduled outpatient follow-up visits for gradual tapering of therapy.
All images regarding COVID-19-related myocarditis, including electrocardiogram, echocardiographic images, chest CT, and CMR, are reported in Figure 1.
At three months, the patient fully recovered LVEF, leading to discontinuation of corticosteroid therapy. She remained asymptomatic and regained good functional capacity (NYHA class I). A six-month CMR confirmed an LVEF of 60% and the resolution of myocardial edema, with no evidence of LGE. As a result, she discontinued the beta-blocker in September 2023.
In January 2025, the patient presented to the emergency department with intermittent chest pain and mild dyspnea. She reported cough and fever in the preceding days, which had been managed with nonsteroidal anti-inflammatory drugs. She was hemodynamically stable upon admission, with normal oxygen saturation and an ECG showing sinus tachycardia at 100 bpm without repolarization abnormalities.
Blood tests showed a recurrent increase in high-sensitivity troponin T (0.037 μg/L to 0.132 μg/L, normal value ≤ 0.014 μg/L) and an elevated CRP level of 1.44 mg/dL (normal value ≤ 0.6 mg/dL). The echocardiogram showed a preserved LVEF (55%) but revealed hypokinesia of the basal inferoposterolateral segments and mild pericardial effusion. Suspecting recurrent myocarditis, she was admitted to the cardiac ICU.
Over the following days, the 12-lead electrocardiogram showed sinus tachycardia with repolarization abnormalities (negative T waves) in the inferior and lateral leads (Figure 2A). Moreover, LVEF declined to 25% with global hypokinesia, showing reduced left ventricular stroke volume (Figure 2B), though she remained hemodynamically stable. Given the rapid decline in LVEF and the need for inotropic support with levosimendan, an endomyocardial biopsy was proposed to achieve a definitive histological diagnosis and to guide tailored immunosuppressive therapy. However, the procedure was not performed due to the patient’s refusal, thus limiting the possibility of histopathological confirmation in this episode. Comprehensive laboratory testing, including bacterial cultures, autoimmunity panels, and toxicology screening, was repeated and yielded negative results. As an endomyocardial biopsy was not performed, the etiological diagnosis relied on virological testing, which identified H1N1 by nasopharyngeal swab. Based on this finding, specific antiviral therapy with oseltamivir was promptly initiated.
A CMR confirmed diffuse subepicardial edema and increased T1 and T2 mapping values (increased if compared to the previous acute event), and meso-subepicardial LGE in the inferior and inferolateral walls of the left ventricle (Figure 2D-J). Given her previous positive response to high-dose corticosteroids, treatment was reinitiated (intravenous methylprednisolone 3 mg/kg/day for 3 days, then 1 mg/kg/day), along with levosimendan. The intravenous methylprednisolone regimen was maintained for two weeks, followed by oral prednisone (1 mg/kg/day) for an additional two weeks, subsequently tapered to 25 mg/day. Overall, the patient was treated with high-dose corticosteroids, antiviral therapy with oseltamivir, and levosimendan.
Despite worsening systolic function, she remained stable without requiring mechanical circulatory support. Follow-up echocardiograms showed progressive improvement, with a full recovery of LVEF to 60% by the time of discharge. Laboratory parameters showed progressive normalization of cardiac and inflammatory biomarkers.
The patient was asymptomatic and hemodynamically stable upon discharge. Discharge therapy included a beta-blocker (bisoprolol 2.5 mg once daily) and oral corticosteroid (prednisone 25 mg daily). At the six-month follow-up visit, the patient was asymptomatic and in stable clinical condition (NYHA Class I). Transthoracic echocardiography demonstrated preserved biventricular systolic function without regional wall motion abnormalities. CMR confirmed the complete resolution of myocardial edema, showing only minimal residual areas of non-ischemic, meso-subepicardial LGE in the lateral and inferior walls. Considering the overall clinical stability and imaging findings, maintenance therapy with low-dose oral prednisone (5 mg/day) and bisoprolol (2.5 mg/day) was continued. Moreover, genetic testing was done due to her young age and recurrent myocarditis to study predisposition, but the results are still pending.
All images regarding influenza-related myocarditis, including electrocardiogram, echocardiographic images, chest X-ray, and CMR, are reported in Figure 2.
A detailed comparison of the clinical presentation, hemodynamic status, therapeutic approaches (including immuno
| COVID-19 fulminant myocarditis (March-April 2023) | Influenza A myocarditis (January-February 2025) | |
| Age | 27 | 29 |
| Triggering virus | SARS-CoV-2 | Influenza A |
| Hemodynamic status at admission | Cardiogenic shock, VA-ECMO required | LVEF reduction, but no mechanical support needed |
| ICU support | Inotropes (noradrenaline, dobutamine, levosimendan); VA-ECMO (7 days) | Mechanical circulatory support not required; levosimendan administered |
| Immunosuppressive therapy | Methylprednisolone IV high dose (3 mg/kg/day for 3 days, then 1 mg/kg/day for one month, followed by tapering to 0.33 mg/kg/day) | Methylprednisolone IV high dose (3 mg/kg/day for 3 days, then 1 mg/kg/day for 2 weeks), then oral prednisone 1 mg/kg/day for 2 weeks, subsequently tapered to 25 mg/day |
| Antiviral therapy | Intravenous remdesivir | Oral oseltamivir |
| Other immunomodulators | Monoclonal anti-SARS-CoV-2 antibodies (500 mg IV) | None |
| Other key therapies | Bisoprolol 5 mg/day | Bisoprolol 2.5 mg/day |
| Outcome at discharge | Asymptomatic, LVEF 60%, scheduled follow-up and CMR | Asymptomatic, LVEF 60%, scheduled follow-up and CMR |
| Follow-up | Cardiology clinic, CMR at 6 months, lab tests | Cardiology clinic, CMR at 6 months, lab tests, genetic screening |
| Therapy at 6 months | Discontinuation of corticosteroids at 3 months and bisoprolol at 6 months | Continuation of low-dose prednisone (5 mg/day) and bisoprolol (2.5 mg/day) |
This case describes a fulminant myocarditis associated with SARS-CoV-2 infection in a young woman who required mechanical circulatory support in the first episode; the second occurrence was likely triggered by H1N1. In both cases, the early initiation of high-dose corticosteroids, along with antiviral therapy, led to a complete recovery of LVEF. The recurrence during H1N1 infection raises questions about autoimmune mechanisms and the need for more straightforward therapeutic guidelines in non-COVID viral myocarditis.
SARS-CoV-2-related myocarditis is believed to occur primarily through an immune-mediated mechanism rather than direct viral injury. Although SARS-CoV-2 can enter cardiac cells via ACE2 receptors, postmortem studies revealed low or undetectable levels of viral genome in myocardial tissue, with predominant macrophage infiltration and limited direct cardiomyocyte damage[3,4,16]. Molecular mimicry, cytokine storm, and extracellular vesicle-mediated antigen pre
Nevertheless, the use of corticosteroids in viral myocarditis remains controversial, and the supporting evidence remains limited. The myocarditis treatment trial, a randomized placebo-controlled study in patients with biopsy-proven lymphocytic myocarditis and reduced LVEF, did not demonstrate significant benefits of immunosuppressive therapy, specifically prednisone in combination with azathioprine or cyclosporine, in terms of survival or improvement in ventricular function[17]. Subsequent studies have suggested that immunosuppressive therapy may be effective in specific patient subgroups. The tailored immunosuppression in inflammatory cardiomyopathy trial demonstrated that a six-month course of prednisone and azathioprine significantly improved LVEF and functional status in patients with virus-negative inflammatory cardiomyopathy and ongoing myocardial inflammation[13].
More specifically, evidence supporting the use of corticosteroids in viral myocarditis has progressively emerged. A recent case report described a young patient who experienced a recurrence of myocarditis three months after an initial episode. The diagnosis of recurrence was confirmed by CMR imaging, which showed findings consistent with active myocarditis. A viral etiology was suspected based on positive serologies for Coxsackie B2 and B5. The patient was treated with high-dose intravenous methylprednisolone followed by an oral taper, in combination with intravenous immunoglobulin, resulting in complete clinical and echocardiographic recovery at follow-up[18]. In a prospective randomized study of pediatric patients with persistent systolic dysfunction three months after acute viral myocarditis, treatment with oral prednisolone for four weeks significantly improved LVEF compared to standard heart failure therapy alone, with a higher proportion of patients achieving normalization of systolic function[19]. Moreover, a 2013 Cochrane meta-analysis of eight randomized controlled trials on corticosteroid therapy in viral myocarditis reported no significant reduction in mortality, but found modest improvements in LVEF and reductions in cardiac biomarkers such as creatine phos
Despite these findings, the use of corticosteroids in virus-positive myocarditis remains controversial due to the potential risk of enhancing viral replication and the absence of proven clinical benefits[21]. A randomized, international trial (MYTHS - MYocarditis THerapy with Steroids) is currently ongoing to evaluate the efficacy and safety of intra
Recent evidence supporting the use of corticosteroids in SARS-CoV-2-related myocarditis remains limited, relying on systematic reviews that include case reports and small case series. The specific pathophysiology of SARS-CoV-2 infection, characterized by an exaggerated immune response rather than direct viral cytotoxicity, has reconsidered its role. A systematic review by Kamarullah et al[8] found that approximately 72% of COVID-19 myocarditis cases treated with corticosteroids experienced significant clinical improvement, mainly when high-dose methylprednisolone was administered early. Similarly, Sawalha et al[9] reported that in their review of published cases, corticosteroid therapy was the most used treatment, associated with an 85% survival rate among treated patients. In line with these findings, an observational study by Kovalenko et al[10] involving 60 patients with acute myocarditis, diagnosed by cardiac magnetic resonance imaging 1-2 months after SARS-CoV-2 infection, showed that oral methylprednisolone administered over six months significantly improved LVEF and myocardial strain parameters, and reduced inflammatory signs at CMR. Approximately 42% of patients achieved normalization of systolic function. These findings suggest that corticosteroids may favorably modulate the inflammatory response in selected cases where immune-mediated injury is predominant[21,23]. In our patient, the rapid recovery of cardiac function and resolution of cardiogenic shock following high-dose methylprednisolone, alongside antiviral and monoclonal antibody therapy, supports this hypothesis and highlights the potential benefit of early targeted immunosuppression in COVID-19-related myocarditis. Despite these encouraging findings, the evidence is limited by the lack of standardized diagnostic criteria, variable therapeutic protocols, and the absence of randomized controlled trials specifically evaluating corticosteroids in COVID-19-related myocarditis.
Recurrent myocarditis is a rare but clinically meaningful entity. Its pathophysiology remains incompletely understood but is increasingly recognized to involve an interplay between immune dysregulation and genetic predisposition. A recent systematic review and meta-analysis by Monda et al[24] demonstrated that a significant proportion of patients with acute myocarditis harbor pathogenic or likely pathogenic variants in genes traditionally associated with cardiomyopathies, such as desmosomal and sarcomeric genes, suggesting a genetic substrate underlying susceptibility to myocardial inflammation and adverse remodeling. Based on these findings, Ammirati et al[25] proposed a “two-hit” model in a recent editorial, in which viral infections act as external triggers that unmask a latent genetic predisposition, thereby triggering or exacerbating myocardial injury. Considering her young age and the recurrence of myocarditis, our patient underwent genetic testing, which may provide further insights into the role of inherited susceptibility in the pathogenesis and prognosis of recurrent myocarditis.
The recurrence of myocarditis in our patient was triggered by a different viral agent (H1N1), underscoring the pos
In particular, comparing both episodes, early recognizing and treating fulminant myocarditis is essential for improving outcome. Actually, the episode of myocarditis occurred during H1N1 infection was apparently less severe than the initial COVID-19-related presentation. Several factors may account for this difference, among which the earlier recognition of the condition and the prompt initiation of supportive and immunosuppressive therapy are likely to have played a key role. These elements may have contributed to preventing fulminant deterioration during the recurrence.
These observations underscore the need for prospective studies to assess the role of immunomodulatory therapies in viral myocarditis, to identify more precise patient subsets that may benefit from such interventions and to establish correct timing for follow-up of this condition. From the perspective of evaluating immune activation and efficacy of immunosuppression, increasing evidence emphasizes the relevance of specific biomarkers, especially pro-inflammatory cytokines like interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-α), which may influence both the pathogenesis and clinical trajectory of viral myocarditis. Elevated serum IL-6 levels have been consistently associated with impaired left ventricular function, need for mechanical circulatory support, and adverse outcomes[30,31], while higher TNF-α concentrations characterize the acute phase of disease and may help differentiate it from recovery[32]. These observations suggest that IL-6 and TNF-α could serve as valuable prognostic biomarkers in the future. However, their clinical application is currently limited by the absence of large prospective studies or standardized validation. Given that corticosteroid therapy exerts an immunosuppressive effect, it will be important for future investigations to assess whether changes in these inflammatory markers correlate with treatment response, but evidence to support this hypothesis is currently lacking.
Because treatment responses remain unpredictable and prognostic biomarkers are not yet validated for routine use, careful long-term follow-up is crucial in patients with recurrent viral myocarditis. Such monitoring not only facilitates the timely recognition of new episodes but also helps identify patients at risk of developing dilated cardiomyopathy. Echocardiography provides essential information on ventricular function, but CMR offers unique value for follow-up by enabling tissue characterization and detecting residual inflammation or fibrosis. The persistence, extent, and distribution of LGE have been consistently associated with adverse outcomes, while its resolution is generally linked to a more favorable course[33]. Improvement or normalization of left ventricular function at 6 months has also been associated with favorable long-term outcomes in biopsy-proven myocarditis[34]. Nevertheless, our case illustrates that recurrence may occur even after apparent full recovery on CMR, underlining both the prognostic utility and the limitations of current imaging, and reinforcing the need for structured long-term surveillance.
In conclusion, this case highlights the importance of a comprehensive understanding of viral myocarditis mechanisms, encompassing the interplay between host immunity, genetic predisposition, and pathogen-specific factors. Further studies are required to define the roles of immunosuppressive and antiviral therapies in COVID-19 and non-COVID-19 viral myocarditis, and to establish individualized treatment approaches.
The main limitation of this clinical case concerns the absence of histological confirmation via endomyocardial biopsy, which was precluded in the first episode by the patient’s critical condition and the need for anticoagulation on VA-ECMO. During the second episode, the endomyocardial biopsy was not performed due to the patient’s refusal. Furthermore, genetic testing results are still pending, limiting our ability to draw definitive conclusions regarding her predisposition. Finally, as a single-patient report, generalizability is limited.
The present case illustrates the complexity of diagnosing and managing acute fulminant viral myocarditis in the post-COVID era. This case, including two distinct episodes of severe myocardial inflammation triggered by different viral pathogens, highlights the potential therapeutic benefit of corticosteroids in this challenging condition. The favorable response observed both in SARS-CoV-2-related and influenza-associated myocarditis suggests that high-dose corticosteroids may exert a beneficial effect by modulating the dysregulated immune response that underlies myocardial injury, irrespective of the specific viral trigger.
This case highlights the need for further prospective, randomized studies to define the role of corticosteroids in managing the immune response in virus-related myocarditis, to identify patients most likely to respond, and to establish evidence-based recommendations on timing, dosing and tapering strategies. Genetic testing and structured long-term follow-up programs may also play a crucial role in improving risk stratification and guiding personalized management.
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