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Right Ventricular Dysfunction: An Early Sign of Anthracycline Induced Cardiotoxicity - Case Series

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Abstract Background: Anthracycline-induced cardiotoxicity is clinically distinguished by a reduction in left ventricular ejection fraction (LVEF) exceeding 10% and an LVEF below 50%. Due to these guidelines, alterations in right ventricular (RV) structure and function are often neglected as indicators of cardiotoxicity. In this report, we present two cases of anthracycline-induced cardiotoxicity that initially manifested as RV dilation and dysfunction. Case presentations: Patient One, A 41-year-old woman with a history of sub-massive pulmonary embolism and obesity, was diagnosed with right pulmonary artery sarcoma and treated with surgical resection, radiation therapy, and adjuvant doxorubicin. Months after starting chemotherapy, she experienced progressive dyspnea on exertion and lower extremity swelling; a follow-up TTE demonstrated normal LV size and function, RV dilation, and RV pressure and volume overload. Since LVEF did not fall under the definition of cardiotoxicity, she continued doxorubicin treatment. Her clinical condition worsened, leading to severe RV dilation, reduced function, and new ECG abnormalities. Eventually, a cardiac MRI revealed reduced biventricular function and RV volume overload, with a final diagnosis of biventricular failure due to chemotherapy. Patient Two, a 21-year-old male diagnosed with osteosarcoma at age 12, underwent surgical resection, endoprosthesis reconstruction, and adjuvant chemotherapy with cisplatin and doxorubicin. A 7-year post-chemotherapy follow-up echocardiogram noted increased RV pressure suggestive of pulmonary hypertension. Follow-up TTE showed normal LVEF with borderline normal GLS, visually normal RV size and systolic function, and borderline elevated RVSP of 35 mmHg. Subsequent cardiac MRI revealed reduced right and left ventricular function and non-ischemic cardiomyopathy. Conclusions: These cases illuminate a critical gap in the current diagnostic criteria and definition of cardiotoxicity, emphasizing the necessity for more comprehensive echocardiographic approaches to assess cardiotoxicity. Specifically, they underscore the importance of including changes in right ventricular (RV) structure and function, which are often overlooked but can serve as early indicators of cardiotoxicity.
Title: Right Ventricular Dysfunction: An Early Sign of Anthracycline Induced Cardiotoxicity - Case Series
Description:
Abstract Background: Anthracycline-induced cardiotoxicity is clinically distinguished by a reduction in left ventricular ejection fraction (LVEF) exceeding 10% and an LVEF below 50%.
Due to these guidelines, alterations in right ventricular (RV) structure and function are often neglected as indicators of cardiotoxicity.
In this report, we present two cases of anthracycline-induced cardiotoxicity that initially manifested as RV dilation and dysfunction.
Case presentations: Patient One, A 41-year-old woman with a history of sub-massive pulmonary embolism and obesity, was diagnosed with right pulmonary artery sarcoma and treated with surgical resection, radiation therapy, and adjuvant doxorubicin.
Months after starting chemotherapy, she experienced progressive dyspnea on exertion and lower extremity swelling; a follow-up TTE demonstrated normal LV size and function, RV dilation, and RV pressure and volume overload.
Since LVEF did not fall under the definition of cardiotoxicity, she continued doxorubicin treatment.
Her clinical condition worsened, leading to severe RV dilation, reduced function, and new ECG abnormalities.
Eventually, a cardiac MRI revealed reduced biventricular function and RV volume overload, with a final diagnosis of biventricular failure due to chemotherapy.
Patient Two, a 21-year-old male diagnosed with osteosarcoma at age 12, underwent surgical resection, endoprosthesis reconstruction, and adjuvant chemotherapy with cisplatin and doxorubicin.
A 7-year post-chemotherapy follow-up echocardiogram noted increased RV pressure suggestive of pulmonary hypertension.
Follow-up TTE showed normal LVEF with borderline normal GLS, visually normal RV size and systolic function, and borderline elevated RVSP of 35 mmHg.
Subsequent cardiac MRI revealed reduced right and left ventricular function and non-ischemic cardiomyopathy.
Conclusions: These cases illuminate a critical gap in the current diagnostic criteria and definition of cardiotoxicity, emphasizing the necessity for more comprehensive echocardiographic approaches to assess cardiotoxicity.
Specifically, they underscore the importance of including changes in right ventricular (RV) structure and function, which are often overlooked but can serve as early indicators of cardiotoxicity.

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