Myocardial Strain Analysis in a Doxorubicin-Induced Cardiomyopathy Model

Piegari, Elena; Salvo, Giovanni Di; Castaldi, Biagio; Vitelli, Maria Redenta; Rodolico, Gabriella; Golino, Paolo; Calabrò, Raffaele; Rossi, Francesco; Berrino, Liberato

doi:10.1016/j.ultrasmedbio.2007.08.002

Cited by 31 publications

(26 citation statements)

References 30 publications

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“…This setting shows that the present findings were not affected by any hyperkinetic state but were related to cardiotoxicity. Piegari et al [18] administered doxorubicin to 14 rats and performed standard echocardiography and STE prior to the therapy and 2 and 4 weeks following therapy, as well as histological sampling. They reported that there was cardiac damage based on the histological samples and the STE results 2 weeks post therapy, whereas the standard echocardiography performed at the same time showed normal findings.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Cardiotoxicity via Speckle-Tracking Echocardiography in Patients Treated with Anthracyclines

Doğru¹,

Çabuk²,

Şahı̇n

et al. 2013

Onkologie

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Background: The aim of this study was to examine the cardiac effects of anthracycline therapy based on speckle-tracking echocardiography (STE) and to identify patients at risk for cardiotoxicity. Patients and Methods: The study included 35 breast cancer (BC) and 15 lymphoma patients who were treated with anthracycline-based chemotherapy. Conventional echocardiography and STE were performed 1 month prior to and 1 month after chemotherapy. Longitudinal strain analysis was performed via STE using automated functional imaging. Results: The ejection fraction (EF) and the fractional shortening values were significantly lower in the lymphoma group. There was a positive correlation between anthracycline dose and subclinical heart failure (p = 0.024). There was an increase in the myocardial performance index in both groups. After therapy, STE showed regional decreases in the longitudinal strain values in the BC group, but the global strain values did not differ. In the lymphoma group, the apical long-axis, the 4-chamber, and the global longitudinal strain values were significantly lower after therapy (p = 0.002, 0.041, and 0.004, respectively). The long-axis and global longitudinal strain values were significantly lower in the lymphoma patients with normal EF values (p = 0.01 and 0.05, respectively). Conclusion: Cardiotoxicity during the early phase of anthracycline treatment can be detected via STE prior to the observation of systolic function deterioration.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Cardiotoxicity via Speckle-Tracking Echocardiography in Patients Treated with Anthracyclines

Doğru¹,

Çabuk²,

Şahı̇n

et al. 2013

Onkologie

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“…If early ventricular dysfunction in antineoplastic drug-treated patients is the intended clinical target, then it would be essential to demonstrate that the novel cardioprotective therapy can prevent early the left ventricular ejection fraction drop C10 % or even more sensitive parameters of left ventricular function at echocardiography or magnetic resonance imaging (MRI) when administered just prior or at the onset of anticancer treatment [99]. However, a decrease in left ventricular ejection fraction does not always predict early cardiac damage.…”

Section: Preclinical Models Of Chemotherapy-induced Cardiotoxicitymentioning

confidence: 99%

Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardiotoxicity and Cardioprotection

et al. 2015

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Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal models of chemotherapy-induced cardiomyopathy. This Position Paper of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology aims to: (1) define the distinctive etiopatogenetic features of cardiac toxicity induced by cancer therapy in humans, which include new aspects of mitochondrial function and oxidative stress, neuregulin-1 modulation through the ErbB receptor family, angiogenesis inhibition, and cardiac stem cell depletion and/or dysfunction; (2) review the new, more promising therapeutic strategies for cardioprotection, aimed to increase the survival of patients with severe antineoplastic-induced cardiotoxicity; (3) recommend the distinctive pathological features of cardiotoxicity induced by cancer therapy in humans that should be present in animal models used to identify or to test new cardioprotective therapies.

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“…Current monitoring recommendations should therefore be revised [72]. Feasibility studies of new cardiac surveillance modalities would be valuable to clinicians treating patients with anthracyclines or other potentially cardiotoxic chemotherapeutic agents [73,74]. In this respect, preclinical evidence for a higher diagnostic value of myocardial strain and strain rate as detected by Doppler echocardiography needs to be validated as a surrogate end point before such determinations could be routinely employed for monitoring anthracycline cardiotoxicity [75][76][77].…”

Section: Detection and Monitoringmentioning

confidence: 99%

Cancer Treatment-Induced Cardiotoxicity: a Cardiac Stem Cell Disease?

Prezioso¹,

Tanzi²,

Galaverna

et al. 2010

CHAMC

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Cardiovascular diseases and cancer represent respectively the first and second cause of death in industrialized countries. These two conditions may become synergistic when cardiovascular complications of anti-cancer therapy are considered. More than 70% of childhood and 50% of adult cancer patients can be cured, however this important success obtained by the biological and medical research is obfuscated by emerging findings of early and late morbidity due to cardiovascular events. Although anthracyclines are effective drugs against cancer a dose-dependent cardiotoxic effects whose mechanism has not been elucidated resulting in failure of therapeutic interventions limit their use. Unexpectedly, tyrosine/kinase inhibitors (TKIs) aimed at molecularly interfering with oncogenic pathways, have been implicated in cardiac side effects. Possible explanations of this phenomenon have been ambiguous, further strengthening the need to deepen our understanding on the mechanism of cardiotoxicity. In addition to a detailed description of anthracyclines and TKIs-related cardiovascular effects, the present review highlights recent observations supporting the hypothesis that the cellular target of anthracyclines and TKIs may include myocardial compartments other than parenchymal cells. The demonstration that the adult mammalian heart possesses a cell turnover regulated by primitive cells suggests that this cell population may be implicated in the onset and development of cardiovascular effects of anti-cancer strategies. The possibility of preventing cardiotoxicity by preservation and/or expansion of the resident stem cell pool responsible for cardiac repair may open new therapeutic options to unravel an unsolved clinical issue.

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Myocardial Strain Analysis in a Doxorubicin-Induced Cardiomyopathy Model

Cited by 31 publications

References 30 publications

Evaluation of Cardiotoxicity via Speckle-Tracking Echocardiography in Patients Treated with Anthracyclines

Evaluation of Cardiotoxicity via Speckle-Tracking Echocardiography in Patients Treated with Anthracyclines

Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardiotoxicity and Cardioprotection

Cancer Treatment-Induced Cardiotoxicity: a Cardiac Stem Cell Disease?

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