Philadelphia, PA, May 5, 2014 New cancer therapies, particularly agents that block vascular endothelial growth factor (VEGF) signaling, have improved the outlook for patients with some cancers and are now used as a first line therapy for some tumors. However, almost 100% of patients who take VEGF inhibitors (VEGFIs) develop high blood pressure, and a subset develops severe hypertension. The mechanisms underlying VEGF inhibitor-induced hypertension need to be better understood and there is a need for clear guidelines and improved management, say investigators in a review article published in the Canadian Journal of Cardiology.
"Exactly how VEGFIs cause hypertension is unknown. However, what is clear is that inhibition of VEGF in the vasculature directly increases blood pressure because hypertension develops acutely in response to VEGFIs and blood pressure returns to normal once the treatment is stopped," says senior investigator Rhian M. Touyz, MD, PhD, of the Institute of Cardiovascular and Medical Sciences, University of Glasgow, Scotland.
Angiogenesis inhibitors are a new class of cancer drugs that are designed to prevent the formation of new blood vessels, thereby stopping or slowing the growth or spread of tumors. Angiogenesis requires the binding of signaling molecules, such as VEGF, to receptors on the surface of normal endothelial cells. When VEGF and other endothelial growth factors bind to their receptors on endothelial cells, signals within these cells are initiated that promote the growth and survival of new blood vessels, which are necessary for tumor growth. Angiogenesis inhibitors interfere with various steps in this process.
Increased blood pressure has been observed in every trial involving VEGFIs and is the most common cardiovascular complication; it has an associated increased risk of fatal adverse cardiovascular events. According to some studies, VEGFI-induced hypertension is not a side effect of treatment,
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Elsevier Health Sciences