Abstract
Cardiovascular diseases and cancer are the leading cause of morbidity and mortality globally. Cardiotoxicity from chemotherapeutic agents results in substantial morbidity and mortality in cancer survivors and patients with active cancer. Cardiotoxicity induced by 5-fluorouracil (5-FU) has been well established, yet its incidence, mechanisms, and manifestation remain poorly defined. Ischemia secondary to coronary artery vasospasm is thought to be the most frequent cardiotoxic effect of 5-FU. The available evidence of 5-FU-induced epicardial coronary artery spasm and coronary microvascular dysfunction suggests that endothelial dysfunction or primary vascular smooth muscle dysfunction (an endothelial-independent mechanism) are the possible contributing factors to this form of cardiotoxicity. In patients with 5-FU-related coronary artery vasospasm, termination of chemotherapy and administration of nitrates or calcium channel blockers may improve ischemic symptoms. However, there are variable results after administration of nitrates or calcium channel blockers in patients treated with 5-FU presumed to have myocardial ischemia, suggesting mechanisms other than impaired vasodilatory response. Clinicians should investigate whether chest pain and ECG changes can reasonably be attributed to 5-FU-induced cardiotoxicity. More prospective data and clinical randomized trials are required to understand and mitigate potentially adverse outcomes from 5-FU-induced cardiotoxicity.
Highlights
In recent years, important progress in the oncological field has led to an increase in cancer survival rates in high-income countries [1]
Fluoropyrimidines, such as 5-fluorouracil (5-FU) and its oral prodrug capecitabine, are the third most common drug used for the treatment of solid malignancies such as breast, colorectal, head, neck, gastrointestinal, and bladder cancer [4,5,6]
This review aims to examine the characteristics and the role of vasospasm and the potential role of microcirculatory dysfunction in patients with fluoropyrimidines-induced ischemic heart disease
Summary
Important progress in the oncological field has led to an increase in cancer survival rates in high-income countries [1]. Cardiovascular toxicity is not uncommon, with more and more oncological patients having to co-exist with cardiovascular comorbidities This has led to the concept of “cardio-oncology” [2,3]. Fluoropyrimidines, such as 5-fluorouracil (5-FU) and its oral prodrug capecitabine, are the third most common drug used for the treatment of solid malignancies such as breast, colorectal, head, neck, gastrointestinal, and bladder cancer [4,5,6]. Capecitabine is a prodrug converted to 5-FU through thymidine phosphorylase, an enzyme highly present inside tumor cell This results in higher intratumor concentrations of 5-FU compared with normal tissue [11]
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