The Great Imitator: A Case of Lyme Carditis Mimicking ST Elevation Myocardial Infarction

Abstract

Lyme disease, caused by Borrelia burgdorferi and transmitted via Ixodes ticks, is a common vector-borne illness in the United States, with an estimated 476,000 annual cases. While primarily known for its neurological and rheumatological manifestations, Lyme disease can also involve the cardiac system, known as Lyme carditis, which occurs in about 4% to 10% of cases. This case report details a rare instance of Lyme carditis presenting as ST-segment elevation myocardial infarction (STEMI) in a 31-year-old female with no significant medical history. The patient exhibited symptoms of chest pressure and shortness of breath, with laboratory results showing significantly elevated troponin levels and other indicative markers. Notably, cardiac catheterization revealed no coronary occlusion, suggesting an alternative diagnosis to acute coronary syndrome (ACS). Further testing confirmed Lyme carditis through positive serological tests for Lyme-specific IgM antibodies. The case underscores the importance of considering Lyme myopericarditis in differential diagnoses for STEMI in Lyme-endemic areas and in patients without typical risk factors for coronary artery disease. This report aims to increase clinical awareness of this condition, highlighting the need for thorough investigation in atypical cardiac presentations.

Introduction

Lyme disease, a multisystem illness caused by the spirochete Borrelia burgdorferi, is the most prevalent vector-borne disease in the United States. Approximately 476 000 patients are diagnosed with Lyme disease every year. ¹ Transmission to humans occurs through the bite of infected Ixodes ticks. ² Clinically, it typically manifests in stages, beginning with the localized infection characterized by erythema migrans, followed by disseminated infection which may involve neurological, rheumatological, and less commonly, cardiac complications. ³

Cardiac involvement in Lyme disease, termed Lyme carditis, is an infrequent but significant manifestation, occurring in approximately 4% to 10% of the cases. ⁴

The pathophysiology of Lyme carditis involves the dissemination of Borrelia burgdorferi to bloodstream leading to myocardial inflammation. ⁴ The clinical presentation can vary from mild nonspecific symptoms to severe life-threatening complications such as high-grade atrioventricular blocks. ⁴ The most common cardiac manifestation is conduction system disease; however, cases of endocarditis, myocarditis, and pericarditis have been reported. ⁵

Acute Lyme carditis presenting as ST-segment elevation myocardial infarction (STEMI) is an even rarer occurrence. In the literature review, there are only 2 cases of Lyme carditis presenting as STEMI.^6,7 Such presentations pose a significant diagnostic challenge because they mimic the more common atherosclerotic coronary artery disease. Despite its rarity, Lyme carditis is potentially reversible when recognized early and treated appropriately, contrasting with the often irreversible damage from classical myocardial infarctions.

The case we present illustrates a nonclassical presentation of Lyme carditis, manifesting as STEMI on electrocardiogram (EKG) without the coronary artery occlusions typically seen in acute coronary syndrome (ACS). This report aims to raise clinical awareness about Lyme carditis as a differential diagnosis for STEMI, particularly in regions endemic for Lyme disease and during peak seasons for tick activity. It also underscores the critical importance of a thorough workup in patients presenting with symptoms of myocardial ischemia, where initial investigations do not reveal the expected cardiac pathology.

Case Presentation

We present here a 31-year-old female with no known past medical history, living in New Jersey, presented to hospital with a chief complaint of chest pressure associated with shortness of breath, fatigue, and chills for 1 day. On presentation, the patient was normotensive with a blood pressure of 101/61 mm hg, heart rate of 88 per minute, afebrile, saturating 99% on room air. On physical examination, patients had a regular rate and rhythm, without any murmurs, gallops, or rubs. Laboratory results were significant for an elevated troponin of 8712 pg/mL (Normal value <17 pg/mL) and C-reactive protein of 30 mg/L (normal value of <9.9 mg/L), urine toxicology was negative. Initial EKG interpreted as sinus rhythm with a rate of approximately 84, normal axis with ST elevation in leads 2, 3, and AVF and ST segment depression in leads 1 and AV (Figure 1). Immediately, STEMI code was activated, the patient received 325 mg of aspirin and taken for cardiac catheterization which did not show any occlusion, (Figure 2) was suggestive of myopericarditis. Shortly afterwards, a 2D transthoracic echocardiogram was performed to better visualize the heart which showed a normal left ventricular ejection fraction of 55% to 60% with a mildly dilated left atrium, no wall motion abnormalities.

Figure 1.

EKG showing normal sinus rhythm, ST elevation in leads II, III, AVF and ST depression in leads I and AVL.

Figure 2.

Left heart catheterization: (A) left circumflex artery and left anterior descending artery, (B) right coronary artery, and (C) left ventriculography.

Immediately after the procedure, the patient was hypotensive, was started on empiric broad spectrum antibiotics, and transferred to the cardiac critical care unit for further monitoring. Patient complained of intermittent positional chest pain and was started on colchicine 0.6 mg twice a day along with celecoxib 100 twice a day with improvements in symptoms. Further myopericarditis work up revealed positive Lyme IgM antibodies (ab) with negative IgG ab on enzyme-linked immunosorbent assay (ELISA). Patient was already on empiric piperacillin-tazobactam. Western blot test was also positive for IgM (p23 and p41 bands) ab, confirming Lyme carditis. Patients chest pain improved after administering celecoxib and colchicine. The patient clinically improved after 10 days of IV antibiotics, remained hemodynamically stable, chest pain resolved, troponin down trended and EKG normalized, discharged to home.

Discussion

Borrelia burgdorferi, transmitted by the Ixodes tick, undergoes gene expression enabling local tissue invasion and inflammation, subsequently leading to blood vessel and tissue invasion. The bacteria continue replicating in the invaded tissues, eliciting systemic inflammation and tissue colonization. ⁸ Most of the tissue damage is thought to be a consequence of the host’s inflammatory response rather than bacterial evasion, due to the evidence of a low bacterial load in the affected tissues. ⁸

Lyme carditis occurs when Borrelia burgdorferi invades cardiac tissue after disseminating in the bloodstream. The bacteria predominantly affect the atrioventricular conduction system but may also infect the endocardium, myocardium, pericardium, coronary vessels, and heart valves. ⁹

Lyme carditis can present as varying degrees of atrioventricular (AV) block, leading to symptoms like palpitations, dizziness, fainting, or shortness of breath. In severe cases, a complete heart block can occur. Myo-pericarditis may manifest as chest pain, along with other nonspecific symptoms like fatigue or fever, reflecting the systemic nature of Lyme disease. ⁹

The diagnostic approach for Lyme carditis typically involves a combination of clinical evaluation and serologic tests. The Suspicious Index in Lyme Carditis (SILC) is a risk assessment tool developed to evaluate the risk of high-degree AV block caused by Lyme carditis. ¹⁰ It assigns points to various factors: constitutional symptoms (eg, fever, fatigue, malaise, and joint pain), outdoor activity in endemic areas, male sex, tick bite history, age under 50 years, and erythema migrans. The total score categorizes suspicion levels into low (0-2), intermediate (3-6), or high (7-12), aiding clinicians in diagnosing Lyme carditis based on these combined factors. Patients with intermediate and high scores should undergo Lyme serologic tests and start empiric intravenous antibiotics. ¹¹

The lack of specific risk assessment protocols for identifying Lyme carditis in cases resembling ST elevation myocardial infarction complicates the diagnostic process. Compared to previously reported cases of Lyme carditis presenting as STEMI, this case presentation is distinct, with significantly elevated Troponin levels^6,7 and ST elevation in leads II, III, and aVF with reciprocal ST depressions in I and AVL ⁷ and lack of erythema migrans. ⁷ Included in our case in New Jersey, all of the 3 cases were from Lyme disease endemic areas.^6,7 The diagnosis in this case was challenging due to the patient’s lack of typical risk factors for coronary artery disease and the atypical presentation. Elevated troponin levels combined with ST-segment elevation in leads II, III, and aVF rather than diffuse elevation and reciprocal ST segment depression in leads I and AVL, as is common in acute inferior myocardial infarction. However, the absence of coronary occlusion during angiography suggested an alternative diagnosis. The use of ELISA and Western blot tests for Lyme disease was crucial. Identifying Lyme-specific IgM antibodies on ELISA and Western Blot confirmed Lyme carditis. ¹² This highlights the need for a high suspicion index and appropriate serological testing in atypical cardiac presentations, particularly when the patient has a history or likelihood of tick exposure. Lyme carditis can be promptly treated with antibiotics with no long-term sequela, as demonstrated by the patient’s rapid improvement following antibiotic therapy.

An echocardiogram may be used for differentiating ACS from Lyme carditis in the setting of elevated cardiac biomarkers and EKG changes suggestive of ACS. In ACS, focal wall motion abnormalities would be expected; however, in Lyme carditis, global wall hypokinesis is more likely. ¹³ Cardiac magnetic resonance imaging (MRI) findings in Lyme carditis may include wall edema indicating myocardial inflammation, late gadolinium enhancement, and pericardial effusion. ¹⁴

Lyme carditis may spontaneously resolve; however, antibiotic therapy shortens the duration of the disease. ¹¹ Serologically confirmed Lyme carditis should be treated with IV antibiotics (the first line being ceftriaxone) for 10 to 14 days and can subsequently be transitioned to oral doxycycline, amoxicillin, or cefuroxime axetil for a total antibiotic duration of 14 to 21 days. ¹¹ In addition to antibiotic therapy, cardiac monitoring should be implemented, especially in patients presenting with AV block. Patients with symptomatic or high-degree AV block should be treated with temporary pacemakers and re-evaluated after 14 days for the necessity of a permanent pacemaker. ¹¹

Conclusion

This case exemplifies the complexity and diagnostic challenge of Lyme carditis, particularly when presenting as STEMI without typical coronary occlusions. The patient’s recovery following appropriate antibiotic therapy reinforces the necessity for a high index of suspicion and comprehensive serological testing in similar scenarios. The inclusion of Lyme carditis in differential diagnoses is crucial, especially in endemic regions and during peak tick activity seasons. This case contributes to the growing body of evidence suggesting that Lyme carditis, though rare, is a significant and treatable condition. It highlights the need for awareness among clinicians to consider Lyme disease in patients presenting with myocardial ischemia symptoms, especially when standard investigations do not reveal the expected cardiac pathology. The successful management of this patient with antibiotics, without the long-term sequelae often associated with classical myocardial infarctions, further underscores the importance of early recognition and treatment of Lyme carditis.