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

1985 ◽  
Vol 3 (2) ◽  
Author(s):  
RobertS. Benjamin ◽  
SantP. Chawla ◽  
MichaelS. Ewer ◽  
C.Humberto Carrasco ◽  
Bruce Mackay ◽  
...  
Author(s):  
Robert H. Liss ◽  
Frances A. Cotton

Daunomycin, an antibiotic used in the clinical management of acute leukemia, produces a delayed, lethal cardiac toxicity. The lethality is dose and schedule dependent; histopathologic changes induced by the drug have been described in heart, lung, and kidney from hamsters in both single and multiple dose studies. Mice given a single intravenous dose of daunomycin (10 mg/kg) die 6-7 days later. Drug distribution studies indicate that the rodents excrete most of a single dose of the drug as daunomycin and metabolite within 48 hours after dosage (M. A. Asbell, personal communication).Myocardium from the ventricles of 6 moribund BDF1 mice which had received a single intravenous dose of daunomycin (10 mg/kg), and from controls dosed with physiologic saline, was fixed in glutaraldehyde and prepared for electron microscopy.


Author(s):  
Xia Mingyu ◽  
Ma Wengshu ◽  
Wu Xiangh ◽  
Chen Dong

This paper describes morphological and cytochemistry changes of endomyocardial biopsy in 94 patients. The samples of myoicardium were taken from 32 patients with dilated cardiomyopathy, and sdudied with light and electron microscop. The cytochemical studies in some of these patients were performed at histological and ultrastructure level. This paper also reported the result of myocardial biopsy in 33 patients with serious dysrythmia.The result of this controlled study indicates that morphological assessment in both cardiomyopathy and congenital or rheumatic heart diseases showed no special changes. In patients of dilated cardiomyopathy, the decreased activity of myosin ATPase was secondary to cardial failure. The change of succinate dehydrogenase (SDHase) was not significant with light microscopy. But ultrastructural localization of SDHase activity is valuable. Its activity was found to be localized in endomembrane and ridge of the mitochondria, the activity of this enzyme was decrease, normal, or increase. SDHase activity was more intense in cardial myocytes well-functioning, or ultrastructurally well preserved hearts.


1984 ◽  
Vol 2 (4) ◽  
pp. 647-656 ◽  
Author(s):  
William D. Edwards

2000 ◽  
Vol 18 (6) ◽  
pp. 0743-0744 ◽  
Author(s):  
Michael E. Mullins ◽  
Deborah G. Robertson ◽  
Robert L. Norton

2013 ◽  
Vol 5 (3) ◽  
pp. 193-197
Author(s):  
Emiko Ejima ◽  
Koichiroh Matsumura ◽  
Fumiyuki Hayashi ◽  
Kensaku Shibata ◽  
Masahiro Mizobuchi ◽  
...  

Author(s):  
Miao Chen ◽  
Vijaya Paul Samuel ◽  
Yi Wu ◽  
Minyan Dang ◽  
Yukiat Lin ◽  
...  

2020 ◽  
Vol 04 (05) ◽  
Author(s):  
Sander Trenson ◽  
Daniel Hofer ◽  
Mateusz Sokolski ◽  
Fran Mikulicic ◽  
Frank Ruschitzka ◽  
...  

2021 ◽  
Vol 3 (3) ◽  
pp. 100-112
Author(s):  
Sarah Martinez Roth ◽  
Eveline E. Vietsch ◽  
Megan E. Barefoot ◽  
Marcel O. Schmidt ◽  
Matthew D. Park ◽  
...  

Thoracic high-dose radiation therapy (RT) for cancer has been associated with early and late cardiac toxicity. To assess altered rates of cardiomyocyte cell death due to RT we monitored changes in cardiomyocyte-specific, cell-free methylated DNA (cfDNA) shed into the circulation. Eleven patients with distal esophageal cancer treated with neoadjuvant chemoradiation to 50.4 Gy (RT) and concurrent carboplatin and paclitaxel were enrolled. Subjects underwent fasting blood draws prior to the initiation and after completion of RT as well as 4–6 months following RT. An island of six unmethylated CpGs in the FAM101A locus was used to identify cardiomyocyte-specific cfDNA in serum. After bisulfite treatment this specific cfDNA was quantified by amplicon sequencing at a depth of >35,000 reads/molecule. Cardiomyocyte-specific cfDNA was detectable before RT in the majority of patient samples and showed some distinct changes during the course of treatment and recovery. We propose that patient-specific cardiac damages in response to the treatment are indicated by these changes although co-morbidities may obscure treatment-specific events.


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