P1.1 Anti-Angiogenic Treatment in Cancer Patients Causes Arterial Dilation and Stiffening Beyond the Blood Pressure Effect

• Published in: Artery research Vol. 8; no. 4; p. 129
• Main Authors: Spronck, B., De Lepper, A., Alivon, M., Boutouyrie, P., Reesink, K.
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 2014; Springer Nature B.V; BMC
• Subjects: Blood pressure; Cancer; Carotid arteries; Poster Abstract Presentations
• ISSN: 1872-9312; 1876-4401; 1876-4401
• DOI: 10.1016/j.artres.2014.09.082

Introduction Anti-angiogenic treatment (AAT) prescribed in cancer patients often induces hypertension and is associated with increased pulse wave velocity (PWV). PWV is known to depend on blood pressure (BP). Therefore, we assessed whether AAT changes PWV beyond an estimated first-order BP effect. Methods We obtained carotid artery systolic and diastolic cross-sectional areas (echo-tracking) and corresponding BPs in 17 cancer patients with metastatic solid tumours at baseline, and after 3 weeks of treatment (22.1 ± 3.2 days) with sorafenib, sunitinib or bevacizumab. For each patient, we derived local PWV (Bramwell-Hill) and a single-exponential P-A curve. Based on baseline P-A curves and measured follow-up pressures, we estimated the BP-induced PWV change at follow-up. By comparing estimated and measured changes in PWV at follow-up, we assessed the PWV increase beyond the BP effect. In the same way, we assessed whether diastolic cross-sectional area (A d ) changed beyond the BP-induced amount. Results Based on the increase in SBP/DBP from (mean±SD) 115±15/70±8mmHg at baseline to 126±13/78±10mmHg at follow-up, follow-up PWV was an estimated 7.2±1.0m/s, whereas measured PWV was higher at 7.8±1.7m/s (p = 0.068). Measured follow-up Ad markedly increased beyond the estimated pressure dilation (from 38.1±9.5mm 2 to 41.1±10.6mm 2 , p = 0.034). Conclusion AAT increases carotid PWV and cross-sectional area beyond the BP effect. While AAT is known to cause peripheral arterial vasoconstriction, this is not the case in the carotid artery. This finding may be explained by the deleterious influence of AAT on carotid vasa vasorum, possibly causing smooth muscle cell hypoxia and thereby wall stiffening (Stefanadis et al., Circulation 1995).