Isolated Right Atrial Myocarditis Secondary to Listeria Monocytogenes

Abstract

Background

Myocarditis secondary to Listeria monocytogenes is rare but life-threatening.

Case Summary

A 54-year-old woman with a prior history of systemic lupus erythematous on immunosuppression presented with chest pain and fever. Troponin and C-reactive protein levels were elevated, and an electrocardiogram showed T-wave inversion. Fludeoxyglucose F18 positron emission tomography showed right atrial (RA) uptake. Cardiac magnetic resonance identified RA wall thickening, akinesia, and late gadolinium enhancement, with an associated RA thrombus. Blood cultures were positive for L. monocytogenes. She received antibiotics and anticoagulation. Repeat imaging demonstrated resolution of both RA dysfunction and thrombus resolution.

Discussion

Myocarditis with atrial involvement is uncommon, often associated with inflammatory or autoimmune conditions. Infectious causes must be excluded before starting immunosuppressive therapy. Cardiac involvement by L. monocytogenes is unusual but may not be infrequent in immunocompromised patients. Early identification and treatment are critical.

Take-Home Messages

Rare causes of myocarditis should always be considered, particularly in immunocompromised patients. Multimodality imaging can help with diagnosis and guide treatment.

Graphical Abstract

History of Presentation

A 54-year-old woman presented with a 3-day history of chest pain, shortness of breath on exertion, and fever. She was hemodynamically stable, and physical examination results were unremarkable. The electrocardiogram showed a junctional rhythm with fractionated QRS and anterolateral T-wave inversion (Figure 1). Blood test demonstrated raised troponin (troponin T 980 ng/L, normal <14 ng/L) and C-reactive protein (100 mg/L) levels, with normal white blood cell count (9.6 × 10⁹/L).

Figure 1.

12-Lead Electrocardiogram Demonstrating a Junctional Rhythm With Fractionated QRS and Anterolateral T-Wave Inversion

Past Medical History

She had been diagnosed with systemic lupus erythematous 15 years before and had been on various steroid and steroid-sparing immunosuppressive medications including biologic agents (rituximab). Because of recent worsening of myositis, confirmed by raised creatine kinase levels, the dose of steroid had been increased to 40 mg once a day. She had received the second dose of the Moderna COVID vaccine 2 weeks before presentation.

Differential Diagnosis

Myocarditis secondary to systemic lupus erythematosus or recent Moderna vaccination was favored, though infectious causes could not be ruled out.

Investigations

An echocardiogram showed normal biventricular size and function, no regional wall motion abnormalities, normal valvular function, and mild pericardial effusion. A computed tomography coronary angiogram did not show any significant coronary artery disease.

Management

Given the likelihood of autoimmune-related myocarditis, she received 3 days of intravenous methylprednisolone along with her usual dose of prednisolone 40 mg once a day and was transferred to our tertiary center for further management and investigations. The initial electrocardiogram demonstrated a junctional rhythm, which spontaneously reverted to sinus rhythm 2 days after admission. Cardiac magnetic resonance (CMR) imaging was not initially undertaken because of claustrophobia. After a carbohydrate-restricted diet and 12 hours of fasting, a fludeoxyglucose F18 positron emission computed tomography (FDG-PET/CT) was performed. β-Hydroxybutyrate levels to confirm ketosis were not measured. The scan showed increased right atrial (RA) uptake with soft tissue infiltration, raising suspicion for cardiac sarcoma or lymphoma. No ventricular uptake was observed (Figure 2).

Figure 2.

FDG-PET/CT Images

FDG-PET/CT demonstrating right atrial uptake (star). There was no ventricular uptake. FDG-PET/CT= fludeoxyglucose F18 positron emission computed tomography.

Given the result of the FDG-PET/CT, CMR was attempted before considering cardiac biopsy. CMR confirmed the presence of thickening and akinetic RA wall along with late gadolinium enhancement (Figure 3). There was a laminar thrombus extending to the inside of the inferior vena cava (Figure 4). The ventricles had normal size, thickness, and function, with no ventricular late gadolinium enhancement or signs of myocardial inflammation. There was no history of recent central venous catheter insertion, making catheter-related thrombus or infection less likely.

Figure 3.

CMR Images

(A, C) A still image of a 4-chamber view and a short-axis stack at the level of the right atrium (star) and demonstrates the presence of right atrial thickening. (B, D) A late gadolinium enhancement 4-chamber and short-axis stack at the level of the right atrium (star) and demonstrates the presence of laminar thrombus (white arrow) and right atrial enhancement (blue arrow). CMR = cardiac magnetic resonance.

Figure 4.

CMR Image

CMR image showing a right atrial stack and the presence of a laminar thrombus in the right atrium (1) extending to the inside of the inferior vena cava (2). CMR = cardiac magnetic resonance.

Because of the presence of a fever, blood cultures were taken and subsequently grew L. monocytogenes. She was therefore started on intravenous amoxicillin 2 g/4 hours and gentamicin 450 mg/d.

Outcome and Follow-Up

A working diagnosis of isolated RA L. monocytogenes myocarditis with RA thrombus was made, and anticoagulation with enoxaparin 135 mg daily was started. Once the inflammatory markers and creatine kinase normalized, prednisolone was reduced to 30 mg daily. Antibiotic therapy with gentamicin was continued for 7 days, and amoxicillin was continued for a total of 6 weeks, and she was discharged home on warfarin.

A repeat CMR 6 months later showed recovery of the RA function with resolution of the RA thickening and thrombus but persistence of the RA enhancement (Figure 5). Anticoagulation was stopped at that time. At 1-year follow-up, she remained asymptomatic with no evidence of cardiac thrombus on further imaging and was discharged from the cardiology clinic.

Figure 5.

CMR Images 6 Months After Starting Treatment

(A, C) A still image of a 4-chamber view and a short-axis stack at the level of the right atrium demonstrating resolution of right atrial thickening. (B, D) A late gadolinium enhancement 4-chamber and short-axis stack at the level of the right atrium showing resolution of atrial thrombus and showing some persistence of right atrial enhancement. CMR = cardiac magnetic resonance.

Discussion

Myocarditis is a myocardial inflammation predominantly affecting the ventricles that usually presents with chest pain, shortness of breath, or in more severe cases with cardiogenic shock or ventricular arrhythmias.¹ Atrial myocarditis is less frequently described, and it may manifest with atrial arrhythmias and conduction disease. Isolated atrial myocarditis is particularly rare and has been reported in giant cell and eosinophilic myocarditis.^2,3 Reports of atrial-predominant myocarditis remain limited in the literature and are often associated with inflammatory cardiomyopathy or autoimmune disease, highlighting its rarity and the diagnostic value of multimodality imaging in these cases.⁴

L. monocytogenes is a foodborne gram-positive bacterium that most commonly affects immunocompromised patients, elderly adults, pregnant women, and newborns. It is transmitted via contaminated food, particularly dairy products, deli meats, and raw fruits and vegetables. It causes a wide range of clinical syndromes, including sepsis, encephalitis, gastroenteritis, hepatitis, and liver abscesses. Diagnosis is typically confirmed through the identification of the pathogen in blood cultures or cerebrospinal fluid analysis. The standard treatment involves ampicillin or amoxicillin in combination with gentamicin for 2 to 3 weeks. In severe infections or complicated cases, prolonged therapy may be required.⁵

On rare occasions, when bacteremia occurs, it can also cause endocarditis, which is linked to high mortality if the bacterium is not identified and treated appropriately.⁶ Myocarditis due to L. monocytogenes and its association with RA involvement is very uncommon. To date, it has been previously reported in 3 case reports.7, 8, 9 Cases of pericarditis with pericardial fluid and cardiac tamponade have also been reported.¹⁰

This case is highly unusual due to the rare combination of isolated RA myocarditis and L. monocytogenes infection. The diagnosis was particularly challenging due to the patient's claustrophobia and initial use of the FDG-PET/CT, which revealed active inflammation but lacked the specificity of CMR and failed to detect the thrombus. In similar settings, CMR should be facilitated with open magnetic resonance imaging scanners or conscious sedation to ensure adequate image acquisition, thus avoiding diagnostic uncertainty associated with less specific imaging modalities.

This case also highlights the importance of considering infectious etiologies in immunocompromised patients presenting with myocarditis. The initial presumption of autoimmune-related myocarditis led to the administration of high-dose intravenous methylprednisolone before infectious causes had been ruled out; this situation can exacerbate disease progression and lead to adverse outcomes. Current European Society of Cardiology guidelines emphasize the need of excluding infectious causes before initiating immunosuppressive therapy in suspected myocarditis, particularly in individuals with systemic symptoms or immunosuppressive backgrounds.¹ In addition, in our case, delayed blood cultures postponed the identification of L. monocytogenes, reinforcing the need for early microbiological testing especially in immunocompromised population. Furthermore, our patient had recently undergone an increase in immunosuppressive therapy and recent COVID-19 vaccination that may have contributed to immune dysregulation and increased susceptibility to this rare presentation. These risk factors should be taken into account when evaluating atypical myocarditis in immunocompromised patients, as they may predispose to uncommon infectious etiologies presenting with unusual features, such as isolated atrial involvement.

Ultimately, this case underscores the importance of integrating clinical context, immune status, and multimodality imaging to accurately diagnose and manage myocarditis, particularly in cases with an atypical presentation.

Conclusions

Cardiac involvement from L. monocytogenes infection is rare but potentially life-threatening and may present in any form. Multimodality imaging clarified the pathophysiology and diagnosis and aided guiding the management and assessing treatment response.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Take Home Messages

• •Rare causes of myocarditis should always be considered in immunocompromised patients, and infectious etiologies must be actively ruled out before initiating immunosuppressive.
• •Multimodality imaging, including echocardiography, cardiac magnetic resonance, and fludeoxyglucose F18 positron emission tomography (if available), plays a crucial role in characterizing myocarditis, guiding management, and monitoring treatment response, particularly in atypical presentations.