Evaluation of mitoxantrone cardiac toxicity by nuclear angiography and endomyocardial biopsy: an update

Sixty-six patients who underwent endomyocardial biopsy for detection of mitoxantrone (Novantrone; dihydroxyanthracenedione) cardiac toxicity were evaluated. All but one had breast cancer, 29 had received prior doxorubicin and 29 of the 37 patients who had not had prior doxorubicin received it or ano...

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Bibliographic Details
Published in:Investigational new drugs 1985-01, Vol.3 (2), p.117-121
Main Authors: Benjamin, R S, Chawla, S P, Ewer, M S, Carrasco, C H, Mackay, B, Holmes, F
Format: Article
Language:English
Subjects:
Adult
Aged
Angiocardiography
Anthraquinones - adverse effects
Antineoplastic Agents - adverse effects
Biopsy
Breast Neoplasms - drug therapy
Doxorubicin - adverse effects
Female
Heart - drug effects
Heart Failure - chemically induced
Humans
Microscopy, Electron
Middle Aged
Mitoxantrone
Myocardium - pathology
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Summary:Sixty-six patients who underwent endomyocardial biopsy for detection of mitoxantrone (Novantrone; dihydroxyanthracenedione) cardiac toxicity were evaluated. All but one had breast cancer, 29 had received prior doxorubicin and 29 of the 37 patients who had not had prior doxorubicin received it or another anthracycline subsequently. Endomyocardial biopsy was carried out initially after four courses of chemotherapy with increasing intervals thereafter. Although cardiac ejection fraction was determined before each course of chemotherapy, our data are limited to cardiac ejection fractions from our own institution which were repeated approximately every four courses. Endomyocardial biopsy changes consisting of dilatation of the sarcoplasmic reticulum with vacuole formation, and myofibrillar dropout are similar to the early changes of anthracycline cardiomyopathy. While there was a slight suggestion of increasing biopsy grade with increasing mitoxantrone dose, no significant changes in cardiac ejection fraction could be associated, regardless of prior doxorubicin therapy. We concluded that mitoxantrone does show morphologic evidence of cardiac toxicity; however, the structural changes are minor and are haemodynamically insignificant. Determination of how much mitoxantrone treatment may contribute to the deterioration of pre-existing doxorubicin damage must await the outcome of longer follow-up.
ISSN:0167-6997
1573-0646
DOI:10.1007/BF00174158