ECE depicts ischemically injured but salvaged myocardium, as well as infarcted myocardium in patients with AMI. The myocardium at risk and infarcted myocardium after reperfusion can be retrospectively assessed by the combination of ECE and LCE.

Immunoglobulin therapy completely suppressed acute CB3 myocarditis by transferring the neutralizing antibody into the host in the acute viremic stage and induced an anti-inflammatory effect in the subsequent aviremic stage; the reduction of the splenic B-cell population may be closely associated with an anti-inflammatory effect.

Nitric oxide inhibition increases myocardial virus titers, resulting in the aggravation of cardiac pathology in the early stage of coxsackievirus B3 myocarditis. In the late stage, it induces more severe cardiomyopathic lesions. Nitric oxide plays a defensive role in the pathogenesis of coxsackievirus B3 myocarditis.

The effects of captopril on murine coxsackievirus B3 (CB3) myocarditis were investigated, with focus on interstitial fibrin deposition and changes in the connective tissue matrix. Captopril was administered intraperitoneally at a dose of 0.1 mg/g to CB3-infected mice daily on days 10-30 in experiment I (inflammatory phase) and on days 30-60 in experiment II (fibrotic phase). In experiment I, mouse survival was higher in the captopril-treated group than in the untreated group. Histological improvement, including prevention of extravasated fibrin deposition, maintenance of connective tissue architecture, suppression of myocyte hypertrophy, and prevention of myosin isoform shift from alpha to beta, was observed in captopril-treated mice in experiment I, but not in experiment II; in experiment II, captopril administration suppressed thickening of the interstitial reticulin fibers. Captopril inhibited inflammatory fibrin deposition, postmyocarditic myocyte hypertrophy, and ventricular remodeling during the inflammatory phase, but not during the fibrotic phase, of CB3 myocarditis in mice.

No abstract

The results suggest that superoxide anion is mostly responsible for myocyte injury in CB3 myocarditis in mice, and that hydrogen peroxide formed as a result of dismutation of superoxide anion may not play a significant role in the development of myocarditis. Superoxide anion is one of the most important factors in free radical mediated injury in CB3 myocarditis in mice and the administration of PEG-SOD alone has therapeutic potential in clinical CB3 myocarditis.

The improvement of cardiac pathology in the 1 x 10(3) and the 5 x 10(3) U.kg-1 x d-1 PEG-SOD groups seems to have resulted not from the reduction in myocardial virus titres but from inhibition of generation of oxygen free radicals. The mechanism of the impaired survival and aggravation of cardiac pathology in the 1 x 10(5) U.kg-1 x d-1 PEG-SOD group is unknown. The results suggest that oxygen free radicals may be involved in the pathogenesis and development of CB3 myocarditis and that appropriate dosages of PEG-SOD have therapeutic potential for clinical CB3 myocarditis, although caution must be paid to the treatment window.

Autoimmune mechanisms might operate in mice with post-CB3 myocarditis and could be transferred in to SCID mice by the antigen-sensitized lymphocytes. An in vivo model of autoimmune post-viral myocarditis in SCID mouse was demonstrated.