We report a 54-year-old woman with an stage IIA (T2N0M0) RE and RP negative and HER2-positive ductal invasive breast cancer who developed a reversible cardiotoxicity associated with chemotherapy. After surgery, she received four cycles of doxorubicin and cyclophosfamide. Later, she used paclitaxel and trastuzumab. At the 7th cycle of trastuzumab, she had symptoms of heart failure with left ventricle ejection fraction = 59%. Trastuzumab dosage was reduced in 25%, and heart function progressively improved. Two years after her discharge, the patient remains asymptomatic. Systolic function of the left ventricle was normal before the initial dosis of trastuzumab, but significantly worsened following the beginning of drug administration. Moreover, a clear improvement of heart function was observed soon after the daily dose of trastuzumab was reduced. Better knowledge of risk factors for cardiotoxicity related to chemotherapy, and longstanding surveillance with serial echocardiograms can avoid more severe cardiotoxicity by chemotherapy.

Download full-text PDF

Source
http://dx.doi.org/10.4067/S0034-98872012000600010DOI Listing

Publication Analysis

Top Keywords

reversible cardiotoxicity
8
54-year-old woman
8
left ventricle
8
heart function
8
cardiotoxicity chemotherapy
8
trastuzumab
6
cardiotoxicity 54-year-old
4
woman treated
4
treated trastuzumab
4
trastuzumab report
4

Similar Publications

Dehydroevodiamine Alleviates Doxorubicin-Induced Cardiomyocyte Injury by Regulating Neuregulin-1/ErbB Signaling.

Cardiovasc Ther

January 2025

Department of Cardiothoracic Surgery, Ningbo Medical Center Lihuili Hospital of Ningbo University, No. 57, Xingning Rd, Ningbo City 315041, Zhejiang Province, China.

Doxorubicin (DOX) is a widely used antitumor drug; however, its use is limited by the risk of serious cardiotoxicity. Dehydroevodiamine (DHE) is a quinazoline alkaloid which has antiarrhythmic effects. The aim of this study was to investigate the protective effect of DHE on doxorubicin-induced cardiotoxicity (DIC) and its potential mechanism.

View Article and Find Full Text PDF

Objectives: This study assessed the electrocardiographic pattern and cardiac inflammatory response of doxorubicin-induced myocardial injury in Wistar rats treated with ethanol extract.

Methods: Female Wistar rats (190-200 g) were assigned into five groups of seven rats each. The Group 1 (Control group) was given rat chow and drinking water while the Group 2 (doxorubicin group) received intraperitoneal administration of doxorubicin (2 mg/kg) once weekly for three weeks.

View Article and Find Full Text PDF

Urolithin A attenuates Doxorubicin-induced cardiotoxicity by enhancing PINK1-regulated mitophagy via Ambra1.

Chem Biol Interact

December 2024

Department of Cardiology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, 250021, China; Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; JiNan Key Laboratory of Cardiovascular Disease, Jinan, China. Electronic address:

Doxorubicin (Dox) is a widely used antineoplastics although its clinical usage is greatly limited by its cardiotoxicity. Several studies have depicted an essential role for dampened mitophagy and mitochondrial injury in Dox cardiotoxicity. However, preventative measure to alleviate Dox-evoked cardiotoxicity via targeting mitophagy and mitochondrial integrity remains elusive.

View Article and Find Full Text PDF

Background: Doxorubicin-induced cardiotoxicity is still an important medical problem associated with a high mortality rate in cancer survivors. p53 plays a key role in doxorubicin-induced cardiotoxicity. Diacylglycerol kinase ζ (Dgkζ), a 130-kDa enzyme abundant in cardiomyocytes, regulates the p53 protein expression level in neurons.

View Article and Find Full Text PDF

Canagliflozin reverses doxorubicin-induced cardiotoxicity via restoration of autophagic homeostasis.

Toxicol Appl Pharmacol

December 2024

Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China; Cardiovascular Center, the Sixth Affiliated Hospital, School of Medicine, South China University of Technology, Foshan, Guangdong, China. Electronic address:

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been reported as successful for preventing doxorubicin (DOX) -induced cardiotoxicity (DIC), but the underlying mechanisms are elusive. This study aimed to determine whether canagliflozin, an SGLT2i, protects against DIC by regulation of autophagic flux in cardiomyocytes through a mechanism independent of SGLT2. The differentially expressed autophagy-related genes (ARGs) in DIC were analyzed.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!