Revised: May 22, 2026
Accepted: June 8, 2026
Published online: July 26, 2026
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Pericardial involvement in Lyme carditis is rare, and its clinical spectrum and outcomes are not systematized. To summaries knowledge on epidemiology, pa
Core Tip: Pericardial involvement in Lyme carditis is rare but can range from asymptomatic effusion to tamponade. This review of 15 documented cases highlights that electrocardiogram changes may mimic myocardial infarction, serological confirmation is key, and timely antibiotic therapy leads to favorable outcomes. Clinicians in endemic regions should consider Lyme disease in unexplained pericarditis, especially in young patients.
- Citation: Pereverzeva KG, Yakushin SS. Lyme carditis with pericarditis: A review of clinical cases. World J Cardiol 2026; 18(7): 121524
- URL: https://www.wjgnet.com/1949-8462/full/v18/i7/121524.htm
- DOI: https://dx.doi.org/10.4330/wjc.121524
Lyme disease (Lyme borreliosis) is the most common tickborne disease in the Northern Hemisphere, caused by spiro
Cardiac involvement in Lyme disease is relatively rare. In untreated patients, it occurs in 0.3%-4% of cases in Europe and in 0.5%-10% in the United States[5-7,9,10]. Pericarditis as a separate manifestation is diagnosed in 23% of patients with Lyme carditis in Europe[1] and in 2-5% of patients in the United States[1,5,11]. However, these figures may be underestimated due to the transience of symptoms, the lack of systematic echocardiographic screening, and difficulties in etiological verification[5,7].
Risk factors for the development of Lyme carditis include male sex[1,5,7,8], and age, as the disease usually affects young and middleaged individuals[4,12]. Most cases occur between June and December, reflecting the seasonal activity of Ixodes ticks[5,6]. Living in or travelling to endemic areas further increases the risk of infection[6,11].
Lyme carditis most often manifests as atrioventricular conduction disturbances of various degrees, from a slight prolongation of the PR interval to complete atrioventricular block, which can develop suddenly and become persistent[12,13]; the frequency of atrioventricular blocks reaches 90%-93%[4,14]. Pericardial involvement is less common but can occur with or without conduction disturbances[5,15]. Patients with Lyme pericarditis may experience chest pain, dyspnea, fever, and a pericardial friction rub[5,12]. The electrocardiogram (ECG) usually shows ST-segment elevation[5,15], and pericardial effusion may be absent, small, or large up to cardiac tamponade[5,6,15].
The pathophysiology of Lyme pericarditis consists of two main mechanisms. First, direct spirochetal invasion of the pericardium is possible, as confirmed through the detection of Borrelia burgdorferi in pericardial tissue and fluid[5,9]. Second, immune-mediated inflammation that occurs in response to the infection plays an important role in processes such as cross-reactive autoimmune reactions and lymphoplasmacytic infiltration of the pericardium[5,15]. Review articles emphasize that the combination of direct microbial damage and immune mechanisms underlies the clinical manifestations of Lyme pericarditis[5,7,15].
Despite more than 40 years of research on Lyme carditis, existing reviews on the topic are devoted mainly to atrioventricular conduction disturbances, whereas pericardial involvement has not yet been systematized, and most publications on Lyme pericarditis comprise single clinical observations or short case series. Thus, the aim of this narrative review is to systematize all documented cases of pericarditis, myopericarditis, and pericardial effusion associated with Lyme disease published in the available literature, with a detailed analysis of demographic data, clinical manifestations, instrumental findings, laboratory confirmation, treatment methods and outcomes.
The search was conducted on the PubMed and Scopus databases for the period from January 1980 to March 2025. The following search query was used: (“Lyme disease” OR “Lyme carditis” OR “Borrelia burgdorferi”) AND (“pericarditis” OR “pericardial effusion”). As a result of the search, 58 articles were selected in PubMed, and 11 in Scopus.
After merging and deduplication, the total number of unique records was 64. As this is a narrative minireview, a formal metaanalysis was not conducted and a Preferred Reporting Items for Systematic Reviews and Meta-analyses flow diagram was not used. The study selection process is detailed below.
Initial screening was performed on the titles and abstracts based on the following inclusion criteria: (1) Documented pericardial involvement (clinical diagnosis of pericarditis, presence of effusion according to echocardiography/computed tomography, effusion during pericardiocentesis, histological confirmation); (2) Established association with Lyme disease; and (3) Sufficient clinical information for analysis.
The exclusion criteria included the following: A lack of reliable confirmation of pericardial involvement, publications with no clinical data (reviews, editorial articles, in vitro studies, veterinary cases), and cases where an alternative tick
Cases with documented coinfections were not systematically excluded provided that a clear causative link to Lyme disease was established (serological confirmation, direct pathogen detection, or typical erythema migrans). If an alternative tickborne pathogen was the more likely cause and the association with Borrelia burgdorferi could not be reliably determined, the case was excluded from the analysis. After critical reappraisal, one potential coinfection case[16] was excluded because the authors concluded that anaplasmosis was the most likely diagnosis and the link to Lyme disease could not be ascertained. Consequently, no confirmed cases of coinfection remained in the final analysis.
After full-text analysis, 15 clinical cases[4,17-28] meeting the inclusion criteria were selected for the final review.
For each selected case, the following were extracted: Demographic data, type of pericardial involvement, ECG changes (localization of ST elevations/depressions, PR changes, rhythm and conduction disturbances), echocardiography/computed tomography data, presence of migratory erythema, tick bite, time from contact to cardiac manifestations, extracardiac symptoms, laboratory confirmation methods, antibiotic therapy, and other treatment methods, complications, and outcomes.
Statistical analysis was performed using descriptive statistics (means, medians, proportions) in Microsoft Excel. Only descriptive statistics were used; no inferential statistical tests (e.g., t-tests, χ2, regression) or metaanalytic methods were applied, which is appropriate for a narrative minireview.
The analysis included 15 documented cases of pericarditis, myopericarditis, or pericardial effusion etiologically asso
| No. | Ref. | Age, Sex | Pericardial involvement | ECG findings | Echo/imaging | Other symptoms/history | Laboratory confirmation | Time from TB/EM | Treatment | Complications | Outcome |
| 1 | Steere et al[4], 1980 | Pericardial friction rub | ST-T changes (myopericarditis) | EM (presumed) | Clinical (EM) | Recovery | |||||
| 2 | Steere et al[4], 1980 | Small effusion | Diffuse ST↓ (anterolateral) | Echo: Small effusion; LVEF 52% | EM (presumed) | Clinical (EM) | Mild LV dysfunction | Recovery, LVEF normalized | |||
| 3 | Veyssier et al[17], 1987 | 59 (male) | Recurrent effusion (no tamponade) | ST↑ (concave) D3, aVF, V1-V6; later T↓ | Echo: Small posterior effusion (relapse) | Rural area; no skin/neuro signs; later arthralgias | IFA: 1:1024; CSF 1:4 to negative post-treatment | No TB, no EM | Aspirin, penicillin 1 million U/day × 21 days | Recovery, arthralgias persisted | |
| 4 | Veyssier et al[17], 1987 | 38 (male) | Myopericarditis (moderate effusion + LV hypokinesis) | Sinus tachycardia 110, incomplete RBBB, mild ST↓ (D3, aVF) | Echo: Moderate effusion to almost disappeared | Fever, headache, myalgias; later arthralgias, conjunctivitis, uveitis | IFA: 1:2048 | Indomethacin, penicillin 1 million U/day × 20 days | Good general condition, serology still positive | ||
| 5 | Cary et al[18], 1990 | 31 (male) | Fibrinous pericarditis (at autopsy) | Complete AVB (narrow QRS) | Farmworker; no systemic illness or rash | ELISA: 41 U; IFA 1:512; direct IgM IF: Negative | No TB, no EM | Complete AVB, death | Death | ||
| 6 | Bergler-Klein et al[19], 1993 | 22 (male) | Acute myopericarditis, no effusion | Sinus tachycardia 120, ST↑ I, II, aVL, aVF, V3-V5; later T↓; no AVB | Echo: Normal LV/RV, no effusion; MRI: Epicardial enhancement; scintigraphy: Diffuse uptake | Arthralgias, flu-like illness 3 weeks prior; no EM, no remembered TB | ELISA IgG + (OD 0.875/0.890); silver stain of biopsy: Spirochetes | No TB, no EM | Nitrates, heparin, aspirin (no antibiotics) | Spontaneous resolution within weeks | |
| 7 | Bruyn et al[20], 1994 | 59 (male) | Large effusion, tamponade (750 mL) | Atrial fib to ST↑ V2-V4 after cardioversion | Echo: Large effusion to small after PC | Chest pain, fever, dyspnea; arthralgias (3 years); recalled TB 10 years prior with EM | IFA: IgM 1:128, IgG 1:256; spirochetes in pericardial fluid and synovium (silver stain) | TB 10 years, EM at that time | PC (750 mL); IV ceftriaxone 2 g/day × 14 days | Tamponade, PC | Recovery within days |
| 8 | Guex-Crosier and Herbort[21], 1994 | 31 (male) | Acute pericarditis (2 episodes) | Recurrent uveitis, pars planitis (since 1982); first pericarditis 1988 | IFA 1:128; WB strongly positive (10 bands) | First episode: Augmentin + aspirin; recurrence: Indomethacin; then ceftriaxone 2 g/day IV × 14 days + doxycycline 200 mg/day × 2 weeks | Relapse-free > 4 years | ||||
| 9 | Horowitz and Belkin[22], 1995 | 23 (male) | Acute myopericarditis, no effusion | ST↑ inferior and precordial | Echo: Mild diffuse LV hypokinesis, no effusion | Fever, headache, stiff neck; TB 3 weeks before (not attached); EM next day after admission | On admission: WB indeterminate; at 4 weeks: WB + (IgG 41, 58; IgM 41, 39, 25, 37, 30) | TB 3 weeks, EM found day after admission | Azithromycin (no effect); ceftriaxone IV; then PO amoxicillin | Recovery by day 5 | |
| 10 | Gasser et al[23], 1998 | 54 (female) | Recurrent effusion, hemodynamic compromise (800 mL) | Extensive effusion, “swinging heart” | Dyspnea, joint pain, paresthesia; TB 1 years before with EM | Serology IgG (positive; also, in fluid) | 1 year | Colchicine, steroids, multiple PC (failures); finally, ceftriaxone 2 g/day × 14 days + PC | Recurrent effusion, multiple PC | Recovery, no recurrence at 1 year | |
| 11 | Briant et al[24], 1997 | 69 (male) | Pericarditis, no effusion (tamponade ruled out) | Diffuse ST↑ all leads; shortened PR | Echo: No effusion; pleural effusion (left) | Esophageal pain (referred), syncope, nausea; Lyme disease 1 week prior | Lyme disease clinical (method not stated) | IV nitroglycerin, heparin; ceftriaxone | Syncope, hypotension, bradycardia | Recovery | |
| 12 | Ocon et al[25], 2018 | 61 (male) | Hemorrhagic pericarditis, large effusion, tamponade (1400 mL) | Large circumferential effusion, tamponade physiology | Tick bite, EM 8 week prior; fever, chest pressure, arthralgia; AOSD diagnosed | Initial equivocal, later neg; clinical disease of Lyme; AOSD by Yamaguchi criteria | Approximately 8 weeks | Pericardiotomy, drainage; IV ceftriaxone; methylprednisolone + anakinra to prednisone | Tamponade, pericardiotomy | Recovery, symptom-free at 3 months | |
| 13 | Nedeljković et al[26], 2018 | 32 (male) | Acute pericarditis, circular effusion (22 mm) | Signs of pericarditis (no details) | Circular effusion; CT: Bilateral pleural effusion | SOB, chest pain (1 week), later fever (CRP 285) | IgM ELISA (positive), WB (positive) | Ibuprofen + colchicine to amoxicillin/clavulanate + azithromycin to piperacillin-tazobactam to ceftriaxone | Resolution, effusion gone after 5 days ceftriaxone | ||
| 14 | Ameer et al[27], 2024 | 18 (male) | Pericarditis, no effusion | ST↑ V2; PR↓ II; PR↑ aVR | Echo: EF > 70%, no effusion | Chest pain, dyspnea, palpitations; EM on back (5 inches × 3 inches) | Initial Lyme Ab (negative); clinical diagnosis (EM) | Rash 1 week before admission | Aspirin, ibuprofen, colchicine, IV doxycycline to IV ceftriaxone, then PO doxycycline 14 days | NSVT, diarrhea | Recovery, lost to FU |
| 15 | Agho 2025[28] | 69 (female) | Acute pericarditis, moderate to large effusion, tamponade physiology (450 mL drained) | CT: Large effusion; echo: Moderate-large effusion, RA collapse (< 50% cycle) | Chest pain, SOB, low-grade fever; asthma, factor V Leiden; no EM or TB mentioned | Lyme Ab screen > 1.23; WB: IgM reactive to 2 of 3 proteins | PO doxycycline 3 weeks, ibuprofen, colchicine; PC (450 mL) | Tamponade physiology, PC | Recovery, symptom-free at 2 months |
Among the 15 cases, sex was reported in 13 patients: 11 (84.6%) were men and 2 (15.4%) were women (sex was not reported in the two cases from Steere et al[4]). Age was reported in 13 patients (excluding the two Steere et al[4] cases, where age was not specified). The mean age was 43.5 years (median: 38 years; range: 18-69 years).
Types of pericardial involvement included pericarditis without effusion (7 cases, 46.7%), pericarditis with effusion (without tamponade; 5 cases, 33.3%), and pericarditis with tamponade (3 cases, 20.0%).
ECG data were available in 11 cases. The most common ECG finding was diffuse ST segment elevations, recorded in four cases (36.4%): In two cases (18.2%), ST elevations were localized (anterior or inferolateral leads), which initially simulated acute myocardial infarction, while ST depressions (without elevations) were noted in the other two cases (18.2%). In one case (9.1%), ECG changes were not detailed, and in four cases, ECG was not described.
PR interval changes were recorded in two patients: PR shortening (one case) and PR depressions typical of pericarditis combined with PR elevation in lead augmented vector right (one case). Atrioventricular blocks (first-degree and third-degree) were identified in two (18.2%) patients, and atrial fibrillation in one (9.1%) patient.
Pericardial effusion (from small to massive) was found in eight patients (53.3%). In three of them (20.0% of all cases), effusion was accompanied by tamponade, which required urgent pericardiocentesis. Effusion recurred in two cases (one recurrence after discontinuation of nonsteroidal antiinflammatory drugs, another after inadequate antibiotic therapy).
Erythema migrans (EM) was noted in seven patients (46.7%), and a confirmed tick bite in four patients (26.7%). The median time from tick bite or erythema migrans to the development of pericarditis (excluding one case with a 10-year interval) was 3 weeks (ranging from 1 week to 1 year).
In four patients (26.7%), pericarditis was combined with other extracardiac manifestations: Arthritis (two cases), uveitis (two cases), and meningoencephalitis (one case). In the case reported by Ocon et al[25], a patient developed adult-onset Still’s disease.
Serological confirmation (enzyme immunoassay and/or western blot) was obtained in 10 cases (66.7%). Direct detection of the pathogen (culture, polymerase chain reaction, silver impregnation, immunofluorescence of pericardial fluid or tissue) was achieved in two cases (13.3%)[19,20], including the patient with tamponade[20] in whom spirochetes were detected in the pericardial fluid using three independent methods. In five cases (33.3%), the diagnosis was made clinically (presence of migratory erythema and typical response to antibiotic therapy) with negative or equivocal serology at an early stage.
Antibiotic therapy was administered in 13 patients (86.7%). The most commonly used agents were intravenous ceftria
In one case[20], the presence of spirochetes in pericardial fluid during tamponade was demonstrated for the first time; the interval from tick bite to pericarditis was 10 years. In three cases[19,22,24], the ECG picture of acute pericarditis/myopericarditis was initially misinterpreted as myocardial infarction, emphasizing the need for differential diagnosis.
The present review combined 15 documented cases of pericarditis, myopericarditis, and pericardial effusion etiologically associated with Lyme disease, published in the available literature from 1980 to 2025. The obtained data allow us to clarify the clinical spectrum, diagnostic difficulties, and outcomes of this rare form of Lyme carditis.
Our analysis confirmed a strong male predominance: Among the 13 patients with known sex, men accounted for 84.6%. This is consistent with larger series of Lyme carditis, where the maletofemale ratio ranges from 3:1 to 7:1[1,2]. This sex disparity has been attributed to possible hormonal, immunological, or behavioral factors, but the exact mechanism remains unclear[3]. The mean age of patients was 43.5 years, which is comparable to classical descriptions in which Lyme carditis typically affects young to middle-aged adults[4]. The presence of two patients older than 65 years[24,28] and one with a 10-year interval from tick bite to carditis[20] points to the possibility of late diagnosis and chronic course, as also noted in earlier observations[4].
In our series, pericarditis without effusion was the most frequent presentation (46.7% of all cases). Pericarditis with effusion without tamponade occurred in 33.3%, and with tamponade in 20.0%. Tamponade in Lyme pericarditis was previously considered extremely rare: Only isolated observations were known[20,23]. Our review shows that with a targeted search; tamponade may be detected in one-fifth of patients with pericardial effusion. This high proportion likely reflects publication bias (severe cases are more often reported) but also suggests that tamponade may be underdiagnosed. Our findings emphasize the need for echocardiographic monitoring in all patients with suspected Lyme pericarditis, even those with minimal symptoms. In all cases of tamponade, prompt pericardiocentesis and antibiotic therapy led to complete recovery.
Conduction disturbances (atrioventricular block) were present in only 18.2% of patients with available electrocardiographic data. This contrasts sharply with classical Lyme carditis, where atrioventricular block is reported in > 90% of cases[4,13]. This discrepancy is expected because our review focused specifically on pericardial involvement, whereas most published series of Lyme carditis are dominated by patients with conduction system disease. In a large retrospective analysis of hospitalized patients[14], conduction system disease was noted in 93% of patients with Lyme carditis, confirming that isolated pericardial involvement without atrioventricular block is a rare but important subtype. Thus, pericardial involvement in Lyme disease represents a distinct clinical subset that often spares the conduction system, a point also emphasized by Lamaison[15].
Electrocardiographic changes in Lyme pericarditis can be misleading. Diffuse ST elevations (classic for acute pericarditis) were observed in 36.4% of cases with described ECG. In 18.2%, localized ST elevations mimicking myocardial infarction were noted, leading to an initial misdiagnosis of acute coronary syndrome in three reports[19,22,24]. This highlights the need to consider Lyme pericarditis in young patients from endemic areas presenting with suspected ST-elevation myocardial infarction but normal coronary arteries. The combination of PR depression and PR elevation in lead aug
Two main mechanisms underlie Lyme pericarditis. Direct spirochetal invasion is documented by the detection of borrelia burgdorferi in pericardial fluid or tissue[19,20]. Immunemediated injury is suggested by postinfectious autoimmune syndromes (e.g., adult-onset Still’s disease after Lyme infection[25]), lymphoplasmacytic infiltrates without detectable spirochetes at autopsy[18], and elevated serum IgM and cryoglobulins in early Lyme carditis series[4]. These mechanisms are not mutually exclusive and may coexist in the same patient.
Serological confirmation (enzyme immunoassay and/or western blot) was obtained in 66.7% of cases. In 33.3%, the diagnosis was made clinically based on the presence of erythema migrans and a characteristic course with negative or equivocal early serology. This underscores the importance of repeating serological testing after 4-6 weeks if clinical suspicion remains high, as recommended by current guidelines[10]. Direct detection of borrelia in pericardial fluid or tissue was achieved in only 13.3% of cases[20,19], mainly in patients requiring pericardiocentesis or biopsy, confirming the invasive nature of these methods. In one case, spirochetes were visualized in synovial biopsy by silver stain[20], illustrating that alternative specimens may be useful in selected situations.
Antibiotic therapy was administered to 86.7% of patients, with ceftriaxone and doxycycline being the most commonly used agents, in line with current recommendations[13,16]. Pericardiocentesis was required in 26.7% of cases, 75% of which were related to tamponade. Complete recovery was achieved in 93.3% of cases; the only fatal outcome occurred in a patient diagnosed postmortem before the era of widespread antibiotic use[18]. This confirms that timely diagnosis and appropriate antibiotic therapy result in a favorable prognosis, as previously reported[11].
Our findings have several practical implications. First, Lyme disease should be included in the differential diagnosis of acute pericarditis in young patients from endemic areas, especially when systemic symptoms are present (fever, arthralgias, erythema migrans). Second, a normal ECG or the absence of conduction disturbances does not rule out Lyme carditis: 81.8% of our patients with pericardial involvement had no atrioventricular blocks. Third, persistent or recurrent effusion after nonsteroidal anti-inflammatory drugs should prompt serological testing for Lyme disease.
Prospective, multi-center registries are needed to determine the true incidence and natural history of Lyme pericarditis. Standardized diagnostic algorithms - including routine echocardiography in all suspected Lyme carditis patients - would clarify the frequency of effusion. Research should explore the role of advanced imaging (cardiac magnetic resonance) in distinguishing Lyme pericarditis from myocarditis.
The present review has a number of limitations characteristic of a narrative review of published cases. First, publication bias may be present (predominance of unusual, severe, or successfully treated cases). Second, the lack of a uniform diagnostic standard (serological tests varied in sensitivity, echocardiography was not performed in all cases) may have resulted in incomplete data. Third, due to the rarity of the condition, we were unable to apply meta-analytic methods. Fourth, many of the cited studies are relatively old, which is understandable given the rarity of Lyme pericarditis and the limited number of reported cases; this historical nature of the evidence base is acknowledged. Nevertheless, the collected information represents the most complete set of documented cases of Lyme pericarditis to date.
Pericardial manifestations of Lyme borreliosis are rare but can range widely, from asymptomatic effusion to cardiac tamponade. In most cases, they develop in young and middle-aged men, are often associated with migratory erythema, arthritis or neurological symptoms, and generally have a favorable prognosis with timely antibiotic therapy. The electrocardiographic pattern may mimic acute myocardial infarction, requiring a high index of suspicion, especially in young patients in endemic regions. Serological confirmation (two-tiered testing) remains the mainstay of diagnosis, but if results are negative in the early stages, testing should be repeated after 4-6 weeks. Pericardiocentesis is indicated for tamponade or refractory effusion. Early initiation of antibiotic therapy (ceftriaxone, doxycycline) ensures complete recovery in the vast majority of cases. Further prospective studies are needed to clarify the true prevalence and optimal management strategies for patients with Lyme pericarditis.
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