Long-term Cardiac Sequelae in Lyme Carditis: A Review

INTRODUCTION: Lyme disease, primarily caused by Borrelia burgdorferi in North America, is a common spirochetal infection transmitted via tick bites. The dissemination of Lyme spirochetes can result in multisystem complications, including Lyme carditis. METHODS: This review incorporated data from observational studies, retrospective analyses, systematic reviews, and case reports involving patients with confirmed or presumed Lyme carditis. Key outcomes included prevalence, reversibility, and chronicity of cardiac involvement, as well as diagnostic and prognostic implications. RESULTS: Atrioventricular block represents the most prevalent conduction abnormality in Lyme carditis, occurring in up to 90% of cases, with high-degree of persistent blocks potentially necessitating temporary or permanent pacing. While the majority of conduction abnormalities resolve with appropriate antimicrobial therapy, a subset of patients experience persistent dysfunction. Structural complications, including myocarditis, pericarditis, and, less frequently, endocarditis and dilated cardiomyopathy, have been documented. Emerging evidence suggests that persistent myocardial inflammation and autoimmune mechanisms may contribute to the development of long-term cardiac remodeling and dysfunction. Reports of coronary artery involvement and aneurysmal changes, though rare, raise further concern regarding chronic cardiovascular risk. DISCUSSION: This review highlights several cardiovascular complications of Lyme carditis that can persist despite medical therapy. While permanent conduction abnormalities, fulminant myocarditis, and subsequent ventricular dysfunction have been reported, studies on chronic heart failure are limited, and coronary artery involvement remains underrecognized, necessitating further research. CONCLUSION: While Lyme carditis is generally self-limited with timely therapy, accumulating evidence indicates the potential for lasting cardiac sequelae. Further longitudinal studies are warranted to delineate risk factors, pathophysiologic mechanisms, and optimal strategies for longterm surveillance and management.