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Updated: Jun 23, 2026

Percutaneous Contrast Echocardiography-guided Intramyocardial Injection and Cell Delivery in a Large Preclinical Model
Published on: January 21, 2018
Doxorubicin cardiomyopathy: evaluation by phonocardiography, endomyocardial biopsy, and cardiac catheterization
Insights
Doxorubicin treatment causes dose-related heart muscle damage, especially in patients over 70 or with prior radiation. Combining multiple assessment methods improves heart failure risk management in these patients.
Area of Science:
- Cardiology
- Oncology
- Pathology
Background:
- Doxorubicin is a widely used chemotherapy agent.
- Cardiac toxicity is a significant concern with doxorubicin therapy.
- Early detection and management of doxorubicin-induced cardiotoxicity are crucial.
Purpose of the Study:
- To evaluate the relationship between doxorubicin dosage and myocardial damage.
- To identify risk factors for doxorubicin-associated heart failure.
- To assess the efficacy of different methods for dose limitation.
Main Methods:
- Right ventricular endomyocardial biopsy was performed in 33 adult patients receiving doxorubicin.
- Right heart catheterization and systolic time intervals were utilized.
- Histopathological analysis assessed myocyte damage and degenerative changes.
Main Results:
- Doxorubicin administration showed a dose-dependent increase in myocyte damage.
- Significant myocyte damage was observed in 27 of 29 patients at doses ≥ 240 mg/m2.
- Pre-existing mediastinal radiation and age ≥ 70 years were identified as risk factors for heart failure.
Conclusions:
- Doxorubicin causes dose-related myocardial injury, with significant damage at cumulative doses of 240 mg/m2.
- The pre-ejection period to left ventricular ejection time ratio (PEP/LVET) indicated a threshold effect at 400 mg/m2.
- Combined clinical, noninvasive, invasive, and morphologic criteria offer superior dose limitation for preventing doxorubicin-induced cardiotoxicity.
Abstract:
Right ventricular endomyocardial biopsy, right heart catheterization, and systolic time intervals were done in 33 adult patients receiving doxorubicin (AdriamycinTM). Doxorubicin administration was associated with a dose-related increase in the degree of myocyte damage, and 27 of 29 patients biopsied at doses greater than or equal to 240 mg/m2 had doxorubicin-associated degenerative changes identified on biopsy. The pre-ejection period to left ventriculr ejection time ratio (PEP/LVET) showed a threshold phenomenon and did not begin to increase until a total dose of 400 mg/m2 had been reached. Seven patients with catheterization-proven heart failure had a significantly greater amount of myocyte damage on biopsy than dose-matched control subjects (P less than 0.01). Preveious mediastinal radiation appeared to potentiate the doxorubicin-associated degenerative process. Mediastinal radiation and age greater than or equal to 70 years appeared to be risk factors for doxorubicin-associated heart failure. Dose limitation by combined clinical, noninvasive, invasive, and morphologic criteria offered an advantage over empirical dose limitation or dose limitation by PEP/LVET alone.
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