Sir,
The cardiovascular toxicity of cisplatin-based chemotherapy of testicular cancer (TC) patients has been well recognised since the late eighties (Doll et al, 1986), but the underlying pathogenetic pathways are still poorly understood.
van Schinkel et al (2013) addressed the question of cardiac toxicity of cisplatin-based chemotherapy with a quite novel method. By performing cardiac magnetic resonance imaging (MRI) before and again after chemotherapy, the authors found a significant deterioration of diastolic heart function secondary to cisplatin-based therapy. This result is in line with previous findings in echocardiographic examinations (Altena et al, 2009).
The authors rightly discuss that cardiac dysfunction after chemotherapy may be caused either by direct impact of chemotherapy on cardiomyocytes or by endothelial damage. Unfortunately, the authors solely point to select experimental data to support the endothelial damage caused by systemic therapy (Nuver et al, 2010). In fact, there is an ever growing body of clinical evidence of acute cardiovascular toxicity of chemotherapy in TC patients that is probably based on vascular wall damage. Clearly, the readers should be informed accordingly. In a survey performed in German treatment centres, we found a calculated incidence 0.3% of major cardiovascular events during chemotherapy of testicular cancer (Dieckmann et al, 2010). Noteworthy, the clinical features of those cases were strongly suggestive of (acute) thrombo-embolic origin rather than (chronic) atherosclerotic origin of the events. Further cases have been reported since the publication of that survey. As a consequence, it appears quite rational to suggest endothelial apoptosis as one probable pathogenetic pathway of cardiac toxicity of chemotherapy. As pointed out by van Schinkel et al (2013), cardiomyocytic damage may be another one.
The authors suggested to determine troponine I levels in TC patients during chemotherapy to evaluate cardiac toxicity early. Accordingly, such serum levels have been found to be completely unchanged in a longitudinal study on 33 TC patients. Yet, von Willebrand factor antigen increased significantly, thus lending support to the endothelial damage hypothesis (Dieckmann et al, 2011).
Caution should be used to interpret the increase of serum levels of low-density lipoprotein and total cholesterol. These results are based on just 14 patients and they are clearly conflicting with several other reports involving much more patients (Fenton et al, 2002; Hisamatsu et al, 2005; Dieckmann et al, 2011; Koc et al, 2011).
In all, the results of the cardiac MRI examinations appear quite promising. However, owing to the small number of patients (n=14), the results certainly need confirmation in further studies, and this is particularly true with respect to the serum lipid profile measurements.
References
Altena R, De Haas EC, Nuver J, Brouwer CA, van den Berg MP, Smit AJ, Postma A, Sleijfer DT, Gietema JA (2009) Evaluation of sub-acute changes in cardiac function after cisplatin-based combination chemotherapy for testicular cancer. Br J Cancer 100: 1861–1866.
Dieckmann KP, Gerl A, Witt J, Hartmann JT Group. GTCS (2010) Myocardial infarction and other major vascular events during chemotherapy for testicular cancer. Ann Oncol 21: 1607–1611.
Dieckmann KP, Struss WJ, Budde U (2011) Evidence for acute vascular toxicity of cisplatin-based chemotherapy in patients with germ cell tumour. Anticancer Res 31: 4501–4505.
Doll DC, List AF, Greco FA, Hainsworth JD, Hande KR, Johnson DH (1986) Acute vascular ischemic events after cisplatin-based combination chemotherapy for germ-cell tumors of the testis. Ann Intern Med 105: 48–51.
Fenton DW, Verma S, Venner P, Sawhney R, Mackey JR (2002) The lack of long-term effect of Cisplatin based combination chemotherapy on serum cholesterol for treatment of testicular cancer. J Urol 168: 1971–1974.
Hisamatsu E, Kawai K, Hinotsu S, Miyanaga N, Shimazui T, Akaza H (2005) Serum creatinine and cholesterol levels of testicular cancer patients in long-term follow up. Int J Urol 12: 751–756.
Koc G, Divrik TR, Unlu N, Bulut V, Zorlu F (2011) Does cisplatin-based chemotherapy effect on blood lipid levels of patients with germ cell testicular tumor in long-term follow-up? Int Urol Nephrol 43: 1095–1100.
Nuver J, De Haas EC, Van Zweeden M, Gietema JA, Meijer C (2010) Vascular damage in testicular cancer patients: a study on endothelial activation by bleomycin and cisplatin in vitro. Oncol Rep 23: 247–253.
van Schinkel LD, Willemse PM, van der Meer RW, Burggraaf J, van Elderen SG, Smit JW, De Roos A, Osanto S, Lamb HJ (2013) Chemotherapy for testicular cancer induces acute alterations in diastolic heart function. Br J Cancer 109: 891–896.
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Dieckmann, KP. Comment on ‘Chemotherapy for testicular cancer induces acute alterations in diastolic heart function’. Br J Cancer 110, 264–265 (2014). https://doi.org/10.1038/bjc.2013.703
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DOI: https://doi.org/10.1038/bjc.2013.703
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