Letter to Editor
Imaging and Histopathologic Evidence of Cardiotoxicity after Chemotherapy
Raymundo-Martinez GI1, Gopar-Nieto R1, Anibal-de Leon W1, Aranda-Fraustro A2, Rodríguez-Chávez LL3 and Espinola- Zavaleta N4*
1Department of Cardiology, National Institute of Cardiology Ignacio Chavez, Mexico
2Department of Pathology, National Institute of Cardiology Ignacio Chavez, Mexico
3Out-Patient Clinic, National Institute of Cardiology Ignacio chavez, Mexico
4Department of Nuclear Cardiology, National Institute of Cardiology Ignacio Chavez, Mexico
*Corresponding author: Nilda Espinola-Zavaleta, Department of Nuclear Cardiology, National Institute of Cardiology Ignacio Chavez, Juan Badiano Nº 1, Colonia Sección XVI, Tlalpan, C.P. 14080, Ciudad de México, México,
Published: 18 Aug, 2018
Cite this article as: Raymundo-Martinez GI, Gopar-
Nieto R, Anibal-de Leon W, Aranda-
Fraustro A, Rodríguez-Chávez
LL, Espinola- Zavaleta N. Imaging
and Histopathologic Evidence of
Cardiotoxicity after Chemotherapy. Clin
Oncol. 2018; 3: 1504.
Letter to Editor
Cardiotoxicity is a well-established complication of anticancer therapy. The increased risk of
cardiovascular disease and cardiovascular disease-related death in cancer survivors is
multifactorial, including cardiotoxic effects of chemotherapy, comorbidities and harmful lifestyle
habits. Cardiovascular adverse effects can range from coronary heart disease, pericardial disease,
valvular disease, myocarditis, thromboembolism, and arrhythmias; the risk of cardiotoxicity varies
according to the type and dose of chemotherapy. Heart failure incidence rates associated with the
commonly-prescribed chemotherapy agents include 0.14% to 48% for anthracyclines. For highdose
cyclophosphamides the risk ranges from 7% to 28%, for trastuzumab is 1% and for tyrosine
kinase inhibitors is 8% to 12.5%.
The management of patients with cancer under chemotherapy must be multidisciplinary in
order to cure them but with a lower risk of cardiotoxicity. (Figure 1). Female 65-years-old, with
history of colorectal cancer (stage IIIB) since September 2015, who received chemotherapy with
capecitabine and oxaliplatin with remission in October 2017. She presented recurrence in
December 2017, so she started with oxaliplatin and 5-fluoracil (5-FU). Minutes after the 5-FU
infusion she began with typical angina at rest. The initial ECG (Figure 1A) showed elevation of the
J point of 0.5 mm with hyperacute T waves in all precordial leads. The ECG performed 4 hrs later
(Figure 1B) with elevation of the ST segment in V2-V3 of 0.5 mm. She underwent primary
percutaneous coronary intervention, but no angiographically significant coronary lesions were
found, except for vasospasm in the left anterior descending coronary artery (Figure 1C). The
cardiotoxic effect of some chemotherapeutic agents that cause myocardial ischemia is due to
coronary vasospasm, endothelial injury and acute thrombosis, as well as changes in lipid
metabolism due to premature atherosclerosis.
(Figure 2). Female 65-years-old with cervical cancer in 1996 and intestinal Hodgkin
lymphoma in 2012, treated surgically and 6 cycles of CHOP, in remission. She had 2-year history
of heart failure. On physical examination, tachycardia, pulse pardus et tardus and aortic, mitral
and tricuspid valvular murmurs were found. ECG showed atrial fibrillation and left ventricular
hypertrophy and cardiomegaly in chest X-ray (Figure 2A). No coronary artery lesions were
detected (Figure 2B).
Two and three-dimensional echocardiography revealed severe
double mitral lesion (Figure 2C1 to 2, Clip 1), moderate double
aortic lesion (Figure 2C1, Clip 2) and moderate tricuspid
regurgitation (Figure 2C-3). She underwent double valvular
replacement and 3 days later died due to uncontrolled bleeding.
Histopathological findings demonstrated extensive plurivalvular
thickening, fibrosis and dystrophic calcification (Figure 2D-1 to 3).
Neither neovascularity nor Aschoff bodies were found, which are
specific for rheumatic carditis. We consider that chemotherapy was
responsible for the purivalvular affection in this patient.