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.