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Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy
D Cardinale1, M T Sandri, A Martinoni
1Cardiology Unit, Istituto Europeo di Oncologia, University of Milan, Italy. daniela.cardinale@ieo.it
Journal of the American College of Cardiology
|August 10, 2000
Summary
Cardiac troponin I (cTnI) elevation in patients receiving high-dose chemotherapy (HDC) for aggressive cancers predicts future left ventricular ejection fraction (LVEF) depression, serving as a reliable marker of myocardial damage.
Area of Science:
- Cardiology
- Oncology
- Pharmacology
Background:
- High-dose chemotherapy (HDC) poses risks of cardiac toxicity.
- Cardiac dysfunction after HDC can manifest late, necessitating early detection markers.
- Identifying early indicators of myocardial injury is crucial for managing HDC-related cardiotoxicity.
Purpose of the Study:
- To investigate the role of cardiac troponin I (cTnI) as an early marker of myocardial injury in patients undergoing HDC.
- To determine if cTnI levels can predict late left ventricular ejection fraction (LVEF) impairment following HDC.
- To assess the clinical and prognostic implications of cTnI elevation in this patient population.
Main Methods:
- Measured plasma cTnI concentrations in 204 cancer patients undergoing HDC.
- Classified patients into troponin-positive (cTnI > 0.4 ng/ml) and troponin-negative groups.
- Monitored LVEF using echocardiography for seven months post-HDC.
Main Results:
- Troponin-negative patients showed transient LVEF reduction post-HDC.
- Troponin-positive patients experienced more significant and persistent LVEF reduction.
- A strong correlation was observed between short-term cTnI increase and maximal LVEF reduction (r = -0.87, p<0.0001) in cTnI+ patients.
Conclusions:
- Elevated cTnI levels accurately predict future LVEF depression in patients receiving HDC for aggressive malignancies.
- cTnI serves as a sensitive and reliable biomarker for acute, minor myocardial damage.
- cTnI monitoring has significant clinical and prognostic value in managing HDC-induced cardiotoxicity.