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Pathogenesis of myocardial injury in myocarditis and cardiomyopathy
A Matsumori1, I Okada, T Yamada
1Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
Abstract:
The pathogenesis of myocardial cell injury in myocarditis and cardiomyopathy was investigated. The presence of viral genomes in the murine heart in experimental coxsackievirus B3 myocarditis was studied by Northern blotting analysis using a 32P-labeled cDNA probe from the 5' end sequence. The strongest signal of positive autoradiograms was always at about 7.4 kilobases, corresponding to the size of the complete genome of the virus. Successive infections with coxsackievirus and encephalomyocarditis (EMC) virus infection showed simultaneous acute myocarditis and healed myocarditis, and the results suggest that successive virus infections cause additional myocardial damage, and develop lesions similar to chronic myocarditis or dilated cardiomyopathy. Anti-heart auto-antibody, induced during EMC virus infection, reacted predominantly with myosin. Indium-111 antimyosin scintigraphy showed positive in some of the patients with cardiomyopathy, and the uptake was inversely correlated with left ventricular function. When mice were injected with antimyosin antibody, mouse immunoglobulin G was detected in hearts in the chronic stage of EMC virus myocarditis, in myocytes surrounding fibrosis and calcification, suggesting deposition of antimyosin antibody. Although further study is necessary to clarify the mechanism of uptake of antimyosin in cardiomyopathy, antimyosin antibody may accumulate in viable myocytes with ongoing degeneration as well as in necrosis.
Insights
Viral infections can cause myocardial cell injury, leading to myocarditis and cardiomyopathy. Subsequent infections exacerbate damage, potentially causing chronic conditions and auto-antibody responses targeting myosin.
Area of Science:
- Cardiology
- Virology
- Immunology
Background:
- Myocarditis and cardiomyopathy involve myocardial cell injury.
- Viral infections are implicated in the pathogenesis of these conditions.
Purpose of the Study:
- To investigate the pathogenesis of myocardial cell injury in myocarditis and cardiomyopathy.
- To examine the role of viral genomes and auto-antibodies in disease development.
Main Methods:
- Northern blotting analysis to detect viral genomes (coxsackievirus B3).
- Indium-111 antimyosin scintigraphy in patients with cardiomyopathy.
- In vivo studies involving antimyosin antibody injection in mice.
Main Results:
- Complete coxsackievirus B3 genome detected in murine hearts.
- Successive viral infections led to progressive myocardial damage, mimicking chronic myocarditis/dilated cardiomyopathy.
- Anti-heart auto-antibodies, particularly against myosin, were induced by encephalomyocarditis (EMC) virus infection.
- Indium-111 antimyosin uptake correlated inversely with left ventricular function in cardiomyopathy patients.
- Antimyosin antibody deposition observed in hearts of mice with chronic EMC virus myocarditis.
Conclusions:
- Viral infections are a significant factor in myocardial injury, potentially leading to chronic conditions.
- Auto-antibodies against myosin may play a role in the progression of cardiomyopathy.
- Further research is needed to elucidate the precise mechanisms of antimyosin antibody accumulation in cardiomyopathy.