Active myocarditis with fibrosis. Poor correlation of ejection fraction with histology of follow-up biopsy

Marboe, Charles C.; Schwartz, R A; Adelson, David; Escala, Edith; Weiss, Melvin B.; Fenoglio, John J.

doi:10.1093/eurheartj/8.suppl_j.43

Cited by 8 publications

(4 citation statements)

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“…However, there is considerable interobserver variation in the interpretation of histologic findings (8,24). Moreover, as evidenced in this study, the histologic findings are often focal and minimal, and thus easily missed on a small endomyocardial biopsy (25,26). Direct in situ detection of the virus in such a biopsy would be needed to establish the diagnosis.…”

Section: Discussionmentioning

confidence: 84%

Histologic and In Situ Viral Findings in the Myocardium in Cases of Sudden, Unexpected Death

Cioc

Nuovo

2002

Mod Pathol

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Section: Discussionmentioning

confidence: 84%

Histologic and In Situ Viral Findings in the Myocardium in Cases of Sudden, Unexpected Death

Cioc

Nuovo

2002

Mod Pathol

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“…The ability of pertussis toxin treatment to increase the levels of cAMP via its known effect of modifying Gi suggests that the inhibitory limb of the signal transduction system is intact or that pertussis toxin can override an ASCM effect on Gi. Explanations for the involvement of Gi could include 1) the ASCM-induced production of a ligand that binds to a Gi-coupled receptor, 2) changes in the mass of Gi, 3) changes in the structure of Gi, such as phosphorylation or production of an isoenzyme of Gi, or 4) membrane effects to enhance the inhibitory capacity of Gi. Only explanation 2 would seem doubtful, given the present data ( Figure 7B).…”

Section: Pertussis Toxin Adp-ribosylationmentioning

confidence: 99%

Mechanism of cytokine inhibition of beta-adrenergic agonist stimulation of cyclic AMP in rat cardiac myocytes. Impairment of signal transduction.

Chung

Gulick

Rotondo

et al. 1990

Circulation Research

200

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Studies conducted in our laboratory have demonstrated that activated immune cells produce a soluble inhibitor(s) of cardiac myocyte contractile and cyclic AMP (cAMP) responses to beta-adrenergic stimulation. To examine the mechanism of this effect, metabolic assays were conducted on cultured rat cardiac myocytes incubated in the presence and absence of supernatants harvested from rat activated splenocyte cultures. Intracellular cAMP accumulation in response to isoproterenol was inhibited by up to 74% in a dose-dependent fashion by conditioned media containing soluble cytokines from activated immune cells. By use of myocyte cultures in which contaminating nonmyocyte proliferation was inhibited by nonlethal irradiation, this phenomenon was shown to be independent of mitogenic effects. Isobutylmethylxanthine, a phosphodiesterase inhibitor, did not ablate cytokine-induced inhibition of cAMP accumulation. Parameters of beta-adrenergic receptor binding and affinity were also unaffected. cAMP suppression was maintained after cholera toxin stimulation of cAMP production via stimulatory G protein ADP-ribosylation. cAMP inhibition was not apparent when cells were stimulated with forskolin, a direct adenylate cyclase activator. Importantly, pertussis toxin treatment significantly ablated cytokine-induced cAMP inhibition. Thus, interference with agonist-occupied beta-adrenergic receptor coupling to adenylate cyclase to produce cAMP and subsequent contractile responses is induced by a factor(s) elaborated by activated immune cells. This interference occurs at the level of signal transduction across the membrane, can be overridden by pertussis toxin, and may involve changes in the coupling of the stimulatory/inhibitory G proteins to adenylate cyclase. These results demonstrate a novel mechanism of cytokine-induced myocyte dysfunction and may have important pathophysiological ramifications in immune-mediated myocardial diseases.

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“…At least two groups [42,43] have looked at the correlation of structure with function (as measured by left ventricu lar ejection fraction); in neither of the stud ies was there a good association of histology with change in ejection fraction. The group at the Massachusetts General Hospital stud ied 17 patients with acute onset of heart fail ure and a biopsy diagnosis of myocarditis, initially and after 6-12 weeks of treatment that included immunosuppression.…”

Section: Natural History Of Myocarditis and Response To Therapymentioning

confidence: 99%

“…There was no significant clinical improvement in either group. In another study [43] a total of 66 follow-up biopsies from 29 patients were examined. All patients were treated supportively and 16 also received prednisone alone or with aza thioprine.…”

Section: Natural History Of Myocarditis and Response To Therapymentioning

confidence: 99%

Pathology and Natural History of Human Myocarditis

Marboe

Fenoglio

1988

Path Immunopathol Res

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Active myocarditis with fibrosis. Poor correlation of ejection fraction with histology of follow-up biopsy

Cited by 8 publications

References 0 publications

Histologic and In Situ Viral Findings in the Myocardium in Cases of Sudden, Unexpected Death

Histologic and In Situ Viral Findings in the Myocardium in Cases of Sudden, Unexpected Death

Mechanism of cytokine inhibition of beta-adrenergic agonist stimulation of cyclic AMP in rat cardiac myocytes. Impairment of signal transduction.

Pathology and Natural History of Human Myocarditis

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