Reversible ventricular dysfunction in rheumatic fever reactivation: insights from imaging and corticosteroid therapy

Abstract Background Rheumatic fever (RF) remains a major global health issue, especially in low- and middle-income countries, with underreported incidence due to diagnostic challenges. Chronic valvular heart disease is its most severe consequence, often leading to heart failure, hospitalizations, and surgeries. While valvulitis is the hallmark of rheumatic carditis, recent evidence suggests that myocarditis during RF reactivation in adults may cause ventricular dysfunction, independent of severe valvular disease, and may be reversible with corticosteroid therapy. However, data on this phenomenon remain limited. This study aimed to evaluate clinical, laboratory, and echocardiographic characteristics of patients with RF reactivation and myocarditis. Methods This single-center, retrospective study included 68 patients with RF reactivation and myocarditis, confirmed by 18F-FDG PET/CT and/or gallium-67 scintigraphy (Figure 1A/B). Patients underwent three echocardiographic assessments: baseline, during myocarditis, and post-corticosteroid treatment. They were classified into: Group 1 (n=15): Normal left ventricular ejection fraction (LVEF) during myocarditis. Group 2 (n=53): Reduced LVEF during myocarditis. Results The median age was 47 years, with 69% over 40 years and 70% women. Only 30.9% were regularly using benzylpenicillin prophylaxis. NYHA class III/IV heart failure was significantly higher in Group 2 (73.6%) vs. Group 1 (28.6%, p=0.005), whereas arthralgia was more common in Group 1 (28.6% vs. 3.9%, p=0.017). Myocarditis was confirmed in 42 patients (61.8%) via PET scan and 39 patients (57.4%) via gallium-67 scintigraphy, with 97.4% showing mild-to-moderate tracer uptake. As expected, Group 2 had left ventricular dysfunction while Group 1 did not (LVEF: 32% 24–40% vs. 50% 34–66%, p=0.001). Right ventricular dysfunction was observed in 44.4% of all patients, and only 55.88% had moderate-to-severe valvular dysfunction, with no significant difference between groups. Pericardial effusion was present in 14.7% of cases, more frequent in Group 1 (20%) (p=0.038). Group 2 showed a significant LVEF decline during myocarditis, followed by marked improvement after corticosteroid therapy (Figure 1C). The overall mortality rate was 11.8%, with a median follow-up of 702 days 1289–326, showing no significant difference between groups (Figure 1D). Conclusion This study highlights myocarditis as a cause of reversible left ventricular dysfunction during RF reactivation, independent of severe valvular disease. Corticosteroid therapy significantly improved LVEF, reinforcing its role in treatment. Multimodal imaging (18F-FDG PET/CT and gallium-67 scintigraphy) confirmed myocardial inflammation, challenging the assumption that RF-related heart failure is solely valvular. These findings emphasize the need for further research on myocarditis in RF and its long-term cardiac impact.