Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy.
OBJECTIVE
We investigated the role of cardiac troponin I (cTnI) in patients with aggressive malignancies treated with high-dose chemotherapy (HDC).


BACKGROUND
High dose chemotherapy is potentially limited by cardiac toxicity. Considering the fact that cardiac dysfunction may become clinically evident weeks or months after HDC, the availability of an early marker of myocardial injury, able to predict late ventricular impairment, is a current need.


METHODS
We measured, in 204 patients (45+/-10 years) affected by cancer resistant to conventional treatment, the cTnI plasma concentration after every single cycle of HDC. According to the cTnI value (< or = or >0.4 ng/ml), patients were divided into a troponin positive (cTnI+, n = 65) and a troponin negative (cTnI-, n = 139) group. All patients underwent echocardiographic examination during the following seven months.


RESULTS
In the cTnI- group, left ventricular ejection fraction (LVEF) progressively decreased after HDC, reaching a maximal reduction after three months; however, myocardial depression was transient and no longer detectable at later follow-up. By contrast, in the cTnI+ group LVEF reduction was more marked and still evident at the end of the follow-up. In cTnI+ patients, a close relationship between the short-term cTnI increment and the greatest LVEF reduction was found (r = -0.87, p<0.0001).


CONCLUSIONS
The elevation of cTnI in patients undergoing HDC for aggressive malignancies accurately predicts the development of future LVEF depression. In this setting, cTnI can be considered a sensitive and reliable marker of acute minor myocardial damage with relevant clinical and prognostic implications.
Cardiology Unit, Istituto Europeo di Oncologia, University of Milan, Italy. daniela.cardinale@ieo.it
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Cardinale
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Sandri
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Martinoni
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Tricca
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Civelli
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Lamantia
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Cinieri
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Martinelli
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Cipolla
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Fiorentini
D000328:Adult; D000970:Antineoplastic Agents / Q000008:administration & dosage* / Q000009:adverse effects; D015415:Biomarkers / Q000097:blood; D001943:Breast Neoplasms / Q000188:drug therapy; D018288:Carcinoma, Small Cell / Q000188:drug therapy; D005260:Female; D006689:Hodgkin Disease / Q000188:drug therapy; D006801:Humans; D008171:Lung Diseases / Q000188:drug therapy; D008228:Lymphoma, Non-Hodgkin / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D010051:Ovarian Neoplasms / Q000188:drug therapy; D011237:Predictive Value of Tests; D013318:Stroke Volume; D019210:Troponin I / Q000097:blood*; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000139:chemically induced
D000970:Antineoplastic Agents; D015415:Biomarkers; D019210:Troponin I