A case report of cardiac cysticercosis in a returning traveller: a rare cause of myocarditis.

Background: A 38-year-old male of Indian origin presented via ambulance directly to the cardiac catheter lab with chest pain and electrocardiogram changes suggestive of an ST-elevation myocardial infarction. Serum troponin was recorded at >10 000 ng/L. Case summary: Angiogram revealed normal coronary arteries. Echocardiography showed myocardial lesions and a subsequent cardiac magnetic resonance imaging showed myocardial cysticercosis. Discussion: This is a case of myocardial cysticercosis causing myocarditis. He was treated successfully with albendazole for Taenia solium infection and non-steroidal anti-inflammatory drugs and colchicine for myocarditis.

Myocardial cysticercosis is rare but has to be taken into consideration in patients who have travelled to countries where Taenia solium is prevalent.

Optimal imaging is with cardiac magnetic resonance imaging.

Management is with antihelmintics and anti-inflammatory medications.

Introduction

A 38-year-old male presented with sudden-onset chest pain that woke him from sleep. He had no associated nausea or breathlessness but had been feeling non-specifically unwell. A 12-lead electrocardiogram showed sinus rhythm with subtle ST-segment elevation inferiorly. He underwent an emergency angiography that revealed unobstructed smooth coronary arteries.

Case summary

He had been unwell with fevers for 3 days prior to admission. Systems review revealed no headaches or weakness, no bladder or bowel symptoms, no recent weight loss, or night sweats. He had no significant past medical history, was a non-smoker, consumed around 10–20 units of alcohol a week, and reported no illicit drug use. He was of Indian descent and worked as a marketing director for a clothing company which required frequent travel abroad. On examination, he was afebrile and haemodynamically stable with normal heart sounds. His chest was clear and neurological examination was unremarkable. His abdomen was soft and non-tender with a palpable spleen 2 cm below the left costal margin.

He remained in sinus rhythm, with no detected arrhythmias whilst an inpatient and blood tests were unremarkable apart from a troponin I of 3000 ng/L which peaked at 17 000 ng/L (normal range 0–40 ng/L) on Day 2. An echocardiogram showed preserved left ventricular (LV) systolic function with no valvular abnormalities. Cardiac magnetic resonance imaging (MRI) showed a high signal on the T2-weighted short tau inversion recovery (STIR) sequence and late gadolinium enhancement in the subepicardial basal inferior and lateral walls indicating extensive myocardial oedema consistent with acute myocarditis ( and ) with preserved LV systolic function. There were also non-enhancing cysts seen within the myocardium, skeletal muscle, subcutaneous tissue, and lung parenchyma ( and ) consistent with systemic cysticercosis infection. A computed tomography scan of the head showed vesicles within the cerebellum, temporal lobe, and frontal lobe () consistent with neurocysticercosis. The patient had no evidence of cysticerci in the eyes. Stool analysis was negative for cysts, and therefore, the diagnosis was made on imaging alone. Serum autoantibody and viral screen as part of myocarditis work up were negative. Management was with albendazole 400 mg twice daily for 3 days for parasitic infection in combination with diclofenac 75 mg twice daily for 7 days and colchicine 0.5 mg twice daily for 3 months for myocarditis. The patient’s fevers and chest pain resolved. He was well on follow-up at 4 months and a repeat cardiac MRI showed resolution of myocardial oedema and cyst on T2-weighted imaging and residual late gadolinium enhancement in the subendocardial inferior and lateral walls consistent with myocardial fibrosis.

Short-axis T2-weighted STIR sequence demonstrates high signal along the basal inferior and lateral walls in keeping with extensive myocardial oedema (block white arrow).

Short-axis late gadolinium sequence shows extensive subepicardial and mid myocardial high signal along the basal inferior and lateral walls (block white arrows).

Axial four-chamber cine stack shows a well-defined round homogenous high signal lesion in the septum (block white arrow). Similar lesions are also seen in the lung (arrowhead) and chest wall musculature (thin white arrow).

Axial four-chamber T1-weighted fat saturated sequence with a well-defined round homogenous high signal lesion in the septum (block white arrow). Similar lesions are also seen in the lung (arrowhead) and chest wall musculature (thin white arrow).

Axial computed tomography brain images without contrast showing a cyst in the left temporal lobe (white block arrow).

Discussion

Cysticercosis is a parasitic infection caused by larval cysts of the pork tapeworm Taenia solium after ingestion of uncooked pork, contaminated food, or by contact with an infected person.[1] It is most common in developing countries in Africa, Asia, and Latin America.[2]

The cysts may go undetected by the host immune system for many years. However, as cysticerci age, their cystic structures can degenerate and rupture, leading to inflammation followed by encasement in a granuloma, most commonly in the brain.[3] Although myocardial cysticercosis has been reported before, this is the first report of it leading to acute and active inflammation seen within the myocardium, likely a response to degeneration of myocardial cysts.

Lead author biography

I am a Specialist Registrar Trainee in Cardiology in the UK. My areas of interest include acute cardiovascular care, cardiac imaging, and intervention.

Supplementary material

Supplementary material is available at European Heart Journal – Case Reports online.

Slide sets: A fully edited slide set detailing this case and suitable for local presentation is available online as Supplementary data.

Consent: The author confirms that written consent for submission and publication of this case series including images and associated text has been obtained from the patients in line with COPE guidance.

Conflict of interest: None declared.

Funding: The authors declare no funding for this case report.

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