Eric J Chow1, Yan Chen2, Leontien C Kremer2, Norman E Breslow2, Melissa M Hudson2, Gregory T Armstrong2, William L Border2, Elizabeth A M Feijen2, Daniel M Green2, Lillian R Meacham2, Kathleen A Meeske2, Daniel A Mulrooney2, Kirsten K Ness2, Kevin C Oeffinger2, Charles A Sklar2, Marilyn Stovall2, Helena J van der Pal2, Rita E Weathers2, Leslie L Robison2, Yutaka Yasui2. 1. Eric J. Chow and Norman E. Breslow, Fred Hutchinson Cancer Research Center, Seattle Children's Hospital, University of Washington, Seattle, WA; Yan Chen and Yutaka Yasui, University of Alberta, Edmonton, Alberta, Canada; Leontien C. Kremer, Elizabeth A.M. Feijen, and Helena J. van der Pal, Emma Children's Hospital and Academic Medical Center, Amsterdam, the Netherlands; Melissa M. Hudson, Gregory T. Armstrong, Daniel M. Green, Daniel A. Mulrooney, Kirsten K. Ness, and Leslie L. Robison, St Jude Children's Research Hospital; Daniel A. Mulrooney, University of Tennessee, Memphis, TN; William L. Border and Lillian R. Meacham, Children's Healthcare of Atlanta, Emory University, Atlanta, GA; Kathleen A. Meeske, Children's Hospital of Los Angeles, University of Southern California, Los Angeles, CA; Kevin C. Oeffinger and Charles A. Sklar, Memorial Sloan-Kettering Cancer Center, New York, NY; and Marilyn Stovall and Rita E. Weathers, University of Texas MD Anderson Cancer Center, Houston, TX. ericchow@u.washington.edu. 2. Eric J. Chow and Norman E. Breslow, Fred Hutchinson Cancer Research Center, Seattle Children's Hospital, University of Washington, Seattle, WA; Yan Chen and Yutaka Yasui, University of Alberta, Edmonton, Alberta, Canada; Leontien C. Kremer, Elizabeth A.M. Feijen, and Helena J. van der Pal, Emma Children's Hospital and Academic Medical Center, Amsterdam, the Netherlands; Melissa M. Hudson, Gregory T. Armstrong, Daniel M. Green, Daniel A. Mulrooney, Kirsten K. Ness, and Leslie L. Robison, St Jude Children's Research Hospital; Daniel A. Mulrooney, University of Tennessee, Memphis, TN; William L. Border and Lillian R. Meacham, Children's Healthcare of Atlanta, Emory University, Atlanta, GA; Kathleen A. Meeske, Children's Hospital of Los Angeles, University of Southern California, Los Angeles, CA; Kevin C. Oeffinger and Charles A. Sklar, Memorial Sloan-Kettering Cancer Center, New York, NY; and Marilyn Stovall and Rita E. Weathers, University of Texas MD Anderson Cancer Center, Houston, TX.
Abstract
PURPOSE: To create clinically useful models that incorporate readily available demographic and cancer treatment characteristics to predict individual risk of heart failure among 5-year survivors of childhood cancer. PATIENTS AND METHODS: Survivors in the Childhood Cancer Survivor Study (CCSS) free of significant cardiovascular disease 5 years after cancer diagnosis (n = 13,060) were observed through age 40 years for the development of heart failure (ie, requiring medications or heart transplantation or leading to death). Siblings (n = 4,023) established the baseline population risk. An additional 3,421 survivors from Emma Children's Hospital (Amsterdam, the Netherlands), the National Wilms Tumor Study, and the St Jude Lifetime Cohort Study were used to validate the CCSS prediction models. RESULTS: Heart failure occurred in 285 CCSS participants. Risk scores based on selected exposures (sex, age at cancer diagnosis, and anthracycline and chest radiotherapy doses) achieved an area under the curve of 0.74 and concordance statistic of 0.76 at or through age 40 years. Validation cohort estimates ranged from 0.68 to 0.82. Risk scores were collapsed to form statistically distinct low-, moderate-, and high-risk groups, corresponding to cumulative incidences of heart failure at age 40 years of 0.5% (95% CI, 0.2% to 0.8%), 2.4% (95% CI, 1.8% to 3.0%), and 11.7% (95% CI, 8.8% to 14.5%), respectively. In comparison, siblings had a cumulative incidence of 0.3% (95% CI, 0.1% to 0.5%). CONCLUSION: Using information available to clinicians soon after completion of childhood cancer therapy, individual risk for subsequent heart failure can be predicted with reasonable accuracy and discrimination. These validated models provide a framework on which to base future screening strategies and interventions.
PURPOSE: To create clinically useful models that incorporate readily available demographic and cancer treatment characteristics to predict individual risk of heart failure among 5-year survivors of childhood cancer. PATIENTS AND METHODS: Survivors in the Childhood Cancer Survivor Study (CCSS) free of significant cardiovascular disease 5 years after cancer diagnosis (n = 13,060) were observed through age 40 years for the development of heart failure (ie, requiring medications or heart transplantation or leading to death). Siblings (n = 4,023) established the baseline population risk. An additional 3,421 survivors from Emma Children's Hospital (Amsterdam, the Netherlands), the National Wilms Tumor Study, and the St Jude Lifetime Cohort Study were used to validate the CCSS prediction models. RESULTS:Heart failure occurred in 285 CCSS participants. Risk scores based on selected exposures (sex, age at cancer diagnosis, and anthracycline and chest radiotherapy doses) achieved an area under the curve of 0.74 and concordance statistic of 0.76 at or through age 40 years. Validation cohort estimates ranged from 0.68 to 0.82. Risk scores were collapsed to form statistically distinct low-, moderate-, and high-risk groups, corresponding to cumulative incidences of heart failure at age 40 years of 0.5% (95% CI, 0.2% to 0.8%), 2.4% (95% CI, 1.8% to 3.0%), and 11.7% (95% CI, 8.8% to 14.5%), respectively. In comparison, siblings had a cumulative incidence of 0.3% (95% CI, 0.1% to 0.5%). CONCLUSION: Using information available to clinicians soon after completion of childhood cancer therapy, individual risk for subsequent heart failure can be predicted with reasonable accuracy and discrimination. These validated models provide a framework on which to base future screening strategies and interventions.
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