Cardiotoxicity is relatively uncommon but a serious and potentially lives threatening adverse event of fluorouracil in a retrospective study 42 patients, who previously have been given fluorouracil or capecitabine were identified. Types of cardiac toxicity developed by the patients included angina, acute arrhythmia, and myocardial infarction. The median number of cycles to the first cardiac event was one. Four patients had cardiac toxicity recognized and anti-anginal therapy initiated with nitrates and calcium antagonists. Despite the interventions they continued to experience further cardiac toxicity with subsequent chemotherapy cycles. Myocardial infraction was reported in 5 patients (12%) and ischemic pain was reported in 20 patients (48%). A recent case report also described the development of Takotsubo syndrome in a patient receiving infusional fluorouracil (along with irinotecan and leucovorin; FOLFIRI regimen. The 48-year-old male with gastric cancer developed tachycardia and dyspnea at the 34th hour of his 46-hour fluorouracil infusion. He was shown to have hypokinesis of the mid-apical segments and hyperkinesis of the basal segments on echocardiogram and his left ventricular ejection fraction was 15%. The patient then developed ventricular fibrillation and required intubation and intensive care for 36 hours. Subsequently, the patient recovered and after 27 days his ejection fraction rebounded to 50%.

A possible alternative for patients developing cardiac toxicity while receiving infusional fluorouracil is to rechallenge with a bolus fluorouracil regimen. In a case series of six patients, administration of bolus fluorouracil, after experiencing cardiotoxicity with infusional fluorouracil or capecitabine, was well tolerated without recurrence of cardiotoxicity.

TYPES

Cardiac toxicity can be reversible or irreversible, with reversibility referring to recovery of cellular or organ function. Myocardial changes such as myocardial cell loss (by necrosis or apoptosis), myofibrillar loss, and mitochondrial degradation are generally considered irreversible in the context of cellular or tissue injury. For example, late anthracycline cardiotoxicity is often perceived to be “irreversible,” given evidence for cardiomyocyte death, and thus led to the classification of “Type 1” or irreversible cardiotoxicity (in contrast to “Type 2” cardiotoxicity with trastuzumab, viewed generally at least to some extent as reversible and occurring during therapy).

The Type 1 and Type 2 classification has fallen out of favor, given a perceived oversimplification of the underlying pathophysiology and natural history of cardiotoxicity. Recent evidence suggests that cardiac function may recover and “reverse” in the setting of anthracycline cardiotoxicity. Moreover, trastuzumab cardiotoxicity is not always reversible. Finally, there may be common mechanisms to cardiotoxicity observed with both strategies.

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