Key result
Early decline in LV shortening fraction predicts anthracycline cardiomyopathy with 100% sensitivity.
Why the study?
Early echocardiographic predictors of left ventricular dysfunction due to anthracycline cardiotoxicity in pediatric oncology patients were not well established.
Do early changes in left ventricular function detected by echocardiography predict subsequent clinical manifestations of anthracycline cardiotoxicity in pediatric oncology patients?
Observational (n=26)
Do early changes in left ventricular function detected by echocardiography predict subsequent clinical manifestations of anthracycline cardiotoxicity in pediatric oncology patients?
Absolute Event Rate: 8.8% vs 2.5%
p-value: p=0.03
A transient early deterioration in left ventricular function detected by standard m-mode echocardiography at 70 mg/m2 of anthracycline may be a sensitive predictor of subsequent clinical cardiomyopathy in pediatric oncology patients.
Early LV shortening fraction decline at 70 mg/m² may flag later cardiomyopathy risk in children; hypothesis-generating and needs prospective validation before guiding practice.
In this study, we attempted to identify echocardiographic findings that can be used as early predictors of left ventricular dysfunction due to anthracyclines in 26 pediatric oncology patients. Retrospective review identified six patients (group 1 mean anthracycline dose = 337 ± 123 mg/m2) who developed clinical evidence of cardiomyopathy and 20 consecutive patients followed prospectively (group 2 mean anthracycline dose = 298 ± 102 mg/m2) who did not. All of the patients had serial m-mode echocardiography before and at approximately every 50 mg/ m2 of anthracycline treatment depending on the dosage schedule. The following measurements were recorded: left ventricular dimensions and wall thickness, indices of left ventricular function, including systolic time intervals, shortening fraction, and ejection fraction. Using digitized echocardiography, the following parameters were recorded: peak and normalized systolic and diastolic velocities of the left ventricular chamber, posterior and septal wall velocities, and percent of posterior wall thickening. Variations from established normal longitudinal bounds and actual changes from pre-anthracycline values were compared for the two groups throughout the course of therapy. At 70 mg/m2 of anthracycline, group 1 showed significant deterioration in shortening fraction (mean change = 8.8 versus 2.5, p = .03), left ventricular velocity in diastole (2.9 versus 0.21, p = .04), left ventricular normalized velocity in systole (.65 versus 0.03, p = .02), and left ventricular normalized velocity in diastole (1.15 versus 0.002, p = .04) compared to group 2. These values were mostly compensated by 125 mg/m2, but they slowly deteriorated again at higher doses of anthracycline, leading to the appearance of clinical evidence of cardiomyopathy. These early changes were 100%, 75%, 75%, 100% sensitive; 82%, 91%, 91%, 73% specific for subsequent cardiomyopathy; and had a predictive accuracy of 67%, 75%, 75%, 57%, respectively. Thus, a transient early deterioration in left ventricular function may be a sensitive predictor of subsequent clinical manifestations of anthracycline cardiotoxicity. This change in left ventricular function may be detected by standard m-mode echocardiography as easily as with digitized echocardiography.
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Sándor et al. (1992) conducted an observational in Anthracycline cardiomyopathy (n=26). Subsequent anthracycline cardiomyopathy vs. No subsequent cardiomyopathy was evaluated on Mean change in shortening fraction at 70 mg/m2 of anthracycline (p=0.03). Early deterioration in left ventricular shortening fraction at 70 mg/m2 of anthracycline predicted subsequent cardiomyopathy (mean change 8.8 vs 2.5, p=0.03) with 100% sensitivity and 82% specificity.
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