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As both the rate of hypertension and cancer rise with age, concomitant hypertension in patients receiving treatment for cancer is very common. Increase in blood pressure during cancer treatment requires careful clinical assessment. Distinction between discontinuation or malabsorption of antihypertensive treatment due to factors such as nausea/vomiting/diarrhea and anti-cancer drug specific effects must be first made. De-novo hypertension during cancer treatment is likely related to anticancer drugs per se. Classical chemotherapeutic agents such as cyclophosphamide, cisplatin and busulfan have been previously linked to rising blood pressure. The concomitant use of high doses of glucocorticoids in some chemotherapy protocols may have a contributory role. However, the recent surge of interest in cancer treatment-related hypertension has been generated by the use of growth receptors’ signaling cascade inhibitors. Hypertension or deterioration in the control of hypertension may be seen in as much as 80% of patients receiving VEGF signaling pathway inhibitors. Agents may target one or more types of VEGF receptors, FGF-, PDGF- and hepatic growth factor receptors; RET and/or signaling elements such as RAF, BRAF, Flt3 and c-KIT. Indeed, at least some rise in blood pressure is actually expected in every patient subjected to this treatment but the rate of evolution of hypertension is variable. Risk factors for significant increase in BP include the type of agent and its dosage, the existence of preceding hypertension, age>60yrs and overweight/obesity. Hypertension may also be more common in subjects previously treated with programmed cell death 1 (PD-1) pathway inhibitors. Potential mechanisms of hypertension include impaired endothelial cell function with decreased NO synthesis and effect with increased endothelin-1 formation; decreased capillary density; increased salt sensitivity; and renal impairment. Hypertension due to VEGF/tyrosine kinase inhibitors is not only common but can evolve within hours/days from the initiation of anti-cancer treatment. This mandates both close BP monitoring and patient awareness to improve outcome. The goals of treatment are 1) to prevent/treat effectively any excessive rise in blood pressure; 2) to allow the anti-cancer treatment to proceed as is dictated by the ocology team, allowing the choice of effective anti-cancer drug dosing. Pre-treatment assessment of blood pressure, preferably by 24 ambulatory monitoring to rule out baseline uncontrolled hypertension and overall cardiovascular risk assessment are desirable. Oncologists should be approached to initiate such work up before the use of agents known to induce/aggravate hypertension or, alternatively, to refer candidates for such treatment to a hypertension specialist. We have formed an Oncological-Hypertension team to promptly address developing hypertension as soon as it is detected by the oncologist or the patients. Aggressive rather than “cautious” treatment of detected increase in BP has been recommended by the Cardiovascular Toxicity Panel of the National Cancer Institute (Am heart J 2012; 163:156). Salt restriction and moderation in the use of NSAIDS may improve the BP response to treatment. In the tailoring of antihypertensive treatment, attention should be given to the emergence of renal impairment and/or proteinuria or heart failure secondary to the anti-cancer drugs. Case-based treatment options will be reviewed.

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