The Importance of Clinical Grading of Heart Failure and Other Cardiac Toxicities During Chemotherapy: Updating the Common Terminology Criteria for Clinical Trial Reporting

Hossain, Akm Mosharraf; Chen, Alice; Ivy, Percy; Lenihan, Daniel J.; Kaltman, Jonathan R.; Taddei-Peters, Wendy C.; Remick, Scot C.

doi:10.1016/j.hfc.2011.03.008

Cited by 15 publications

(16 citation statements)

References 33 publications

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“…Publications use different criteria in their definition of anthracycline cardiotoxicity. The CTCAE for clinical reporting has been advocated 8.We therefore used ejection fraction (EF) <50% (CTCAE Grade 2+) to define cardiotoxicity.…”

Section: Methodsmentioning

confidence: 99%

Anthracycline induced cardiac toxicity in pediatric Ewing sarcoma: A longitudinal study

Brown

Vijarnsorn

Potts

et al. 2013

Pediatric Blood & Cancer

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Section: Methodsmentioning

confidence: 99%

Anthracycline induced cardiac toxicity in pediatric Ewing sarcoma: A longitudinal study

Brown

Vijarnsorn

Potts

et al. 2013

Pediatric Blood & Cancer

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“…To further complicate the matter, the general consensus for the definition of significant cardiotoxicity is an absolute decline of the LVEF by 10 % to a value less than 50 % [10,[19][20][21]. The Common Terminology Criteria (version 4) for the detection of cardiotoxicity defined as HF, symptomatic left ventricular dysfunction (LVD), and reduced LVEF for clinical trial reporting are listed in Table 1 [22]. Unfortunately, LVEF reduction is a late and often irreversible effect of anthracycline therapy.…”

Section: Introductionmentioning

confidence: 99%

Cardiotoxicity due to Chemotherapy: the Role of Biomarkers

Stevens

Lenihan

2015

Curr Cardiol Rep

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An ever-increasing array of chemotherapeutic agents is being used in the treatment of solid organ or hematologic malignancies. The success of many of these agents has led to an increasing survival of patients with cancer. However, many of these agents, particularly anthracyclines and trastuzumab, are associated with the development of cardiotoxicity. The current standard for the evaluation of chemotherapy-associated cardiotoxicity typically involves the use of serial measurements of left ventricular (LV) function by echocardiogram (Echo) and radionuclide ventriculogram (MUGA). Unfortunately, this time-honored method offers low sensitivity to the early prediction or detection of cardiac events. Frequently, by the time cardiotoxicity is detected, significant LV dysfunction has occurred and ultimately this may not respond to standard cardioprotective treatment. Cardiac biomarkers, troponin I and B-type natriuretic peptide, may allow a more accurate and timely monitoring strategy. The current data and a summarized understanding of how to utilize cardiac biomarkers for the prevention and early detection of cardiac dysfunction during chemotherapy are presented.

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“…It has been established that TKIs, especially those that interfere with the vascular endothelial growth factor (VEGF) signaling pathways (VSPs; VSP inhibitors), have a class effect of raising BP significantly, and that effect correlates with CV AEs. Hypertension is an important consideration when treating patients with small-molecule TKIs (e.g., sunitinib, sorafenib, pazopanib, vandetanib, and cabozantinib) and monoclonal antibodies (e.g., bevacizumab) that inhibit the VEGF signaling pathway [9,16,26]. Interaction between the soluble VEGF and its primary receptor, VEGF receptor 2 (VEGFR-2), on endothelial cells leads to multiple important physiologic changes, including increased capillary permeability; upregulated nitric oxide production with secondary relaxation of vascular smooth muscle; and increased proliferation, migration, and survival of endothelial cells under stress [27].…”

Section: Hypertensionmentioning

confidence: 99%

Overview and Management of Cardiac Adverse Events Associated With Tyrosine Kinase Inhibitors

2013

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Background. Small-molecule tyrosine kinase inhibitors (TKIs) may provide an effective therapeutic option in patients with hematologicmalignanciesandsolidtumors.However,cardiovascular (CV) events, including hypertension, heart failure, left ventricular systolic dysfunction, and QT prolongation, have emerged as potential adverse events (AEs) with TKI therapy. Purpose. We review what is known about the mechanism of action of CV AEs associated with TKI use and discuss therapeutic interventions that may prevent and manage these events in clinical practice. Methods. References for this review were identified through searches of PubMed and Medline databases, and only papers published in English were considered. Search terms included "cardiac," "cardiovascular," "cancer," and "kinase inhibitor." Related links in the databases were reviewed, along with relevant published guidelines.Results. Although the link between rising blood pressure (BP) and CV AEs is observed but not proven, good clinical practice supports an aggressive policy on proper long-term BP management. There are insufficient data from randomized controlled clinical trials to show indisputably that aggressive or effective heart failure therapy in patients receiving TKIs will fundamentally change outcomes; however, clinical practice suggests that this is an effective long-term approach. Recognizing that QT prolongation is associated with TKI use facilitates identification of patients at high risk for this CV AE and increases awareness of the need for routine electrocardiograms and electrolyte monitoring for those receiving TKI treatment. Conclusion. Regular monitoring, early recognition, and appropriate interventions for CV AEs can help more patients derive the benefit of long-term TKI therapy. The Oncologist 2013;18: 900 -908 Implications for Practice: Although the antitumor effects of small-molecule tyrosine kinase inhibitors (TKIs) can be considerable, these agents are often associated with cardiovascular (CV) adverse events (AEs), including hypertension, heart failure, and QT prolongation. This review covers the cardiac risks associated with different TKI therapies, including the putative mechanisms through which TKIs may affect cardiac function, as a means to increase both clinician awareness and understanding of these potential side effects in the oncology setting. This paper also provides clinical strategies for optimizing the use of TKI therapy based on careful pretreatment cardiac risk assessment, early recognition of CV AEs through regular monitoring of electrocardiograms and serum electrolytes, and aggressive management of cardiac events that develop in patients receiving TKI treatment. These guideline-based approaches can facilitate the appropriate use of TKI therapy, thereby allowing patients to experience long-term benefits while minimizing the occurrence of CV AEs.

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The Importance of Clinical Grading of Heart Failure and Other Cardiac Toxicities During Chemotherapy: Updating the Common Terminology Criteria for Clinical Trial Reporting

Cited by 15 publications

References 33 publications

Anthracycline induced cardiac toxicity in pediatric Ewing sarcoma: A longitudinal study

Anthracycline induced cardiac toxicity in pediatric Ewing sarcoma: A longitudinal study

Cardiotoxicity due to Chemotherapy: the Role of Biomarkers

Overview and Management of Cardiac Adverse Events Associated With Tyrosine Kinase Inhibitors

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