Key result
5-fluorouracil-induced cardiotoxicity is likely multifactorial, with proposed mechanisms including endothelial injury, increased metabolism leading to energy depletion, oxidative stress, and coronary artery spasm.
Systematic Review (n=26)
5-fluorouracil-induced cardiotoxicity is driven by multifactorial mechanisms including endothelial injury, vasospasm, oxidative stress, and altered red blood cell metabolism, rather than a single pathway.
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Multifactorial mechanisms warrant comprehensive cardiac monitoring during 5-FU therapy; confirms prior hypotheses and directs targeted prevention trials.
Dyhl-Polk et al. (2014) conducted a systematic review in 5-fluorouracil-induced cardiotoxicity (n=26). 5-fluorouracil (5-FU) or capecitabine was evaluated on Pathophysiological mechanisms of 5-FU-induced cardiotoxicity. 5-fluorouracil-induced cardiotoxicity is likely multifactorial, with proposed mechanisms including endothelial injury, increased metabolism leading to energy depletion, oxidative stress, and coronary artery spasm.
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