Annals of Oncology 13:1952-1953, 2002
© 2002 European Society for Medical Oncology
Letters to the Editor |
Troponin I, cardiac ventricular dysfunction and causal toxicity of chemotherapy drugs
Service de Médecine Interne, Centre des tumeurs de l’Université Libre de Bruxelles, Bruxelles, Belgique (E-mail: ldelval@swing.be)
I read with great interest the report by Cardinale et al. [1] that elevation of cardiac troponin I (TnI) after treatment with high-dose chemotherapy in breast cancer patients is an early marker of asymptomatic myocardial injury and predicts chemotherapy-induced late ventricular impairment. In their series of 211 consecutive patients, 70 (33%) presented a slight elevation of TnI [mean (± 
) 0.9 ± 0.5 ng/ml] during the treatment period. The increase in TnI occured a few hours after chemotherapy infusion, and a significant reduction in left ventricular (LV) function was observed in the group of patients with positive TnI, compared with the group with no elevation of TnI. However, I am concerned that the authors do not mention the presence (or lack) of other medical conditions or complications of the chemotherapeutic treatment that could, by themselves, be responsible for a secondary cardiac dysfunction.
A clear relationship between elevated TnI and LV dysfunction has been previously established in septic patients [2] and in hypovolemic-hypotensive patients [3]. Studies on the clinical conditions associated with elevation of TnI have shown that TnI was elevated (slight to moderate elevation) in 85% of patients with systemic inflammatory response syndrome, sepsis and septic shock [4]. Kahn et al. reported that 35/102 consecutive patients with slight elevation of TnI [mean (± ) 2.0 ± 1.9 ng/ml] did not have the final diagnosis of acute coronary syndrome, but had various other medical problems including non-ischemic dilated cardiomyopathy, muscular disorders, central nervous system disorders, HIV disease, chronic renal failure, sepsis, lung diseases and endocrine disorders [5]. Thus, elevated TnI, especially slight elevation, should be interpreted with caution.
TnI is likely to be a sensitive early marker of LV dysfunction, but is not a specific marker for the origin of the cardiac dysfunction. Therefore, in the absence of further information about the presence of other medical problems, it cannot be assumed that the LV dysfunction is solely attributable to a cardiotoxic effect of the chemotherapeutic treatment.
Oncologists facing an elevation of TnI should consider the possible causes of the enzyme elevation in their decision making process to modify or discontinue an antineoplastic treatment. Particularly, a sepsis or a hypovolemic-hypotensive problem has to be excluded.
L. Delval
Service de Médecine Interne, Centre des tumeurs de l’Université Libre de Bruxelles, Bruxelles, Belgique (E-mail: ldelval{at}swing.be)
References
1. 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 2002; 13: 710–715.
2. Ver Elst KM, Spapen HD, Nguyen DN et al. Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock. Clin Chem 2000; 46: 650–657.
3. Arlati S, Brenna S, Prencipe L et al. Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study. Intensive Care Med 2000; 26: 31–37.[Web of Science][Medline]
4. Ammann P, Fehr T, Minder EI et al. Elevation of troponin I in sepsis and septic shock. Intensive Care Med 2001; 27: 965–969.[Web of Science][Medline]
5. Khan IA, Tun A, Wattanasauwan N et al. Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes. Am J Emerg Med 1999; 17: 225–229.[Web of Science][Medline]
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