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CLINICAL STUDIES

Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy

Daniela Cardinale, MD^a, Maria Teresa Sandri, MD, Alessandro Martinoni, MD^a, Alessio Tricca LabTech, Maurizio Civelli, MD^a, Giuseppina Lamantia, MD^a, Saverio Cinieri, MD^*, Giovanni Martinelli, MD^*, Carlo M. Cipolla, MD^a and Cesare Fiorentini, MD^a

^a Cardiology Unit, Istituto Europeo di Oncologia, University of Milan, Milan, Italy
^* Hematoncology Unit, Istituto Europeo di Oncologia, University of Milan, Milan, Italy
Laboratory Medicine, Istituto Europeo di Oncologia, University of Milan, Milan, Italy

Manuscript received October 25, 1999; revised manuscript received February 11, 2000, accepted March 30, 2000.

Reprint requests and correspondence: Dr. Daniela Cardinale, Cardiology Unit, Istituto Europeo di Oncologia, Via Ripamonti 435, 20141 Milan, Italy
daniela.cardinale{at}ieo.it

OBJECTIVES

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 >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.

Abbreviations and Acronyms   CK = creatine kinase   CK-MB = creatine kinase, MB fraction   cTnI = cardiac troponin I   EDV = end-diastolic volume   ESV = end-systolic volume   HDC = high-dose chemotherapy   LVEF = left ventricular ejection fraction

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