Delayed gadolinium-enhanced cardiac magnetic resonance in patients with chronic myocarditis presenting with heart failure or recurrent arrhythmias.
Sarcoidosis Subepicardial progressing inwards, basal Amyloidosis Diffuse, subendocardial to epicardial, altered T1 kinetics Anderson-Fabry disease Mid myocardial, basal inferolateral wall, symmetrically hypertrophied myocardium, normal or increased function Myocarditis Subepicardial progressing inwards, inferolateral/lateral/anteroseptal walls, focal wall-motion abnormalities Chronic myocarditis Mid myocardial, linear ARVD RV-free wall-septum, wall-motion abnormalities, fatty replacement Endomyocardial fibrosis Diffuse subendocardial, adherent thrombus Noncompaction Enhancement of noncompacted myocardium Chagas disease Subepicardial, LV apex, inferolateral wall Muscular dystrophies Inferolateral wall
These results indicate that persistence of virus alone is not the determining factor in the development of chronic myocarditis.
Since the innate immune response is critical in determining the development of adaptive immunity (18) and proinflammatory cytokines administered during the innate response determine whether chronic myocarditis develops, we were interested in studying early differences in the cytokine response to CB3 infection in susceptible (BALB/c) or resistant (C57BL/6) mice to see if they could provide clues to the progression to autoimmunity.
Histologic examination of the explanted heart otherwise showed the usual severe chronic myocarditis
characteristic of this disease (Figure, 1A), most extensively involving the left ventricle.