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Allostatic load and cardiovascular outcomes in males with prostate cancer

医学 狼牙棒 危险系数 置信区间 比例危险模型 内科学 静载荷 队列 前列腺癌 心脏病学 癌症 老年学 心肌梗塞 经皮冠状动脉介入治疗
作者
Nickolas Stabellini,Jennifer Cullen,Márcio Sommer Bittencourt,Justin X. Moore,Lifen Cao,Neal L. Weintraub,Ryan A. Harris,Xiaoling Wang,Biplab Kumar Datta,Steven S. Coughlin,Jorge García,John Shanahan,Nelson Hamerschlak,Kristin Waite,Nathanael Fillmore,Martha K. Terris,Alberto J. Montero,Jill S. Barnholtz‐Sloan,Avirup Guha
出处
期刊:JNCI Cancer Spectrum [Oxford University Press]
卷期号:7 (2) 被引量:14
标识
DOI:10.1093/jncics/pkad005
摘要

Abstract Background Cardiovascular disease (CVD) is the leading cause of death in men with prostate cancer (PC). Accumulated stress plays an important role in CVD development. The cumulative burden of chronic stress and life events can be measured using allostatic load (AL). Methods The initial cohort included males aged 18 years and older diagnosed with PC (2005-2019). AL was modeled as an ordinal variable (0-11). Fine-Gray competing risk regressions measured the impact of precancer diagnosis AL and postdiagnosis AL in 2-year major cardiac events (MACE). The effect of AL changes over time on MACE development was calculated via piecewise Cox regression (before, and 2 months, 6 months, and 1 year after PC diagnosis). Results We included 5261 PC patients of which 6.6% had a 2-year MACE. For every 1-point increase in AL before and within 60 days after PC diagnosis, the risk of MACE increased 25% (adjusted hazard ratio [aHR] =1.25, 95% confidence interval [CI] = 1.18 to 1.33) and 27% (aHR = 1.27, 95% CI = 1.20 to 1.35), respectively. Using AL as a time-varying exposure, the risk of MACE increased 19% (aHR = 1.19, 95% CI = 1.11 to 1.27), 22% (aHR = 1.22, 95% CI = 1.14 to 1.33), 28% (aHR = 1.28, 95% CI = 1.23 to 1.33), and 31% (aHR = 1.31, 95% CI = 1.27 to 1.35) for every 1-point increase in AL before, 2 months after, 6 months after, and 1 year after PC diagnosis, respectively. Conclusion AL and its changes over time are associated with MACE in PC patients, suggesting a role of a biological measure of stress as a marker of CVD risk among men with PC.

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