Abstract
In this case report, we describe two previously healthy young males who presented with cardiac symptoms suggestive of Lyme carditis (LC). LC-associated arrhythmia is a potentially fatal complication of Lyme disease, which typically occurs during the early disseminated and late stages. In high endemic areas a high degree of suspicion is vital to avoid misdiagnosis and delayed treatment, and to prevent long-term complications of disseminated infection and potentially fatal outcome.
Learning objective
Lyme carditis (LC) can present with a wide array of symptoms. The following two cases illustrate the diverse clinical manifestations of LC, as well as the potential for ‘doctor’s delay’ in diagnosing patients with LC.
Introduction
Borrelia burgdorferi sensu lato is a collective term for several Borrelia species, the causative agent of Lyme disease (LD), and is transmitted to vertebrate hosts by Ixodes ticks. Untreated, LD can cause disease manifestations in several organs, including the heart [ ].
Lyme carditis (LC) is a potentially fatal complication of LD. In Europe, LC is a rare manifestation of untreated LD, with regional differences and a reported incidence of 0.3–4.0 % [ ]. The most common clinical presentation is high-degree atrioventricular (AV) block, which can progress rapidly [ ]. Most AV blocks resolve with appropriate antibiotic treatment without the requirement for a permanent pacemaker [ ].
This case report discusses two young previously healthy males presenting with cardiac symptoms and AV block. However, neither patient could recall previous tick bites or the pathognomonic erythema migrans (EM), characteristic for the early localized stage of LD. Thus, correct diagnosis and appropriate treatment were delayed in both patients.
Case report
Patient A
An 18-year-old male, residing in western Norway, was admitted to the emergency department (ED) of our regional University Hospital in July 2020 after three weeks of periodic heart palpitations, dyspnea, and dizziness. He had no previous medical history, recent travel history, and did not take any regular medications.
On admission to the ED, the patient reported no symptoms but recalled an unspecific insect bite on his ankle one month prior to admission, with subsequent development of an itchy, red rash around the bite, lasting for two weeks. Clinical examination and vital parameters were unremarkable. Blood tests showed a slightly elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP) level of 709 ng/L (reference range < 85 ng/L). The electrocardiogram (ECG) ( Fig. 1 ) showed second-degree AV block Mobitz type I. Transthoracic echocardiography (TTE) demonstrated slightly reduced left ventricular ejection fraction of 45–50 %, but was otherwise normal. The patient was transferred to the cardiovascular intensive care unit for closer monitoring.

Within hours, the patient reported dizziness while lying flat on his back, and the cardiac telemetry revealed third-degree AV block with a junctional escape rhythm of 26 beats per minute. To maintain an adequate cardiac output, a continuous intravenous isoprenaline infusion was initiated, stabilizing the junctional escape rhythm at 60 beats per minute and improving the patient’s symptoms.
The patient’s progressive AV block, previous reported insect bite, and the fact that the patient resided in an LD endemic region, led to the suspicion of LC as the underlying cause. A Borrelia burgdorferi antibody test was performed and came out positive (IgM 145 AU/mL, IgG 1297 AU/mL) on day two after admission. The patient was started on ceftriaxone 2 g intravenously every 24 h.
Due to hemodynamic instability and continuous need of isoprenaline, a temporary transvenous pacemaker (PM) was placed on day 3. The AV block gradually resolved during the following week, and on day 10 of admission the temporary transvenous PM was removed. The patient was discharged the following day with a one-week course of 100 mg oral doxycycline twice daily. His general practitioner followed the patient after discharge from the hospital, and the patient has had no further reported cardiovascular admissions or events in the three years since discharge.
Patient B
A 19-year-old male was admitted to his local hospital in western Norway in July 2020 with a one-day history of inspiratory chest pain along with intermittent pressure in the chest radiating to his right upper arm. He had no previous medical history and did not take any regular medications or illicit drugs.
On admission, the patient had a temperature of 38.7 °C. Remaining vital parameters and the clinical examination were normal. Blood tests revealed an elevated leukocyte count of 12.3 /L (reference range 4.1–12.0 × 10 9 /L) along with a high-sensitivity cardiac troponin T (hs-cTnT) of 190 ng/L (reference range < 15 ng/L). The ECG showed sinus rhythm with normal AV conduction. Chest X-ray and TTE were described as normal. A non-ST-elevation acute coronary syndrome (NSTE-ACS) was suspected, and the patient was transferred to our hospital for urgent coronary angiography.
Ten hours after initial presentation, the patient was admitted to our hospital. The ECG now showed sinus rhythm with ST elevations in leads I, aVL, and V4 to V6, along with a mild PR-segment depression. Hs-cTnT was 195 ng/L.
Coronary computed tomography angiography (CTA) showed no coronary stenoses. A cardiac magnetic resonance imaging scan (CMR) showed extensive myocardial edema and late gadolinium enhancement (LGE) in the left ventricle (LV) as well as in the free wall of the right ventricle (RV). In addition, signs of inflammation were seen in the pericardium covering the affected myocardium. No significant pericardial effusion was detected ( Fig. 2 A-C ). The left ventricular ejection fraction as measured by the CMR was 58 %. A non-specific viral perimyocarditis was suspected. Treatment with ibuprofen 600 mg three times daily and colchicine 500 μg twice daily was prescribed, and the patient was discharged from hospital after seven days.
