Pathogenesis and preventive and therapeutic trials in an animal model of dilated cardiomyopathy induced by a virus.

Matsumori, Akira; Kawai, Chuichi; Crumpacker, Clyde S.; Abelmann, Walter H.

doi:10.1253/jcj.51.661

Cited by 14 publications

(2 citation statements)

References 6 publications

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“…In another mouse model using EMC virus, severe myocarditis, congestive heart failure, and dilated cardiomyopathy have a high incidence (15). The viral genome of EMC virus was detected by polymerase chain reaction (PCR) in infected mouse hearts consistently during the acute phase of myocarditis and persisted in some hearts up to 3 months in the chronic stage, when infectious virus was no longer detectable (16).…”

Section: Discussionmentioning

confidence: 99%

Prolonged Captopril Therapy in Murine Viral Myocarditis

Reyes

Khatib

et al. 1998

J Cardiovasc Pharmacol Ther

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BACKGROUND: Acute myocarditis can progress to chronic heart muscle disease and cardiomyopathy. In the coxsackievirus B(3) (CB(3)) mouse model of myocarditis, early administration of captopril, an angiotensin-converting enzyme (ACE) inhibitor, ameliorated histopathological changes in inflammation, necrosis, and calcification and reduced heart weight. Late administration of captopril reduced heart weight but did not affect the histological findings. In this study, we investigated the effects of prolonged captopril treatment in the chronic phase of this model. METHODS AND RESULTS: Three-week-old male CD(1) mice were infected with CB(3) and then randomized to receive placebo or captopril starting on day 7 of infection. Captopril, 2 g/L, was given as the drinking water daily for up to 6 months. Autopsies were performed at 6 and 10 months. Heart-to-body weight ratios were obtained, and deaths were tallied. Myocardial fibrosis was graded according to a score system. In addition, picrosirius red stain (PSR) also was used for assessment of collagen deposition. Mean heart weights were similar in both groups. Mean body weight was significantly lower in captopril-treated mice (40.7 g) than in the untreated group (43.6 g) at 6 months (P =.0155), and mortality was higher (8.7 vs 0.87%; P =.009). At 6 months, the mean myocardial fibrosis score in treated mice (0.12) was significantly less than in untreated animals (0.35; P =.035). With PSR, the mean myocardial fibrosis score in the captopril group (1.20) was also significantly less than in the untreated group (1.58; P =.045). At 10 months, fibrosis scores were similar in both groups. CONCLUSIONS: Chronic captopril treatment in CB(3) myocarditis reduces myocardial fibrosis.

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Section: Discussionmentioning

confidence: 99%

Prolonged Captopril Therapy in Murine Viral Myocarditis

Reyes

Khatib

et al. 1998

J Cardiovasc Pharmacol Ther

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“…When newborn Swiss mice were passively immunized by subcutaneous administration of specific antiviral antibodies 24 h before infection with CVB-3, viremia was abbre viated and viral clearance from tissues accel erated with a reduction in mortality from 100 to 0% [16], Similarly, passive maternal immunization with specific antibodies against EMC virus prevents infection in off spring which leads to high early mortality following in utero infection [17]. Although immunization is feasible when a specific vi ral infection is anticipated, human myocar ditis may be initiated by multiple cardio tropic viruses and, hence, vaccination or passive immunization could realistically prevent only a fraction of human viral myo carditis.…”

Section: Immunosuppression In Murine Myocarditismentioning

confidence: 99%