Abstract
Background
Lyme disease, caused by Borrelia burgdorferi, is the most common vector-borne infection in North America. Cardiac involvement occurs in approximately 1% to 10% of untreated infections and most commonly manifests as atrioventricular conduction abnormalities.
Case Summary
A 29-year-old man with arrhythmogenic right ventricular cardiomyopathy underwent orthotopic heart transplantation. Early postoperatively he developed atrial flutter progressing to complete heart block despite preserved graft function and absence of rejection. Donor history revealed recent tick exposure. Warthin-Starry staining of surveillance endomyocardial biopsy demonstrated rare spirochetes consistent with Borrelia species. The patient received intravenous ceftriaxone for presumed donor-derived Lyme carditis but ultimately required permanent pacemaker implantation.
Discussion
This case highlights Lyme carditis as a rare potential cause of early conduction abnormalities after heart transplantation.
Key words: atrioventricular block, Borrelia burgdorferi, donor-derived infection, heart transplantation, Lyme carditis
Visual Summary
History of Presentation
A 29-year-old man with end-stage cardiomyopathy underwent orthotopic heart transplantation. During the early postoperative course, he developed atrial flutter with slow ventricular response and progressive conduction abnormalities that evolved into complete heart block requiring epicardial pacing (Figure 1). On postoperative day 10 he developed hypotension and diaphoresis, prompting evaluation that revealed pericardial tamponade requiring surgical evacuation (Video 1).
Take-Home Messages
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Early atrioventricular block after heart transplantation should prompt evaluation for causes beyond rejection when graft function is preserved.
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Lyme carditis may present with severe conduction abnormalities and should be considered in transplant recipients with potential donor-derived tick exposure.
Figure 1.
Telemetry Demonstrating Complete Heart Block
Telemetry tracing obtained on postoperative day 18 (November 13, 2025) demonstrating underlying complete atrioventricular block.
Past Medical History
The patient had arrhythmogenic right ventricular cardiomyopathy complicated by ventricular arrhythmias and progressive biventricular heart failure requiring orthotopic heart transplantation.
Differential Diagnosis
Early atrioventricular (AV) conduction abnormalities after heart transplantation may occur due to
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ischemia-reperfusion injury
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surgical trauma to the conduction system
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acute rejection
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medication effects
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metabolic disturbances
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infectious etiologies including myocarditis
Investigations
Transthoracic echocardiography demonstrated preserved allograft function with a left ventricular ejection fraction >55%.
Right heart catheterization demonstrated a right atrial pressure of 13 mm Hg, right ventricular pressure of 36/8 mm Hg, pulmonary arterial pressure of 38/20 mm Hg (mean: 27 mm Hg), and pulmonary capillary wedge pressure of 22 mm Hg.
Cardiac output by the Fick method was 8.9 L/min, with a cardiac index of 3.0 L/min/m2. Pulmonary vascular resistance was 0.6 Wood units, and no intracardiac shunt was present (Qp/Qs: 1.0). These findings were consistent with preserved graft function and adequate cardiac output without evidence of graft failure.
Immunologic evaluation did not suggest rejection. Post-transplant crossmatch testing was negative, donor-specific antibodies were absent, and surveillance endomyocardial biopsy performed on postoperative day 8 demonstrated no evidence of acute cellular rejection (0R) or antibody-mediated rejection (pAMR0).
During evaluation of hypotension on postoperative day 10, imaging demonstrated a pericardial effusion with tamponade physiology (Video 1). Emergent surgical exploration revealed approximately 350 mL of sanguineous pericardial fluid and clot without an identifiable surgical bleeding source. The pericardial space was evacuated and drains were placed, with subsequent hemodynamic stabilization (Video 2).
Because the severity and persistence of conduction abnormalities were unusual in the absence of rejection or graft dysfunction, donor history was reviewed, which revealed recent outdoor exposure including participation in a “deer camp,” raising concern for deer tick exposure. Recipient Lyme serologic testing (IgM and IgG) was negative.
Warthin-Starry staining of the surveillance endomyocardial biopsy demonstrated rare spirochetes morphologically consistent with Borrelia species (Figure 2).
Figure 2.
Endomyocardial Biopsy Specimens Demonstrating Spirochetes
(A and B) Warthin-Starry stain of endomyocardial biopsy specimen demonstrating rare spirochetes (arrows) morphologically consistent with Borrelia species.
Additional molecular testing was pursued given the rarity of organisms identified. Next-generation sequencing performed on formalin-fixed paraffin-embedded (FFPE) biopsy tissue did not detect Borrelia burgdorferi, which was suspected to reflect low organism burden below the assay detection threshold and suboptimal performance of next-generation sequencing on FFPE tissue.
Management
Intravenous ceftriaxone (2 g daily) was initiated for treatment of severe Lyme carditis, in accordance with current treatment recommendations.1 Mycophenolate dosing was temporarily reduced.
Despite antimicrobial therapy, complete heart block persisted and the patient ultimately required permanent pacemaker implantation.
Outcome and Follow-Up
The patient completed a 21-day course of intravenous ceftriaxone. Leukocytosis gradually improved and graft function remained preserved on follow-up imaging. However, AV conduction did not recover and the patient remained pacemaker dependent.
Discussion
Lyme disease is the most common vector-borne infection in North America and is caused by the spirochete Borrelia burgdorferi, transmitted by Ixodes ticks.1 Although most infections present with dermatologic, neurologic, or rheumatologic manifestations, cardiac involvement—referred to as Lyme carditis—occurs in approximately 1% to 10% of untreated cases.2,3 Cardiac manifestations most commonly involve the conduction system and may rapidly progress to complete heart block, which is typically transient.4 Pericardial involvement including pericarditis and pericardial effusion has also been reported in Lyme carditis.2
The diagnosis of Lyme carditis typically relies on compatible clinical features supported by serologic testing.1 However, serologic assays may be negative early in infection and may also be difficult to interpret in immunocompromised hosts because antibody responses may be delayed or attenuated.5,6 In these situations, tissue-based diagnostic techniques such as histochemical staining or molecular assays may provide additional evidence, although sensitivity may be limited when organism burden is low.
Transmission of Lyme disease through solid-organ transplantation has not been well documented. Large surveillance studies examining donor-derived infections have not identified B burgdorferi as a transmitted pathogen.7 Similarly, a Centers for Disease Control and Prevention investigation found no evidence of Lyme disease transmission through transplantation, including among recipients of corneal grafts from donors with confirmed Lyme disease.7,8 Because routine donor screening protocols do not include Lyme disease testing, recognition of potential donor-derived infection relies largely on clinical suspicion and targeted diagnostic evaluation.
High-grade AV block after heart transplantation is most commonly attributed to ischemia-reperfusion injury, surgical trauma to the conduction system, rejection, medication effects, or metabolic disturbances.9 In this patient the severity and persistence of conduction disease were disproportionate to the remainder of the clinical picture. Serial echocardiography demonstrated preserved graft function, and repeated immunologic evaluation did not support rejection.
Several features of this case support a donor-derived infectious process involving the cardiac allograft. The onset of conduction abnormalities occurred very early after transplantation, making recipient-acquired tick exposure unlikely. The recipient had no known prior history of Lyme disease, and serologic testing was negative. Review of donor history revealed recent outdoor exposure compatible with tick exposure. Histochemical staining of surveillance endomyocardial biopsy demonstrated rare spirochetes morphologically consistent with Borrelia species. Although confirmatory molecular testing was negative, low organism burden within myocardial tissue may limit the sensitivity of molecular assays performed on FFPE tissue.
Taken together, these findings support the diagnosis of presumptive donor-derived Lyme carditis affecting the transplanted heart.
Although AV conduction abnormalities associated with Lyme carditis typically improve with antimicrobial therapy, persistent conduction disturbances requiring permanent pacing have been reported in a minority of cases.4 In this patient, complete heart block persisted despite antimicrobial therapy, suggesting that conduction system injury may have been related to immunosuppression or had occurred before recognition of infection.
Conclusions
Presumptive donor-derived Lyme carditis may represent a rare cause of conduction abnormalities after orthotopic heart transplantation. When high-grade AV block occurs in the absence of rejection or graft dysfunction, clinicians should consider a broad differential diagnosis that includes infectious etiologies. Recognition may require targeted tissue-based diagnostic testing when serologic studies are negative.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
Appendix
Visual Summary.
| Time | Events |
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| Day 1 | A 29-year-old man with arrhythmogenic right ventricular cardiomyopathy underwent orthotopic heart transplantation. |
| Early postoperative period | The patient developed atrial flutter with slow ventricular response progressing to conduction abnormalities and complete heart block requiring pacing. Graft function was preserved, with no evidence of rejection. |
| Postoperative day 8 | Surveillance endomyocardial biopsy showed no rejection (0R, pAMR0). |
| Postoperative day 10 | Patient developed hypotension and diaphoresis. Imaging revealed pericardial tamponade requiring surgical evacuation of ∼350 mL sanguineous fluid with hemodynamic improvement. |
| Subsequent evaluation | Persistent conduction abnormalities prompted further investigation. Donor history revealed recent tick exposure. Lyme serologies were negative. |
| Diagnostic work-up | Warthin-Starry staining of endomyocardial biopsy demonstrated rare spirochetes consistent with Borrelia species. |
| Management | Initiated intravenous ceftriaxone and reduced immunosuppression. |
| Hospital course | Despite antimicrobial therapy, complete heart block persisted requiring permanent pacemaker implantation. |
| Follow-up | Completed 21-day course of antibiotics. Graft function remained preserved, but patient remained pacemaker dependent. |
Appendix
Point-of-Care Transthoracic Echocardiography
(A) Parasternal long-axis view demonstrating circumferential pericardial effusion. (B) Apical 4-chamber view demonstrating pericardial effusion. (C) Parasternal short-axis view demonstrating pericardial effusion.
Transesophageal Echocardiography Demonstrating Residual Pericardial Effusion
Transesophageal echocardiography obtained on postoperative day 10 demonstrating a small residual pericardial effusion after evacuation of approximately 350 mL of sanguineous pericardial fluid via pericardial window.
References
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Associated Data
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Supplementary Materials
Point-of-Care Transthoracic Echocardiography
(A) Parasternal long-axis view demonstrating circumferential pericardial effusion. (B) Apical 4-chamber view demonstrating pericardial effusion. (C) Parasternal short-axis view demonstrating pericardial effusion.
Transesophageal Echocardiography Demonstrating Residual Pericardial Effusion
Transesophageal echocardiography obtained on postoperative day 10 demonstrating a small residual pericardial effusion after evacuation of approximately 350 mL of sanguineous pericardial fluid via pericardial window.