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Complete atrioventricular block in experimental murine myocarditis
Minoru Ohmae1, Chiharu Kishimoto, Nobuyoshi Tomioka
1Kochi General Rehabilitation Hospital, Kochi 781-8130, Japan.
Insights
Myocarditis can cause complete atrioventricular (AV) block due to conduction system damage or mild edema. Pathological findings guide treatment, with severe lesions requiring permanent pacing and mild edema suggesting transient recovery.
Area of Science:
- Cardiology
- Pathology
- Virology
Background:
- Limited data exists on conduction system pathology in myocarditis.
- This study investigates pathological characteristics of complete atrioventricular (AV) block in myocarditis.
Purpose of the Study:
- To clarify the pathological characteristics of complete AV block in experimental myocarditis.
- To correlate pathological findings with clinical outcomes and treatment strategies.
Main Methods:
- Experimental myocarditis induced by encephalomyocarditis virus in mice.
- Serial electrocardiogram recordings and cardiac pathology examinations up to 360 days.
- Histopathological analysis focused on the His bundle and AV node.
Main Results:
- Complete AV block developed in mice with experimental myocarditis.
- 10.7% of mice with complete AV block showed His bundle lesions and necrosis.
- 17.3% exhibited only edematous changes in the AV node without other evident lesions.
Conclusions:
- Complete AV block in myocarditis can stem from significant conduction system lesions or minor edematous changes.
- Severe lesions necessitate permanent pacing, while edematous changes may indicate transient, recoverable block.
- Understanding these pathological differences is crucial for appropriate clinical management of myocarditis-induced AV block.
Background:
There were few reports on the pathological characteristics of the conduction system in myocarditis. This study was aimed to clarify the pathological characteristics of complete atrioventricular (AV) block in myocarditis.
Methods And Results:
We studied serial electrocardiograms in experimental myocarditis in mice and also examined their cardiac pathology. After taking baseline electrocardiograms, mice were inoculated intraperitoneally with the encephalomyocarditis virus. Electrocardiograms were serially recorded until day 360. Serial electrocardiograms revealed the appearance of complete AV block. Myocardial lesions were found in the hearts of mice with these ectopic beats. Mononuclear cell infiltrations into the His bundle and necrotic lesions of the conduction system were found in 10.7% (18/168) of mice with complete AV block. However, 17.3% (29/168) of mice showed no evident pathological lesions except the edematous changes of AV node.
Conclusions:
The appearance of complete AV block in myocarditis may suggest not only significantly comparable pathological lesions of the conduction system but also the trivial edematous changes; in clinical settings, in the former case, permanent pacing therapy is necessary, and in the latter case, the disease may be transient and could be recovered from complete AV block. This study may shed light on the pathological characteristics of complete AV block in myocarditis.
