Renin-Angiotensin-Aldosterone System Modulates Blood Pressure Response During Vascular Endothelial Growth Factor Receptor Inhibition

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  Figure 1. Flow Diagram for Cohort Selection The database investigated was the Synthetic Derivative (a de-identified version of Vanderbilt University’s electronic health record). Subjects within the Synthetic Derivative with a history of cancer were identified on the basis of their presence in the Vanderbilt Cancer Registry. From these subjects, 3,866 had a mention of a vascular endothelial growth factor inhibitor (VEGFi). Within this group, we required a mention of a vascular endothelial growth factor inhibitor ≥2 times and blood pressure (BP) recorded in any setting 6 weeks before and 6 weeks after initiation of vascular endothelial growth factor inhibitor therapy. These criteria narrowed our cohort to 1,013 subjects. We then narrowed this selection to our final cohort by including only those subjects with outpatient blood pressure recordings. On the basis of these selection criteria we identified 265 patients using renin-angiotensin-aldosterone system inhibitor (RAASi) therapy before initiation of vascular endothelial growth factor inhibitor and 530 patients not using renin-angiotensin-aldosterone system inhibitor therapy before vascular endothelial growth factor inhibitor initiation.

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  Central Illustration. Blood Pressure and Cancer Therapy: Change in Mean Blood Pressure Using Student’s t-test, the change in mean systolic blood pressure in subjects with baseline renin-angiotensin-aldosterone system inhibitor use was 2.46 mm Hg (95% confidence interval [CI]: 0.7 to 4.2), and without renin-angiotensin-aldosterone system inhibitor use it was 4.56 mm Hg (95% CI: 3.5 to 5.6; p = 0.034). The change in mean diastolic blood pressure in subjects with baseline renin-angiotensin-aldosterone system inhibitor use was 3.30 mm Hg (95% CI: 2.2 to 4.4), and without renin-angiotensin-aldosterone system inhibitor use it was 3.82 mm Hg (95% CI: 3.1 to 4.5; p = 0.419). The rise in blood pressure was less in those patients who had renin-angiotensin-aldosterone system inhibitor therapy at baseline.