癌症、遗传易感性和冠状动脉疾病风险:一项前瞻性研究

IF 4.3 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Yidan Wang , Shan Zhong , Na Sun , Yunfei Wu , Jun Lyu , Minghui Piao , Wenbo Qu , Xueyu Wang , Wenjun Ni , Xia Gu , Tianshu Han , Jinwei Tian
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引用次数: 0

摘要

目的癌症幸存者患冠状动脉疾病(CAD)的风险增加。我们引入了CAD多基因风险评分(PRS),并研究了癌症状况与CAD预后的关系。方法:来自英国生物银行,我们通过相关的癌症登记、住院和死亡记录,在464,193名无CAD的参与者中确定了癌症幸存者和CAD结局。CAD-PRS被分为低(最低四分之一)、中(二分之一)和高(最高三分之一)。调整后的Cox模型评估了癌症状态和CAD- prs对CAD预后的联合和相互作用影响。在随访期间(中位11.7年),36,332名参与者发展为CAD。与低CAD- prs相比,中级CAD的风险比(HRs)和95%置信区间(CIs)为1.35(1.31-1.38),高CAD- prs的风险比(HRs)为1.86(1.81-1.91)。癌症幸存者与非癌症患者相比,CAD的HR (95% CI)为1.16(1.13-1.19)。在联合效应分析中,与低CAD- prs和无癌症的参与者相比,CAD的HRs (95% ci)分别为1.37(1.32-1.41)和1.90(1.84-1.96)。对于癌症患者,低、中、高CAD-PRS的hr (95% ci)分别为1.26(1.19-1.33)、1.59(1.51-1.67)和2.13(2.03-2.23)。在CAD- prs和CAD的癌症状态之间观察到显著的乘法相互作用(HR: 0.94, 95% CI: 0.91-0.98)。此外,癌症与高CAD- prs之间存在显著的累加性相互作用,可致死性CAD。结论癌症与冠心病发生风险增高相关,并可能与遗传因素有关,进一步增加冠心病发生风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study

Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study

Objective

Cancer survivors have an increased risk of developing coronary artery disease (CAD). We introduce CAD polygenic risk scores (PRS) and examine associations with cancer status on CAD outcomes.

Methods

From the UK Biobank, we identified cancer survivors and CAD outcomes among 464,193 CAD-free participants using linked cancer registries, hospitalizations, and death records. CAD-PRS was categorized as low (lowest tertile), intermediate (tertile 2), and high (highest tertile). Adjusted Cox models assessed the joint and interaction effects of cancer status and CAD-PRS on CAD outcomes.

Results

Over the follow-up (median 11.7 years), 36,332 participants developed CAD. Compared to low CAD-PRS, the hazard ratios (HRs) and 95% confidence intervals (CIs) for CAD was 1.35 (1.31–1.38) for intermediate and 1.86 (1.81–1.91) for high CAD-PRS. The HR (95% CI) for CAD in cancer survivors was 1.16 (1.13–1.19) compared to those without cancer. In the joint effect analysis, compared to participants with low CAD-PRS and no cancer, the HRs (95% CIs) for CAD were 1.37 (1.32–1.41) and 1.90 (1.84–1.96) for intermediate and high CAD-PRS without cancer, respectively. For those with cancer, the HRs (95% CIs) were 1.26 (1.19–1.33), 1.59 (1.51–1.67), and 2.13 (2.03–2.23) for low, intermediate, and high CAD-PRS, respectively. A significant multiplicative interaction (HR: 0.94, 95% CI: 0.91–0.98) was observed between CAD-PRS and cancer status on CAD. Additionally, a significant additive interaction between cancer and high CAD-PRS was found for fatal CAD.

Conclusion

Cancer was associated with a higher risk of CAD and may further increase the risk of CAD related to genetic factors.
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来源期刊
American journal of preventive cardiology
American journal of preventive cardiology Cardiology and Cardiovascular Medicine
CiteScore
6.60
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审稿时长
76 days
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