Nicholas Camarda1, Richard Travers1,2, Vicky K Yang3, Cheryl London3, Iris Z Jaffe4. 1. Molecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Box 80, Boston, MA, 02111, USA. 2. Department of Medicine, Division of Hematology Oncology, Tufts Medical Center, MA, Boston, USA. 3. Cummings School of Veterinary Medicine, Tufts University, MA, Boston, USA. 4. Molecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Box 80, Boston, MA, 02111, USA. ijaffe@tuftsmedicalcenter.org.
Abstract
PURPOSE OF REVIEW: While vascular endothelial growth factor receptor inhibitors (VEGFRis) have dramatically improved cancer survival, these drugs cause hypertension in a majority of patients. This side effect is often dose limiting and increases cardiovascular mortality in cancer survivors. This review summarizes recent advances in our understanding of the molecular mechanisms and clinical findings that impact management of VEGFRi-induced hypertension. RECENT FINDINGS: Recent studies define new connections between endothelial dysfunction and VEGFRi-induced hypertension, including the balance between nitric oxide, oxidative stress, endothelin signaling, and prostaglandins and the potential role of microparticles, vascular smooth muscle cells, vascular stiffness, and microvessel rarefaction. Data implicating genetic polymorphisms that might identify patients at risk for VEGFRi-induced hypertension and the growing body of literature associating VEGFRi-induced hypertension with antitumor efficacy are reviewed. These recent advances have implications for the future of cardio-oncology clinics and the management of VEGFRi-induced hypertension.
PURPOSE OF REVIEW: While vascular endothelial growth factor receptor inhibitors (VEGFRis) have dramatically improved cancer survival, these drugs cause hypertension in a majority of patients. This side effect is often dose limiting and increases cardiovascular mortality in cancer survivors. This review summarizes recent advances in our understanding of the molecular mechanisms and clinical findings that impact management of VEGFRi-induced hypertension. RECENT FINDINGS: Recent studies define new connections between endothelial dysfunction and VEGFRi-induced hypertension, including the balance between nitric oxide, oxidative stress, endothelin signaling, and prostaglandins and the potential role of microparticles, vascular smooth muscle cells, vascular stiffness, and microvessel rarefaction. Data implicating genetic polymorphisms that might identify patients at risk for VEGFRi-induced hypertension and the growing body of literature associating VEGFRi-induced hypertension with antitumor efficacy are reviewed. These recent advances have implications for the future of cardio-oncology clinics and the management of VEGFRi-induced hypertension.
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