Extract

Drugs targeting the vascular endothelial growth factor (VEGF) pathway represent a successful therapeutic option for several solid malignancies, but are burdened by the risk of developing cardiovascular (CV) and renal adverse events (CVAEs).1 Arterial hypertension, proteinuria and impairment of renal function are the most common AEs due to anti-VEGF drugs.2 For many anticancer therapies, the risk of developing CVAEs is related to the baseline CV risk profile,3 and traditional CV risk factors have, indeed, been shown to predict CVAEs also in subjects receiving anti-VEGF agents.2 Nevertheless, data regarding the prevalence of CV risk factors among oncologic patients are scarce.4 Moreover, in the oncologic setting, CV risk factors are typically defined only on the basis of clinical history (i.e. present/absent), and information regarding their control is frequently missing. Yet, the predisposition that a given CV risk factor confers towards CVAEs due to anticancer therapies is expected to be stronger if it is uncontrolled or untreated; on the other hand, the association may be blunted if it is well controlled.5

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