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Case Reports
. 2021 Mar 2;5(3):ytab079.
doi: 10.1093/ehjcr/ytab079. eCollection 2021 Mar.

Capecitabine-mediated heart failure in colorectal cancer: a case series

Erin N McAndrew  1 , Davinder S Jassal  1   2   3   4 , Benjamin A Goldenberg  1   5 , Christina A Kim  1   5   6
Affiliations
Case Reports

Capecitabine-mediated heart failure in colorectal cancer: a case series

Erin N McAndrew et al. Eur Heart J Case Rep. .

Abstract

Background: Capecitabine is a pyrimidine antimetabolite that inhibits thymidylate synthase and is commonly used in the treatment of colorectal cancer. Adverse cardiac side effects are reported in 1-18% of patients receiving Capecitabine. The most commonly proposed mechanism of cardiotoxicity in the setting of Capecitabine use is vasospasm of the coronary arteries. However, cardiotoxicity can also present as an acute coronary syndrome, arrhythmia, hypertension, and/or sudden cardiac death. Profound non-vasospastic cardiotoxicity is rare.

Case summary: We describe two cases of acute heart failure leading to cardiogenic shock in patients shortly after exposure to Capecitabine. Both patients did not demonstrate the characteristic transient ST elevation seen in patients with coronary artery vasospasms secondary to Capecitabine. Both patients required admission to the Acute Cardiac Care Unit requiring vasopressor and inotropic support. Thorough diagnostic investigations including echocardiography, cardiac magnetic resonance imaging, and cardiac computed tomography did not identify infarction, myocarditis, or any infiltrative process to explain their symptoms. Both patients had complete resolution of cardiac function, with no long-term sequalae.

Discussion: In patients receiving Capecitabine, reversible heart failure leading to cardiogenic shock should be considered as a potential cardiotoxic side effect.

Keywords: Capecitabine; Cardio-oncology; Cardiogenic shock; Cardiotoxicity; Case report; Heart failure.

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Figures

Figure 1
Figure 1
(A) Patient 1: a 12-lead electrocardiogram demonstrating sinus tachycardia with non-specific ST changes. (B) Patient 2: a 12-lead electrocardiogram demonstrating sinus tachycardia.
Figure 2
Figure 2
(A) Patient 1: an apical four-chamber view on transthoracic echocardiography with definity for left ventricular opacification demonstrating severe left ventricular systolic dysfunction with an left ventricular ejection fraction <20%. (B) Patient 1: a horizontal long-axis view on balanced steady-state free precession images demonstrating an improvement in left ventricular systolic function on inotropic support. (C) Patient 2: an apical four-chamber view on transthoracic echocardiography confirming severe left ventricular systolic dysfunction with a left ventricular ejection fraction <20%.(D) Patient 2: a horizontal long-axis view on balanced steady-state free precession images demonstrating an improvement in left ventricular ejection fraction to 32% ∼5 days after the initial transthoracic echocardiography.
None
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