Table 1.

Biomarker of myocardial damage: cardiac troponins.

BIOMARKERS	MECHANISMS	MAIN FINDINGS	REF.
Troponins	Release after cardiomyocyte damage induced by various mechanisms: ischemia, inflammation or oxidative stress	Anthracycline:	26–32
		– cTnI elevation in 1/3 of patients treated; proportion increases with cumulative dose
		– in patients with cTnI level > 0.5 ng/mL, 33%, 27% and 25% of increases occur right after, at 12 hours and 24 hours after dose and predict LVEF decrease at 1 month
		– Patients with cTnI > 0.5 ng/mL have a significant reduction in LVEF persisting for 3–7 months, in contrast to patients with cTnI < 0.5 ng/mL who show a transient decrease in LVEF at 3 months followed by complete recovery at 7 months
		– cTnT levels during the first 90 days after therapy predict cardiotoxicity at 4 years of follow-up
		– cTnI > 0.08 ng/mL persisting 1 month after therapy is associated with 84% risk of cardiotoxicity compared to 37% when the elevation is transient. absence of cTnI elevation early and 1 month after therapy is associated with only 1% risk
		Anthracycline—adjuvant trastuzumab:
		– cTnI elevation early after anthracycline therapy and at 3 months is an independent predictor of cardiotoxicity with a 17.6 times increased risk

Abbreviations: cTn, cardiac troponin; LVEF, left ventricular ejection fraction.