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Sterile Pericarditis in Aachener Minipigs As a Model for Atrial Myopathy and Atrial Fibrillation
Published on: September 24, 2021
Efficacy of steroid therapy for pacing failure in a patient with chronic myocarditis
Nobuyuki Mitsuya1, Ryoji Kishi, Noriyuki Suzuki
1Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki.
Insights
Steroid therapy stabilized pacing thresholds in a patient with chronic myocarditis by reducing inflammation and fibrosis. However, this treatment did not improve overall cardiac function.
Area of Science:
- Cardiology
- Immunology
Background:
- Chronic myocarditis can lead to progressive cardiac conduction abnormalities, such as increased pacing thresholds.
- Pacemaker dependency can arise from inflammatory cardiomyopathies, necessitating careful management.
Observation:
- A 66-year-old male patient experienced a progressive increase in pacemaker pacing threshold over one year due to chronic myocarditis.
- Biomarkers including serum creatine kinase, cardiac myosin light chains, and pro-collagen III peptide decreased after steroid therapy.
Findings:
- Steroid therapy successfully decreased and stabilized the patient's pacing threshold, indicating improved electrical conduction.
- Endocardial biopsy revealed no progression of cardiac fibrosis, suggesting suppression of the inflammatory process.
- Despite improvements in pacing parameters and reduced fibrosis, cardiac function did not show significant improvement.
Implications:
- Steroid therapy may be effective in managing pacing threshold issues in chronic myocarditis by mitigating inflammation and fibrosis.
- The dissociation between improved pacing parameters and unchanged cardiac function highlights the complex pathophysiology of myocarditis.
- Further research is needed to explore strategies for functional recovery in patients with myocarditis treated with immunosuppressants.
Abstract:
A 66-year-old man had a progressive increase in the pacing threshold over a one-year period, resulting from chronic myocarditis. Following steroid therapy, the pacing threshold decreased and became stabilized, and was accompanied by a decrease in the serum creatine kinase, cardiac myosin light chains and pro-collagen III peptide values, but cardiac function did not improve. Endocardial biopsy showed that there was no progression in the fibrosis. The pacing failure improved, but the cardiac function did not. It was believed that the steroid therapy suppressed the progression of the inflammation and fibrosis caused by the chronic myocarditis.
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