Why the study?
Does prior cisplatin-based chemotherapy worsen endothelial function and subclinical atherosclerosis in long-term survivors of testicular cancer?
Does prior cisplatin-based chemotherapy worsen endothelial function and subclinical atherosclerosis in long-term survivors of testicular cancer?
Long-term survivors of testicular cancer who received cisplatin-based chemotherapy show objective evidence of endothelial injury and dysfunction compared to chemotherapy-naive survivors.
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May indicate persistent endothelial dysfunction after cisplatin in testicular cancer survivors; leaves open links to clinical events and needs prospective studies.
BACKGROUND: Long-term survivors of testicular cancer (TC) who received cisplatin-based chemotherapy have an increased risk of cardiovascular disease. A cross-sectional study was performed to objectively assess cardiovascular risk, subclinical atherosclerosis, and endothelial function in long-term survivors of TC. METHODS: Long-term survivors of TC underwent evaluation including determination of body mass index (BMI), Framingham relative risk (RR), brachial artery flow-mediated dilatation (FMD), carotid artery intima-media thickness (IMT), soluble intercellular adhesion molecule-1 (sICAM-1), high sensitivity C-reactive protein (hs-CRP), and flow cytometric analysis of peripheral blood for levels of endothelial progenitor cells (EPCs) and circulating endothelial cells (CECs). TC survivors who received chemotherapy were compared with a chemotherapy naive cohort. RESULTS: Twenty-four patients received cisplatin-based chemotherapy (CBCT) and 15 were chemotherapy-naive (CN). The CBCT cohort demonstrated more impairment of brachial artery FMD than the CN group (5.6% vs 8.8%; P = .05). The mean sICAM was also found to be higher in the CBCT cohort compared with the CN group (P = .04). No significant differences between the groups were noted with regard to BMI, Framingham RR, carotid IMT, or hs-CRP. In a subset of patients, TC survivors who received chemotherapy had a significantly increased level of CECs compared with CN patients (P = .04). No significant difference in EPC levels was detected. CONCLUSIONS: Long-term survivors of TC who received chemotherapy demonstrate objective evidence of endothelial injury and dysfunction, a potential mechanism for increased cardiovascular risk.
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Vaughn et al. (2008) studied this question.
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