Key result
Rising arterial stiffness precedes sunitinib-induced hypertension in a single case report.
Why the study?
Sunitinib treatment is often complicated by hypertension, and early detection methods for sunitinib-induced hypertension are needed.
Does measuring cardio-ankle vascular index (CAVI) allow for early detection of sunitinib-induced hypertension?
Case Report (n=1)
No
Does measuring cardio-ankle vascular index (CAVI) allow for early detection of sunitinib-induced hypertension?
Arterial stiffness assessed by CAVI may be a useful surrogate marker for the early detection of sunitinib-induced hypertension.
CAVI rise may precede sunitinib hypertension in single cases; hypothesis-generating and leaves open utility for early detection.
Cardio-ankle vascular index (CAVI) has been established as a marker of arterial stiffness, which is increased in hypertensive patients. CAVI reflects the stiffness of the aorta, femoral artery, and tibial artery. Sunitinib, multi-targeted tyrosine kinase inhibitor with both anti-angiogenic and anti-tumor activities, has been proved effective in patients with gastrointestinal stromal tumors. However, the treatment with sunitinib is often complicated by side effects such as hypertension. We describe an 84-year-old woman with gastrointestinal stromal tumor, who showed changes in arterial stiffness preceding the appearance of hypertension in the early phase after sunitinib initiation. The patient received sunitinib (50 mg given daily) for gastrointestinal stromal tumor. We assessed the influence of sunitinib on arterial stiffness every 7 days by measuring CAVI. The CAVI, which reflects arterial stiffness, was increased from 9.95 at baseline to 11.65 at 7 days after the initiation of sunitinib, whereas the blood pressure remained unchanged (117/72 and 119/76 mmHg). At 14 days after sunitinib initiation, the blood pressure was increased to 159/89 mmHg, indicating the occurrence of hypertension, while the CAVI was 11.90, the similar level detected at 7 days. Subsequently, sunitinib treatment was discontinued, because of the marked decrease in blood platelets. Both blood pressure and CAVI, together with blood platelets, were restored to the baseline values at 12 days after cessation of sunitinib. In conclusion, the increase in the CAVI preceded the appearance of sunitinib-induced hypertension. Arterial stiffness assessed by CAVI may be useful for early detection of sunitinib-induced hypertension.
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Masugata et al. (2009) conducted a case report in Gastrointestinal stromal tumor (n=1). Sunitinib vs. Baseline was evaluated on Cardio-ankle vascular index (CAVI). In a patient treated with sunitinib, an increase in arterial stiffness assessed by the cardio-ankle vascular index preceded the onset of sunitinib-induced hypertension.
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