Introduction: Angiogenesis is fundamental for tumour development and progression. Thus, anti-angiogenic agents have been developed and are mainly vascular endothelial growth factor (VEGF) pathway inhibitors. However, these agents commonly exhibit cardiac and renal toxicity, proteinuria and hypertension (HT). In fact, with the use of anti-angiogenic agents a rapid dose-dependent increase of blood pressure (BP) is observed. The possible mechanisms of VEGF inhibitors-induced HT include systemic endothelial dysfunction, renal impairment as well as vascular micro- and macroangiopathy. Furthermore, the simultaneous use of non-steroidal anti-inflammatory drugs (NSAIDs) and opioids in these patients results in uncontrolled HT.
Conclusion: Lifestyle changes are the cornerstone of antihypertensive treatment. No clear recommendations for a specific antihypertensive agent can be made. In most cases antihypertensive management needs to be individualized to each patient. Calcium channel blockers (CCBs) are considered as first line option, while renin-angiotensin-aldosterone system (RAAS) blockers should be the agents of choice in patients with proteinuria. Centrally acting antihypertensive agents and diuretics can also be used. Careful monitoring is critical during therapy and BP should be assessed every week and before any new cycle or infusion of anti-VEGF therapy. If BP remains uncontrolled anti-VEGF treatment discontinuation should be considered. Withdrawal of anti-VEGF therapy needs also a re-evaluation of antihypertensive therapy since BP will return to the prior baseline levels.