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Background <p>Myocardial infarction (MI) is an adverse event potentially associated with capecitabine treatment, potentially impacting the continuation of cancer therapy. However, data on its incidence remain limited.</p> Methods <p>Using Danish nationwide registries, we identified patients with gastrointestinal (GI) cancer treated with capecitabine (2004–2016) and compared them to age- and sex-matched controls without cancer. Patients with prior ischemic heart disease were excluded but were subsequently analyzed as a separate secondary cohort. Cumulative incidences of MI and competing risks were calculated, and multivariable regression analyses were performed.</p> Results <p>A total of 23,820 patients with GI cancer treated with capecitabine and 47,640 controls without cancer were included. Differences in comorbidities and antianginal medications were not significantly different (<i>P</i> &gt; 0.05 for all). At 6&#xa0;months, the cumulative incidence of MI was significantly higher for patients treated with capecitabine at 0.6% (95% CI: 0.5%-0.7%) versus 0.3% (95% CI: 0.3%-0.4%) in controls, with a competing risk of death of 15.2% versus 0.7%. At 1&#xa0;year, the cumulative incidence of MI for patients receiving capecitabine was 0.7% (95% CI: 0.6%-0.9%) versus 0.6% (95% CI: 0.5%-0.6%) among controls, with a competing risk for death of 29.7% versus 1.6%. After accounting for competing risks, the sub distribution hazard ratios indicated an increased risk of MI for patients receiving capecitabine compared with control subjects at both 6&#xa0;months (hazard ratio: 2.02; 95% CI: 1.57–2.60; <i>P</i> &lt; 0.001) and 12&#xa0;months (hazard ratio: 1.28; 95% CI: 1.05–1.57; <i>P</i> = 0.015).</p> Conclusion <p>Capecitabine treatment in GI cancer patients was associated with an increased MI risk at 6 and 12&#xa0;months compared to controls, though absolute risks were low. Given the high competing mortality, the clinical relevance of this increased MI risk appears limited. In a secondary analysis of patients with known ischemic heart disease, our findings suggest that cardiovascular risk assessment and monitoring is warranted during capecitabine therapy, rather than routine avoidance of treatment.</p>

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Risk of myocardial infarction following capecitabine treatment in patients with gastrointestinal cancer – a nationwide registry-based study

  • 期刊论文

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  • 发表日期：

    2025年11月10日

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  • Jan Walter Dhillon Shanmuganathan,
  • Kristian Kragholm,
  • Harman Yonis,
  • Morten Schou,
  • Christian Torp-Pedersen,
  • Laurids Østergaard Poulsen,
  • Manan Pareek,
  • Gunnar Gislason,
  • Lars Køber,
  • Dorte Nielsen,
  • Tarec Christoffer El-Galaly,
  • Peter Søgaard,
  • Mamas A. Mamas,
  • Phillip Freeman

摘要

Background

Myocardial infarction (MI) is an adverse event potentially associated with capecitabine treatment, potentially impacting the continuation of cancer therapy. However, data on its incidence remain limited.

Methods

Using Danish nationwide registries, we identified patients with gastrointestinal (GI) cancer treated with capecitabine (2004–2016) and compared them to age- and sex-matched controls without cancer. Patients with prior ischemic heart disease were excluded but were subsequently analyzed as a separate secondary cohort. Cumulative incidences of MI and competing risks were calculated, and multivariable regression analyses were performed.

Results

A total of 23,820 patients with GI cancer treated with capecitabine and 47,640 controls without cancer were included. Differences in comorbidities and antianginal medications were not significantly different (P > 0.05 for all). At 6 months, the cumulative incidence of MI was significantly higher for patients treated with capecitabine at 0.6% (95% CI: 0.5%-0.7%) versus 0.3% (95% CI: 0.3%-0.4%) in controls, with a competing risk of death of 15.2% versus 0.7%. At 1 year, the cumulative incidence of MI for patients receiving capecitabine was 0.7% (95% CI: 0.6%-0.9%) versus 0.6% (95% CI: 0.5%-0.6%) among controls, with a competing risk for death of 29.7% versus 1.6%. After accounting for competing risks, the sub distribution hazard ratios indicated an increased risk of MI for patients receiving capecitabine compared with control subjects at both 6 months (hazard ratio: 2.02; 95% CI: 1.57–2.60; P < 0.001) and 12 months (hazard ratio: 1.28; 95% CI: 1.05–1.57; P = 0.015).

Conclusion

Capecitabine treatment in GI cancer patients was associated with an increased MI risk at 6 and 12 months compared to controls, though absolute risks were low. Given the high competing mortality, the clinical relevance of this increased MI risk appears limited. In a secondary analysis of patients with known ischemic heart disease, our findings suggest that cardiovascular risk assessment and monitoring is warranted during capecitabine therapy, rather than routine avoidance of treatment.