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Journal of Clinical Oncology, Vol 24, No 21 (July 20), 2006: pp. 3508
© 2006 American Society of Clinical Oncology.
DOI: 10.1200/JCO.2006.06.7876

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CORRESPONDENCE

Troponin I and Cardiovascular Risk Stratification in Patients With Testicular Cancer

Daniela Cardinale, Giuseppina Lamantia, Carlo M. Cipolla

Cardiology Unit, European Institute of Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy

To the Editor:

We have read the work of Nuver et al1 with great interest. The authors point out that long-term survivors of testicular cancer have an increased risk for cardiovascular events, and conclude that increase in von Willebrand factor plasma levels, and in the intima-media thickness of carotid artery, may predict cardiovascular complications in this population. Moreover, cardiac troponin I (TnI) was measured in 37 patients at least once during each chemotherapy course. Ten patients (27%) showed an increase of this marker and three of those patients (30%) experienced a cardiovascular event during the study period (two acute myocardial infarctions and one acute pulmonary embolism). However, the authors have not grasped the relevant clinical implications of these findings.

Cardiac troponins are the most specific and sensitive markers of myocardial cell injury. Their utility has been well established for the diagnosis of acute myocardial infarction and for short- and long-term risk stratification of patients with acute coronary syndrome. Moreover, cardiac troponin elevation has been described in several diseases, which were not related to an acute thrombotic coronary event, and in these clinical settings as well, troponin elevation still retained its prognostic value.2

We have previously demonstrated the prognostic relevance of TnI elevation after high-dose chemotherapy, including not only anthracyclines, but also other drugs, such as platinum derivates.3-5 The increase of this marker soon after chemotherapy, particularly when persistent for at least 1 month, not only predicts late cardiac dysfunction, but, more importantly, major adverse cardiac events.

In their work, Nuver et al affirm that "standardized measurements of TnI during each course of chemotherapy are probably of limited value in the early detection of cardiac damage." However, in our opinion, this statement is incorrect, because TnI rise is unequivocally due to myocardial cells damage. What the authors can eventually call into question is the prognostic meaning of TnI rise in their specific study population. Because of the small population considered, no definite conclusion can be drawn from the prognostic value of TnI. Nevertheless, it must be emphasized that previous studies have reported a similar percentage (almost 30%) of patients showing a TnI increase after different chemotherapy schemes.3-8 It is therefore possible that also cisplatin- and bleomycin-containing chemotherapy have cardiotoxic effects that can be detected by TnI. Notably, in 30% of patients with TnI increase, an acute cardiac event occurred, so it is likely that TnI maintains both a diagnostic and prognostic usefulness also in this clinical setting.

In our view, these results should be regarded as promising, albeit preliminary. Because of the increased myocardial infarction risk recognized in testicular cancer survivors9, TnI assessment should be prospectively investigated in a larger population, with repeated measurements, after each course of chemotherapy and during the follow-up,5 and with a longer observation period to definitely characterize the role of TnI in this clinical setting.

Authors' Disclosures of Potential Conflicts of Interest

The authors indicated no potential conflicts of interest.

REFERENCES

1. Nuver J, Smit AJ, van der Meer J, et al: Acute chemotherapy-induced cardiovascular changes in patients with testicular cancer. J Clin Oncol 23:9130-9137, 2005[Abstract/Free Full Text]

2. Jeremias A, Gibson CM: Narrative review: Alterative causes for elevated cardiac troponin levels when coronary syndromes are excluded. Ann Intern Med 142:786-791, 2005[Abstract/Free Full Text]

3. Cardinale D, Sandri MT, Martinoni A, et al: Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy. J Am Coll Cardiol 36:517-522, 2000[Abstract/Free Full Text]

4. Cardinale D, Sandri MT, Martinoni A, et al: Myocardial injury revealed by plasma troponin I in breast cancer treated with high-dose chemotherapy. Ann Oncol 13:710-715, 2002[Abstract/Free Full Text]

5. Cardinale D, Sandri MT, Colombo A, et al: Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation 109:2749-2754, 2004[Abstract/Free Full Text]

6. Lipshultz SE, Rifai N, Sallan SE, et al: Predictive value of cardiac Troponin T in pediatric patients at risk for myocardial injury. Circulation 96:2641-2648, 1997[Abstract/Free Full Text]

7. Lipshultz SE, Rifai N, Dalton VM, et al: The effect of dexrazoxane on myocardial injury in doxorubicin-treated children with acute lymphoblastic leukaemia. N Engl J Med 351:145-153, 2004[Abstract/Free Full Text]

8. Kilickap S, Barista I, Akgul E, et al: CTnT can be an useful marker for early detection of anthracyclines cardiotoxicity. Ann Oncol 16:798-804, 2005[Abstract/Free Full Text]

9. van den Belt-Dusebout AW, Nuver J, de Wit R, et al: Long-term risk of cardiovascular disease in 5-years survivors of testicular cancer. J Clin Oncol 24:467-475, 2006[Abstract/Free Full Text]


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  • In Reply
    Esther C. de Haas, Janine Nuver, Maarten P. van den Berg, Andries J. Smit, Dirk Th. Sleijfer, and Jourik A. Gietema
    JCO 2006 24: 3508-3509 [Full Text]


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