Why the study?
Does the AIDA protocol result in late subclinical cardiotoxicity in patients with acute promyelocytic leukemia in long-term remission?
Does the AIDA protocol result in late subclinical cardiotoxicity in patients with acute promyelocytic leukemia in long-term remission?
Long-term follow-up of APL patients treated with the AIDA protocol reveals significant subclinical diastolic dysfunction despite preserved systolic function, highlighting the importance of diastolic parameters in cardio-oncology screening.
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Subclinical diastolic dysfunction may warrant monitoring in long-term AIDA-treated APL survivors; this cohort study leaves open causality and clinical impact.
Anthracycline chemotherapy remains a critical component of cancer treatment despite its established risk of cardiotoxicity. To investigate whether the AIDA protocol, which combines idarubicin, mitoxantrone, and all-trans retinoic acid (ATRA) for treatment of acute promyelocytic leukemia (APL) results in late cardiotoxicity, 34 APL patients in long-term remission were evaluated. The cumulative dose of idarubicin and mitoxantrone were 80 mg/m(2) and 50 mg/m(2), respectively. Median follow-up was 7 years. Segmental wall motion abnormalities (SWMAs) were detected in 11 AIDA patients who still presented with an ejection fraction (EF) within normal limits (EF 56% in the AIDA group vs 59% in the control group, P=.01). However, parameters of diastolic dysfunction were significantly impaired in the AIDA group (E/A ratio: 1.04 in the AIDA group vs 1.28 in the control group, P=.001; E/E' lateral ratio: 10.04 in the AIDA group vs 5.79 in the control group, P≤.001) as well as left atrial volume (52 mL in the AIDA group vs 35 mL in the control group, P<.001). Cardiac toxicity due to anthracycline therapy is often frequent. Changes in diastolic function are helpful in the detection of subclinical anthracycline cardiotoxicity in long-term cardiac follow-up despite a preserved systolic ventricular function.
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Pellicori et al. (2012) studied this question.
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