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Background <p>Cancer survivors (CSs) are at increased risk of atrial fibrillation (AF), potentially due to cancer-related inflammation and treatment effects. While inflammation has been implicated in both cancer and AF, the association between C-reactive protein (CRP) and AF risk in CSs remains unclear.</p> Methods <p>We analyzed data from 19,677 UK Biobank participants (mean age 60; 34.2% male) with a prior cancer diagnosis. Incident AF was evaluated using competing-risk Cox proportional hazards models, adjusting for sociodemographic, lifestyle, and clinical factors.</p> Results <p>Over a median follow-up of 10.4 years, 836 CSs (4.2%) developed AF.</p> <p>Competing risk analysis revealed that the significant association between elevated CRP (&gt; 2&#xa0;mg/L) and AF risk in CSs, observed in models adjusted for sociodemographic and clinical factors (HR 1.21, 95% CI 1.06–1.37; <i>P</i> = 0.005), progressively attenuated with further adjustment for lifestyle factors (HR 1.14, 95% CI 0.99–1.31; <i>P</i> = 0.076). Despite losing statistical significance in the fully adjusted model, a consistent, suggestive trend was observed. This association was particularly pronounced in individuals not receiving radiotherapy.</p> Conclusions <p>Our findings suggest that systemic inflammation is associated with an increased risk of AF among CSs, particularly in individuals without a history of radiotherapy. Further studies are needed to explore underlying mechanisms and therapeutic implications.</p>

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Association between systemic inflammation and risk of atrial fibrillation in cancer survivors: a population-based cohort study using UK biobank

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月12日

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  • Quan Yang,
  • Jiazhen Zheng,
  • Chunting Zhao,
  • Min Wu,
  • Run Wang,
  • Mingya Liu,
  • Kai-Hang Yiu

摘要

Background

Cancer survivors (CSs) are at increased risk of atrial fibrillation (AF), potentially due to cancer-related inflammation and treatment effects. While inflammation has been implicated in both cancer and AF, the association between C-reactive protein (CRP) and AF risk in CSs remains unclear.

Methods

We analyzed data from 19,677 UK Biobank participants (mean age 60; 34.2% male) with a prior cancer diagnosis. Incident AF was evaluated using competing-risk Cox proportional hazards models, adjusting for sociodemographic, lifestyle, and clinical factors.

Results

Over a median follow-up of 10.4 years, 836 CSs (4.2%) developed AF.

Competing risk analysis revealed that the significant association between elevated CRP (> 2 mg/L) and AF risk in CSs, observed in models adjusted for sociodemographic and clinical factors (HR 1.21, 95% CI 1.06–1.37; P = 0.005), progressively attenuated with further adjustment for lifestyle factors (HR 1.14, 95% CI 0.99–1.31; P = 0.076). Despite losing statistical significance in the fully adjusted model, a consistent, suggestive trend was observed. This association was particularly pronounced in individuals not receiving radiotherapy.

Conclusions

Our findings suggest that systemic inflammation is associated with an increased risk of AF among CSs, particularly in individuals without a history of radiotherapy. Further studies are needed to explore underlying mechanisms and therapeutic implications.