Hypertension and Prohypertensive Antineoplastic Therapies in Cancer Patients

Circ Res. 2021 Apr 2;128(7):1040-1061. doi: 10.1161/CIRCRESAHA.121.318051. Epub 2021 Apr 1.

Abstract

The development of a wide range of novel antineoplastic therapies has improved the prognosis for patients with a wide range of malignancies, which has increased the number of cancer survivors substantially. Despite the oncological benefit, cancer survivors are exposed to short- and long-term adverse cardiovascular toxicities associated with anticancer therapies. Systemic hypertension, the most common comorbidity among cancer patients, is a major contributor to the increased risk for developing these adverse cardiovascular events. Cancer and hypertension have common risk factors, have overlapping pathophysiological mechanisms and hypertension may also be a risk factor for some tumor types. Many cancer therapies have prohypertensive effects. Although some of the mechanisms by which these antineoplastic agents lead to hypertension have been characterized, further preclinical and clinical studies are required to investigate the exact pathophysiology and the optimal management of hypertension associated with anticancer therapy. In this way, monitoring and management of hypertension before, during, and after cancer treatment can be improved to minimize cardiovascular risks. This is vital to optimize cardiovascular health in patients with cancer and survivors, and to ensure that advances in terms of cancer survivorship do not come at the expense of increased cardiovascular toxicities.

Keywords: angiogenesis inhibitors; antineoplastic agents; comorbidity; hypertension; neoplasms; prognosis; risk factors.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Agammaglobulinaemia Tyrosine Kinase / antagonists & inhibitors
  • Antineoplastic Agents / adverse effects*
  • Cancer Survivors
  • Carcinoma, Renal Cell / etiology
  • Cardiotoxicity / etiology
  • Humans
  • Hypertension / chemically induced*
  • Hypertension / complications
  • Hypertension / drug therapy
  • Kidney Neoplasms / etiology
  • MTOR Inhibitors / adverse effects
  • Neoplasms / drug therapy*
  • Neoplasms / etiology
  • Platinum Compounds / adverse effects
  • Poly(ADP-ribose) Polymerase Inhibitors / adverse effects
  • Proteasome Inhibitors / adverse effects
  • Proto-Oncogene Proteins B-raf / antagonists & inhibitors
  • Proto-Oncogene Proteins c-ret / antagonists & inhibitors
  • Risk Factors
  • Vascular Endothelial Growth Factor A / antagonists & inhibitors

Substances

  • Antineoplastic Agents
  • MTOR Inhibitors
  • Platinum Compounds
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Proteasome Inhibitors
  • Vascular Endothelial Growth Factor A
  • Proto-Oncogene Proteins c-ret
  • RET protein, human
  • Agammaglobulinaemia Tyrosine Kinase
  • BTK protein, human
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf