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-fr...
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Elsevier
2025-03-01
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| Series: | American Journal of Preventive Cardiology |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2666667724002952 |
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| author | Yidan Wang Shan Zhong Na Sun Yunfei Wu Jun Lyu Minghui Piao Wenbo Qu Xueyu Wang Wenjun Ni Xia Gu Tianshu Han Jinwei Tian |
| author_facet | Yidan Wang Shan Zhong Na Sun Yunfei Wu Jun Lyu Minghui Piao Wenbo Qu Xueyu Wang Wenjun Ni Xia Gu Tianshu Han Jinwei Tian |
| author_sort | Yidan Wang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-47935dfffa434f14a933fb874daa6079 |
| institution | DOAJ |
| issn | 2666-6677 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | American Journal of Preventive Cardiology |
| spelling | doaj-art-47935dfffa434f14a933fb874daa60792025-08-20T02:45:11ZengElsevierAmerican Journal of Preventive Cardiology2666-66772025-03-012110092610.1016/j.ajpc.2024.100926Cancer, genetic susceptibility and risk of coronary artery disease: A prospective studyYidan Wang0Shan Zhong1Na Sun2Yunfei Wu3Jun Lyu4Minghui Piao5Wenbo Qu6Xueyu Wang7Wenjun Ni8Xia Gu9Tianshu Han10Jinwei Tian11Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin Medical University, Harbin 150001, PR ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Clinical Research, The First Affiliated Hospital of Jinan University, 613 West Huangpu Avenue, Guangzhou 510630, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, ChinaDepartment of Nutrition and Food Hygiene, National Key Discipline, School of Public Health, Harbin Medical University, 157 Baojian Road, Harbin 150081, China; Corresponding author at: Department of Nutrition and Food Hygiene, National Key Discipline, School of Public Health, Harbin Medical University, 157 Baojian Road, Harbin 150081, China.Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin Medical University, Harbin 150001, PR China; Corresponding author at: Department of Cardiology, The second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150081, China.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.http://www.sciencedirect.com/science/article/pii/S2666667724002952Cardio-oncologyCoronary artery diseasePolygenic risk score |
| spellingShingle | Yidan Wang Shan Zhong Na Sun Yunfei Wu Jun Lyu Minghui Piao Wenbo Qu Xueyu Wang Wenjun Ni Xia Gu Tianshu Han Jinwei Tian Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study American Journal of Preventive Cardiology Cardio-oncology Coronary artery disease Polygenic risk score |
| title | Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study |
| title_full | Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study |
| title_fullStr | Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study |
| title_full_unstemmed | Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study |
| title_short | Cancer, genetic susceptibility and risk of coronary artery disease: A prospective study |
| title_sort | cancer genetic susceptibility and risk of coronary artery disease a prospective study |
| topic | Cardio-oncology Coronary artery disease Polygenic risk score |
| url | http://www.sciencedirect.com/science/article/pii/S2666667724002952 |
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