What question did this study set out to answer?

To examine whether doxorubicin-induced cardiac impairment reverses or progressively worsens over time after treatment cessation.

Doxorubicin-induced late cardiotoxicity: delayed impairment of Ca²⁺-handling mechanisms in the sarcoplasmic reticulum in the rat

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May indicate progressive doxorubicin cardiotoxicity after cessation in rats; leaves open clinical relevance and need for human studies.

To examine whether doxorubicin-induced cardiac impairment reverses or progressively worsens over time after treatment cessation.
Administered doxorubicin (2.5 mg/kg, i.v., once weekly for 3 weeks) to rats and evaluated cardiac tissue at 1, 13, and 18 weeks post-treatment.
Measured twitch kinetics, postrest contraction, force-frequency relationships, caffeine-induced contractions in skinned fibers, and [3H]ryanodine binding parameters in isolated atrial and ventricular preparations.
Twitch contraction time to peak and postrest contraction impairments were not significant at 1 week post-treatment, but were significantly prolonged and deteriorated at 13 and 18 weeks.
Caffeine-induced contractions in skinned fibers were reduced at 18 weeks without changes in contractile protein calcium sensitivity.
[3H]ryanodine maximal binding capacity (Bmax) was significantly reduced at 13 and 18 weeks compared to controls, with no significant change in dissociation constant (Kd).

Chugun et al. (2000) studied this question.

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