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Journal of Clinical Oncology, Vol 24, No 15 (May 20), 2006: pp. 2399 © 2006 American Society of Clinical Oncology. DOI: 10.1200/JCO.2006.05.7836
Acute Chemotherapy-Induced Cardiovascular Changes in Patients With Testicular Cancer: Are There Implications for Blood Pressure Management in Patients Receiving Chemotherapy?Radiation Oncology, Department of Medicine, Hematology/Oncology, James P. Wilmot Cancer Center, University of Rochester, Rochester School of Medicine and Dentistry, Rochester, NY To the Editor: We read with interest results of the study evaluating chemotherapy induced cardiovascular complications and complement Nuver et al for highlighting an important aspect of cancer treatment which has received little attention thus far.1 The results demonstrated increased plasma von Willebrand factor levels and intima-media thickness of the carotid artery in young males receiving cisplatin-based chemotherapy. Also observed in the same population was a significant increase in the hypotension event rate, which was not related to infections. This surprising finding could not be explained on the basis of cardiovascular changes monitored during chemotherapy. Therefore, we wonder if chemotherapy-induced neuronal mechanisms may have contributed to significant decrease in systolic and diastolic blood pressure in this largely young, normotensive study population not receiving antihypertensive medications. It would be interesting to know if the Nuver et al evaluated and/or monitored ganglionic and postganglionic sympathetic neuron function (by performing norepinephrine levels) or alternatively, evaluated for autoimmune paraneoplastic antibodies (such as anti-Hu, antibodies to PCA-2 and/or CRMP-5), which have known associations with autonomic failure leading to hypotension in other disease states. Indeed, cisplatin mediated apoptosis of dorsal nerve root ganglions has been described previously in experimental models,2 although its effect on blood pressure has not been defined. Another interesting paradox emerges from the trial results. While cytotoxic agent-induced hypotension was observed in this study, conversely hypertension is seen with antivascular endothelial growth factor (anti-VEGF) antibody therapy which is currently used to treat metastatic colon and renal cancer patients.3 The mechanism of hypertension observed with anti-VEGF antibody therapy is again not clear but may share a neuronal basis as well, because VEGF is known to be expressed in the dorsal nerve root and postganglionic neurons and in vivo appears to have a neurotrophic role.4 It is not clear if interference of this role with VEGF antibody may provoke hypertension by causing autonomic dysfunction. Understanding the mechanism of cytotoxic agent-induced hypotension (or biologic agent-induced hypertension) is important, because it allows planning for appropriate preventive or therapeutic intervention. This is especially relevant in the care of elderly cancer patients with pre-existing hypertension who are treated with platinum or new biologic based treatments. At the very minimum, such patient populations may need a readjustment of ongoing antihypertensive dosage. In addition, prolonged monitoring with or without medical treatment for blood pressure fluctuations may also be needed in symptomatic patients. Finally, the effects of chemotherapy-induced hypotension may in itself also contribute to chronic fatigue in long-term survivors. The prospective study in a young cancer population presents an opportunity to further evaluate some of these clinically pertinent issues. 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 2. McDonald ES, Randon KR, Knight A, et al: Cisplatin preferentially binds to DNA in dorsal root ganglion neurons in vitro and in vivo: A potential mechanism for neurotoxicity. Neurobiol Dis 18:305-313, 2005[CrossRef][Medline] 3. Sparano JA, Gray R, Giantonio B, et al: Evaluating antiangiogenesis agents in the clinic: The Eastern Cooperative Oncology Group Portfolio of Clinical Trials. Clin Cancer Res 10:1206-1211, 2004 4. Kutcher ME, Klagsbrun M, Mamluk R: VEGF is required for the maintenance of dorsal root ganglia blood vessels but not neurons during development. Faseb J 18:1952-1954, 2004 Related Reply
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Copyright © 2006 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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