Table 1. Chemotherapy-related cardiac dysfunction (Ewer and Lippman, 2005).

	Type I (myocardial damage)	Type II (myocardial dysfunction)
Characteristic agent	Doxorubicin	Trastuzumab
Clinical course, response to CRCD therapy	May stabilise, but underlying damage appears to be permanent and irreversible; recurrence in months or years may be related to sequential cardiac stress	High likelihood of recovery (to or near baseline cardiac status) in 2–4 months (reversible)
Dose effects	Cumulative, dose-related	Not dose-related
Mechanism	Free-radical formation, oxidative stress/damage	Blocked ErbB2 signalling
Ultrastructure	Vacuoles; myofibrillar disarray and dropout; necrosis (changes resolve over time)	No apparent ultrastructural abnormalities
Non-invasive cardiac testing	Decreased ejection fraction by ultrasound or nuclear determination: global decrease in wall motion	Decreased ejection fraction by ultrasound or nuclear determination: global decrease in wall motion
Effect of rechallenge	High probability of recurrent dysfunction that is progressive, may result in intractable heart failure and death	Increasing evidence for the relative safety of rechallenge; additional data needed
Effect of late sequential stress	High likelihood of sequential stress-related cardiac dysfunction	Low likelihood of sequential stress-related cardiac dysfunction

Abbreviation: CRCD=chemotherapy-related cardiac dysfunction.

Reproduced with permission from the American Society of Clinical Oncology, from Ewer and Lippman, 2005.