Abstract | INTRODUCTION: Angiogenesis is fundamental for tumor development and progression. Hence, anti-angiogenic drugs have been developed to target VEGF and its receptors (VEGFRs). Several tyrosine kinase inhibitors (TKIs) have been developed over the years and others are still under investigation, each anti-VEGFR TKI showing a different cardiotoxic profile. Knowledge of the cardiac side-effects of each drug and the magnitude of their expression and frequency can lead to a specific approach. AREAS COVERED: This work reviews the mechanism of action of anti-VEGFR TKIs and the pathophysiological mechanisms leading to cardiotoxicity, followed by close examination of the most important drugs individually. A literature search was conducted on PubMed selecting review articles, original studies and clinical trials, with a focus on Phase III studies. EXPERT OPINION: Side-effects on the cardiovascular system could lead both to the worsening of general health status of cancer patients and to the discontinuation of the cancer treatment affecting its efficacy. Cardiologists often have to face new triggers of heart disease in these patients. They need a specific approach, which must be carried out in cooperation with oncologists. It must start before cancer treatment, continue during it and extend after its completion.
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Authors | Giuseppe Bronte, Enrico Bronte, Giuseppina Novo, Gianfranco Pernice, Francesca Lo Vullo, Emmanuela Musso, Fabrizio Bronte, Eliana Gulotta, Sergio Rizzo, Christian Rolfo, Nicola Silvestris, Viviana Bazan, Salvatore Novo, Antonio Russo |
Journal | Expert opinion on drug safety
(Expert Opin Drug Saf)
Vol. 14
Issue 2
Pg. 253-67
(Feb 2015)
ISSN: 1744-764X [Electronic] England |
PMID | 25494575
(Publication Type: Journal Article, Review)
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Chemical References |
- Antineoplastic Agents
- Drugs, Investigational
- Protein Kinase Inhibitors
- Protein-Tyrosine Kinases
- Receptors, Vascular Endothelial Growth Factor
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Topics |
- Antineoplastic Agents
(adverse effects, therapeutic use)
- Cardiovascular Diseases
(chemically induced)
- Drugs, Investigational
(adverse effects, therapeutic use)
- Heart
(drug effects)
- Humans
- Models, Biological
- Molecular Targeted Therapy
- Neoplasms
(blood supply, drug therapy)
- Neovascularization, Pathologic
(drug therapy)
- Protein Kinase Inhibitors
(adverse effects, pharmacology, therapeutic use)
- Protein-Tyrosine Kinases
(antagonists & inhibitors)
- Receptors, Vascular Endothelial Growth Factor
(antagonists & inhibitors)
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