Background Anti‐cancer vascular endothelial growth factor inhibitors (VEGFI) frequently induce a rise in blood pressure (BP). The most effective treatment of this BP rise is currently unknown, and risk factors and its association with survival remain inconclusive. Methods and Results Baseline characteristics and BP readings were retrospectively collected from oncology patients who received oral VEGFI treatment (sorafenib, sunitinib, pazopanib, regorafenib, lenvatinib, or cabozantinib). Risk factors for a clinically relevant BP rise (increase of ≥20 mm Hg in systolic BP or ≥10 mm Hg in diastolic BP) were investigated via logistic regression (relative), efficacy of antihypertensives via unpaired t‐tests, and association of BP rise with survival via Cox regression analysis. In total, 162 (47%) of 343 included patients developed a clinically relevant BP rise ≥7 days after VEGFI treatment initiation. Both calcium channel blockers and renin‐angiotensin system inhibitors effectively reduced systolic BP (−24.1 and −18.2 mm Hg, respectively) and diastolic BP (−12.0 and −11.0 mm Hg, respectively). Pazopanib therapy (odds ratio, 2.71 [95% CI, 1.35–5.42; P =0.005], compared with sorafenib) and estimated glomerular filtration rate <60 mL/min per 1.73 m 2 (OR, 1.75 [95% CI, 0.99–3.18, P =0.054]) were risk factors for a BP rise, whereas a baseline BP ≥140/90 mm Hg associated with a lower risk (OR, 0.39 [95% CI, 0.25–0.62, P <0.001]). Only for renal cell carcinoma, BP rise was associated with a substantially improved median overall survival compared with no BP rise: 45.4 versus 20.3 months, respectively, P =0.003. Conclusions The type of VEGFI, baseline BP, and baseline estimated glomerular filtration rate determine the VEGFI‐induced BP rise. Both calcium channel blockers and renin‐angiotensin system inhibitors are effective antihypertensive treatments. Particularly in patients with renal cell carcinoma, a BP rise is associated with improved overall survival.
Vascular endothelial growth factor inhibitors (VEGFI) are highly effective anti-cancer agents, but frequently induce a rise in blood pressure (BP). The optimal treatment of this BP rise is currently unknown, and risk factors for this rise and its association with survival remain unclear. To this end, baseline characteristics and BP readings were collected from electronic medical records from oncology patients who received oral VEGFI treatment (sorafenib, sunitinib, pazopanib, regorafenib, lenvatinib or cabozantinib) in the period of 2008 until 2020. Risk factors for a clinically relevant BP rise, defined as an increase of ≥20mmHg in systolic BP (SBP) and/or ≥10mmHg in diastolic BP (DBP), were investigated via logistic regression, and their association with survival via Cox regression analysis. In total, 343 patients were included of whom 162 (47%) developed a clinically relevant rise in BP ≥ 7 days after VEGFI treatment initiation. Both calcium channel blockers (CCB) and renin-angiotensin system inhibitors (RASI) effectively reduced SBP (-24.1mmHg and -18,2mmHg, respectively) and DBP (-12.0mmHg and -11mmHg, respectively) when started during VEGFI therapy. Pazopanib therapy (OR: 2.67, 95% CI 1.33-5.34, P =0.006, compared to sorafenib) and eGFR < 60ml/min/1.73m 2 (OR: 1.77, 95% CI 1.00-3.11, P =0.049) were risk factors for a BP rise, whereas a baseline BP of >140/90mmHg was associated with a lower risk (OR: 0.39, 95% CI 0.25-0.62, P <0.001). Only for renal cell carcinoma (RCC) patients, BP rise was associated with substantially improved overall survival (OS) compared to patients without BP rise (median OS 45.4 versus 20.3 months, respectively, P =0.003). No significant difference in OS between patients with and without new antihypertensives during VEGFI therapy was found (median OS 21.9 vs. 18.5 months, respectively, P = 0.143). In conclusion, the VEGFI-induced BP rise is determined by the type of VEGFI, baseline BP, and baseline eGFR. Both CCB and RASI can be used as effective antihypertensive treatment without impairing OS. Our study identified unique risk factors for a VEGFI-induced BP rise and demonstrated that this rise is an indication of treatment efficacy in RCC patients.
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