Patient with native valve infective endocarditis and concomitant bacterial myopericarditis

Abstract

A 39-year-old man with known mitral regurgitation (MR) presented with chest pain, nausea and dizziness. Troponin of 5801 ng/L and scooped ST segments indicated myopericarditis. Cardiac MRI demonstrated an epicardial late gadolinium enhancement pattern consistent with a significantly myocarditic syndrome. Initially afebrile, the patient reported fevers a week earlier when abroad where he received amoxicillin.

The patient then began spiking temperatures and infective endocarditis (IE) was confirmed following blood cultures positive for Streptococcus sanguinis and Transoesophageal echocardiography (TOE) showing a vegetation on the anterior mitral valve leaflet. Patient underwent 6 weeks of intravenous benzylpenicillin and on resolution he was discharged to await valve surgery.

A model is proposed where septic embolism from IE caused bacterial myopericarditis, triggering the initial presenting complaint. It is suggested that prior antibiotic therapy and paracetamol suppressed the systemic symptoms of IE.

Background

This case is unusual as a previously healthy individual (with the significant risk factor of asymptomatic mitral regurgitation predisposing to infective endocarditis) presented with typically acute and clear symptoms/signs consistent with myopericarditis. The initial diagnosis was duly made, but meanwhile the underlying, and more serious, condition of IE remained undetected due to the masking effects of earlier antibiotic treatment. A timely diagnosis of IE was made in this instance because appropriate blood cultures were taken at a comparatively early stage of the recurrent febrile illness.

Case presentation

A 39-year-old man with a well-characterised history of mitral regurgitation (video 1) presented with severe retrosternal chest pain radiating to the lower jaw, shortness of breath, nausea, sweating and dizziness. Also recounting a recent history of fever, chills and arthralgia, he was apyrexial but presently taking oral augmentin dispensed to him when abroad. 1 g of paracetamol was given for pain, and observations were heart rate: 85/min, respiratory rate: 18/min, blood pressure: 120/81 mm Hg, temperature: 36.3°C and saturation of 98% on room air. No adenopathy, skin rash or peripheral signs of endocarditis were noted; sole examination findings of note concerned a pale, clammy appearance and a prominent pansystolic murmur. He was admitted pending invasive coronary angiography and echocardiography.

Video 1.

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DOI: 10.1136/bcr-2018-224907.video01

Echocardiography. TOE from 9 June 2017 showed severe mitral regurgitation, A2 prolapse and flail

Investigations

Initial bloods showed troponin of 5801 ng/L, C reactive protein (CRP) of 45 mg/L and a normal full blood count (FBC). ECGs showed PR depression and 1–2 mm elevated scooped ST segments in lateral leads; while mildly downsloping TP segments in V4/5 were also suggested (figure 1). This, with normal coronary angiography, supported an initial diagnosis of myopericarditis.¹ Transthoracic echocardiography (TTE) reported the overall impression of mildly impaired systolic function in the presence of MR. Troponin peaked at 13 940 ng/L 3 days postadmission and cardiac MRI (CMR) showed a dilated, mildly impaired left ventricle and mid to apical lateral hypokinesia with basal and mid lateral epicardial late gadolinium enhancement typical of significant myocarditic involvement (figure 2). Leucocytes remained within normal limits but CRP peaked at 67 mg/L on the sixth day postadmission, 24 hours after the final temperature spike (figure 3). Chest X-ray showed no focal consolidation and urinalysis was unremarkable.

Figure 1.

ECGs. (A) Admission: PR depression and 1–2 mm elevated scooped lateral ST segments with mildly downsloping TP segments (Spodick’s sign) indicating myopericarditis. (B) Five days postadmission: largely resolved.

Figure 2.

Cardiac MRI. (A) A dilated, mildly impaired left ventricle and mid to apical lateral hypokinesia. (B) Basal and mid lateral epicardial late gadolinium enhancement typical of myocarditis.

Figure 3.

The patient’s temperature and CRP plotted against time postadmission. Patient spiked temperatures 4 days after stopping oral antibiotics. 13 September 2017: TOE showed positive for vegetation (admission+15 days).

On seventh day postadmission, eight samples cultured Streptococcus sanguinis (viridans), exceeding the threshold of three positive paired samples required by Liesman for a microbial diagnosis of IE.² All showed high sensitivity to penicillin, meanwhile blood viral titres returned negative. TOE (video 2) reported severe MR due to anterior leaflet prolapse and flail thickened tip with a vegetation (figure 4).

Video 2.

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DOI: 10.1136/bcr-2018-224907.video02

Echocardiography. TOE conducted on 13 September 2017 (15 days postadmission) reported severe mitral regurgitation due to anterior leaflet prolapse and flail thickened tip with a vegetation

Figure 4.

Echocardiography. (A) TOE from 9 June 2017 showed severe mitral regurgitation (MR), A2 prolapse and flail. (B) TOE conducted on 13 September 2017 (15 days postadmission) reported severe MR due to anterior leaflet prolapse and flail thickened tip with a vegetation.

Treatment

• Intravenous antibiotic therapy: benzylpenicillin (1.2 g intravenous, six times daily—4 weeks).

• Colchicine (500 mg oral, once daily—3 months).

• Ramipril (2.5 mg oral, once daily—life long).

• Ibuprofen (400 mg oral, as required—until asymptomatic), omeprazole (500 mg oral, as required—until asymptomatic).

• Bloods (CRP, FBC) twice weekly and weekly ECGs.

Outcome and follow-up

Chest pain and fevers settled with intravenous antibiotics; CRP levels dropped as the patient recovered. A predischarge TOE showed persistent MR, with a vegetation still visible but presumed sterile (video 3). Four dental extractions were carried out, and no temperatures were recorded following the conclusion of antibiotic therapy. The patient was duly discharged and underwent successful valve repair surgery.

Video 3.

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DOI: 10.1136/bcr-2018-224907.video03

Echocardiography. Predischarge TOE showed persistent mitral regurgitation, with a vegetation still visible but presumed sterile

Discussion

The Dallas criteria describes myocarditis as inflammatory infiltration of the myocardium with necrosis and/or degeneration of adjacent myocytes,³ and is most commonly of viral origin, inciting a cytotoxic effect.⁴ Bacterial myocarditis is ‘an uncommon cause of infectious myocarditis; usually seen in the context of overwhelming sepsis or as part of a specific bacterial syndrome’,⁵ although Malnick et al claim it is probably underdiagnosed and suggest that streptococcal myocarditis may be commoner than previously appreciated.⁶

Symptoms of IE such as loss of appetite, arthralgia and night sweats overlap with many conditions. While fever is almost inevitable, many patients may initially experience only a general malaise as reported here. Diagnosis can therefore be difficult due to varied presentations, which risks delayed admission and treatment.⁷ Li et al remind us that it is typically a syndrome diagnosis but that misdiagnosing it may be a clinical catastrophe.⁸

Embolism represents one of the most severe complications of IE and is not uncommon, having been reported to occur in 13% to 49% (of patients) with IE.⁹ Meanwhile, bacterial spread via direct extension from the endocardium is also perhaps less rare than widely believed. In the preantibiotic era, Flaxman reported that myocardial changes were frequently noted in cases of bacterial endocarditis,¹⁰ and Saphir remarked that typical abscesses were often present which were apparently the result of lodgement of bacterial emboli in minute vessels.¹¹ Meanwhile Weiss and Wilkins described abscesses ‘formed as a direct extension of a small mural pneumococcus vegetation’.¹² More recently, Wasi and Shuter report that the impact of antimicrobial therapy, modern diagnostic techniques and other approaches on the epidemiology of bacterial myocarditis has not been defined.¹³

Study findings of Mahrholdt et al concluded that focal myocardial gadolinium enhancement on CMR, coupled with abnormalities on regional wall motion during echocardiography, yielded a positive predictive value of 71% in myocarditis.¹⁴ Varghese et al advocate CMR for differentiating between Myocardial Infarction (MI) and the less common condition of myocarditis, stating that such unusual CMR appearances obviate the necessity for endomyocardial biopsy.¹⁵ MI was discounted in this case by angiography, and myocarditis was suggested by the epicardial distribution of late gadolinium enhancement^{16 17} but without insight into the pathogenesis behind the diagnosed myopericarditis. Bacterial myopericarditis represents probable sequelae of IE in this case, but endomyocardial biopsy is not recommended by international guidelines within the diagnostic pathway of myocarditis. Meanwhile, IE was not suggested at this stage by the clinical picture, and a myocarditis of viral aetiology was a natural assumption.

Fowler and Bayer state that conditions causing turbulent flow across the endocardium predispose patients to IE. Prolapse of thickened mitral valve leaflets and/or regurgitation increases the risk of endocarditis by about 10-fold over that of the general population.¹⁸ In this case, MR remained the sole presenting feature that bore any correlation with IE until the patient spiked temperatures. Temperatures mandated the taking of blood cultures, which in turn justified the diagnostic TOE. So the symptomatic relief provided by paracetamol and amoxicillin effectively eliminated a minor criterion (fever)¹⁹ and thereby lowered the index of suspicion. The presenting complaint was explained by the convincing diagnosis of myopericarditis. Meanwhile, the subclinical endocarditis (likely causative of the secondary myopericarditis) remained undiagnosed until later.

Treatment protocol was followed according to ESC (European Society of Cardiology) guidelines. Highly penicillin-susceptible S. viridans (sanguinis) group streptococci should demonstrate an expected cure rate of >95%.²⁰ Aminoglycosides were stopped after 1 day of therapy when culture sensitivities were received.

Conclusion

This report describes an unusual presentation of a rare but serious condition. It is explained by the unifying diagnosis of an underlying IE with a complication of myopericarditis due to septic embolism. It was detected in a timely fashion by the simple and prudent step of taking blood cultures in response to an unexplained febrile illness that was inconsistent with myopericarditis.

The delayed presentation of the IE provides some intrigue but can be cautiously explained without contradicting Duke’s criteria. The patient was treated according to protocol and responded well to make a good recovery.

Learning points.

• Mitral regurgitation represented the only significant risk factor in this patient’s presentation with infective endocarditis. Appropriate blood cultures were vital in this case.

• While being only a minor diagnostic criterion, mitral regurgitation raises the index of suspicion for infective endocarditis. Early TOE may be prudent even with negative TTE findings, particularly if the clinical picture is unclear.

• Bacterial myopericarditis, while rarer than viral myopericarditis, should never be discounted even in the absence of an established bacteraemia. This is especially pertinent to patients at increased risk of infective endocarditis.

• Symptomatic remedies and oral antibiotics rendered an acute condition into a subclinical presentation, masking the typical clinical presentation of endocarditis.