Keita Kitagawa, Jacob Ryave, Robert A. Sanders, Ji-Hyun Lee, Zhongyue Zhang, Paulo Vilar Saavedra
{"title":"接受阿霉素单药治疗的荷瘤犬QT顶点的纵向评价","authors":"Keita Kitagawa, Jacob Ryave, Robert A. Sanders, Ji-Hyun Lee, Zhongyue Zhang, Paulo Vilar Saavedra","doi":"10.1111/jvim.70169","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>The cardiac morphologic and functional derangements induced by doxorubicin (DOX) are referred to as DOX-induced cardiotoxicity (DOX-IC). Prolongation of the QT apex (QTa) has been identified as a potential marker for the early detection of DOX-IC in humans.</p>\n </section>\n \n <section>\n \n <h3> Objectives</h3>\n \n <p>Describe changes in QTa that occur in dogs with cancer undergoing DOX monotherapy.</p>\n </section>\n \n <section>\n \n <h3> Animals</h3>\n \n <p>Forty-five client-owned dogs.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>Descriptive analysis of data routinely recorded as part of case management of dogs with cancer. Dogs included in the study had a confirmed malignant neoplasm, received DOX as a monotherapy, and had at least 4 ECGs > 30 s. All ECGs included in the study were recorded before DOX administration. Five heartbeats with a stable signal and minimal artifact were randomly selected from each dog, and the QTa was blindly evaluated in lead II, lead III, or both. Subsequently, a linear mixed model was used to quantify the effect of a cumulative dose of DOX on the QTa interval, adjusting for the effect of the other clinical variables.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Forty-five dogs met the inclusion criteria. Among them, 39/45 received five DOX treatments and 26/45 received six DOX treatments. For ECG analysis, 234 ECGs were evaluated for changes in the QTa. The average cumulative dose of DOX was 154.1 mg/m<sup>2</sup>. There was no significant impact of the DOX treatments on the change in QTa (<i>p</i> = 0.8).</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>Administration of DOX up to a cumulative dose of 154.1 mg/m<sup>2</sup> does not result in QTa prolongation.</p>\n </section>\n </div>","PeriodicalId":49958,"journal":{"name":"Journal of Veterinary Internal Medicine","volume":"39 4","pages":""},"PeriodicalIF":2.2000,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.70169","citationCount":"0","resultStr":"{\"title\":\"Longitudinal Assessment of QT Apex in Tumor-Bearing Dogs Receiving Doxorubicin Monotherapy\",\"authors\":\"Keita Kitagawa, Jacob Ryave, Robert A. Sanders, Ji-Hyun Lee, Zhongyue Zhang, Paulo Vilar Saavedra\",\"doi\":\"10.1111/jvim.70169\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>The cardiac morphologic and functional derangements induced by doxorubicin (DOX) are referred to as DOX-induced cardiotoxicity (DOX-IC). Prolongation of the QT apex (QTa) has been identified as a potential marker for the early detection of DOX-IC in humans.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Objectives</h3>\\n \\n <p>Describe changes in QTa that occur in dogs with cancer undergoing DOX monotherapy.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Animals</h3>\\n \\n <p>Forty-five client-owned dogs.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>Descriptive analysis of data routinely recorded as part of case management of dogs with cancer. Dogs included in the study had a confirmed malignant neoplasm, received DOX as a monotherapy, and had at least 4 ECGs > 30 s. All ECGs included in the study were recorded before DOX administration. Five heartbeats with a stable signal and minimal artifact were randomly selected from each dog, and the QTa was blindly evaluated in lead II, lead III, or both. Subsequently, a linear mixed model was used to quantify the effect of a cumulative dose of DOX on the QTa interval, adjusting for the effect of the other clinical variables.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>Forty-five dogs met the inclusion criteria. Among them, 39/45 received five DOX treatments and 26/45 received six DOX treatments. For ECG analysis, 234 ECGs were evaluated for changes in the QTa. The average cumulative dose of DOX was 154.1 mg/m<sup>2</sup>. 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Longitudinal Assessment of QT Apex in Tumor-Bearing Dogs Receiving Doxorubicin Monotherapy
Background
The cardiac morphologic and functional derangements induced by doxorubicin (DOX) are referred to as DOX-induced cardiotoxicity (DOX-IC). Prolongation of the QT apex (QTa) has been identified as a potential marker for the early detection of DOX-IC in humans.
Objectives
Describe changes in QTa that occur in dogs with cancer undergoing DOX monotherapy.
Animals
Forty-five client-owned dogs.
Methods
Descriptive analysis of data routinely recorded as part of case management of dogs with cancer. Dogs included in the study had a confirmed malignant neoplasm, received DOX as a monotherapy, and had at least 4 ECGs > 30 s. All ECGs included in the study were recorded before DOX administration. Five heartbeats with a stable signal and minimal artifact were randomly selected from each dog, and the QTa was blindly evaluated in lead II, lead III, or both. Subsequently, a linear mixed model was used to quantify the effect of a cumulative dose of DOX on the QTa interval, adjusting for the effect of the other clinical variables.
Results
Forty-five dogs met the inclusion criteria. Among them, 39/45 received five DOX treatments and 26/45 received six DOX treatments. For ECG analysis, 234 ECGs were evaluated for changes in the QTa. The average cumulative dose of DOX was 154.1 mg/m2. There was no significant impact of the DOX treatments on the change in QTa (p = 0.8).
Conclusions
Administration of DOX up to a cumulative dose of 154.1 mg/m2 does not result in QTa prolongation.
期刊介绍：
The mission of the Journal of Veterinary Internal Medicine is to advance veterinary medical knowledge and improve the lives of animals by publication of authoritative scientific articles of animal diseases.
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