1988
DOI: 10.1016/0277-5379(88)90205-2
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Cardiotoxicity of mitozantrone assessed by stress and resting nuclear ventriculography

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Cited by 19 publications
(7 citation statements)
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“…Overall, five studies 16 , 22 , 23 , 25 , 26 showed a benefit, five 18 , 19 , 24 , 27 , 28 showed possible benefit, and four 17 , 20 , 21 , 29 showed no benefit to utilizing cardiac stress tests in identifying evidence of cardiovascular disease in breast cancer survivors.…”
Section: Resultsmentioning
confidence: 94%
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“…Overall, five studies 16 , 22 , 23 , 25 , 26 showed a benefit, five 18 , 19 , 24 , 27 , 28 showed possible benefit, and four 17 , 20 , 21 , 29 showed no benefit to utilizing cardiac stress tests in identifying evidence of cardiovascular disease in breast cancer survivors.…”
Section: Resultsmentioning
confidence: 94%
“…Heart function tests that were performed with stress in the selected studies were scintigraphy (n=5), 17 , 19 , 20 , 28 , 29 single photon emission computed tomography (SPECT) (n=4), 18 , 22 , 24 , 25 echocardiography (n=2), 16 , 23 cardiac magnetic resonance imaging (cMRI) (n=1), 21 nuclear ventriculography (n=1), 26 and ECG (n=5). 17 , 19 , 20 , 22 , 27 The utility of stress among each technique is shown in Figure 2A .…”
Section: Resultsmentioning
confidence: 99%
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“…Though early animal studies sug gested that MTX was devoid of the progres sive cardiotoxic effects typical of anthracy clines [1][2][3], there have been several clinical reports of MTX cardiotoxicity in patients receiving multiple administrations [4][5][6]. Analyses of myocardial biopsy specimens have shown that a cardiomyopathy develops after multiple doses of this drug [7], The car diotoxicity of MTX is mild at total cumula tive doses < 100 mg/m2, and the cellular alterations induced are not severe except for patients receiving total cumulative doses > 200 mg/m2 [7], The latter show structural changes of the heart muscle qualitatively identical to those caused by anthracyclines, consisting of degeneration of myocytes and myofibrillar lysis [7], The presence of focal myopathic changes with a great quantity of fibrosis typical of these cardiomyopathies may give rise to an inhomogeneous propagation of conduction which is the electrophysiologic basis of lowamplitude high-frequency signals in the ter minal portion of the QRS complex and ST segment (late potentials, LP) [8,9], These low amplitude signals have been observed in patients with scarred myocardium and have been proposed as a marker of reentry which plays a major role in the pathophysiology of malignant ventricular arrhythmias [10,11].…”
Section: Introductionmentioning
confidence: 99%