Evidence map›Paper›PMID 29703600›Full record

ReviewJournal of the American Society of Hypertension : JASH2018

Vascular toxicities with VEGF inhibitor therapies-focus on hypertension and arterial thrombotic events.

Rhian M Touyz, Sandra M S Herrmann, Joerg Herrmann

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of the American Society of Hypertension : JASH, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 6 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

115 citing papers in PubMed, 6 syntheses or guidelines pooled it.

  1. Pooled it
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  4. Pooled it
  5. Guideline
  6. Pooled it
  7. Article
  8. Review
  9. Article
  10. [Pathophysiological mechanisms of coagulation dysfunction associated with liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  11. Review
  12. Article
  13. Vascular Toxicities of Cancer Therapies: 2025 Update.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. Article
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  20. Review

55 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Rhian M TouyzInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom.
Sandra M S HerrmannDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, MN, USA.
Joerg HerrmannDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA. Electronic address: herrmann.joerg@mayo.edu.

Funding

The pathophysiological role of the immunoproteasome in atherosclerosisK08HL116952 · NHLBI · MAYO CLINIC ROCHESTER · PI HERRMANN, JOERG · 2014 to 2018
$750k
NHLBI NIH HHS K08 HL116952
6 · The paper itself

Abstract

The vascular endothelial growth factor (VEGF) signaling pathway (VSP) fulfills a cardinal role in endothelial cells and its inhibition has profound cardiovascular impact. This is true not only for the normal vasculature but also for the tumor vasculature when VSP inhibitors are used as anti-angiogenic therapies. Generalized endothelial dysfunction predisposes to vasoconstriction, atherosclerosis, platelet activation, and thrombosis (arterial more than venous). All of these have been reported with VSP inhibitors and collectively give rise to vascular toxicities, the most concerning of which are arterial thromboembolic events (ATE). VSP inhibitors include antibodies, acting extracelluarly on VEGF, such as bevacizumab and tyrosine kinases inhibitors, acting intracellularly on the kinase domain of VEGF receptors, such as sunintib and sorafenib. The addition of bevacizumab and VSP tyrosine kinase inhibitor therapy to the cancer treatment regimen is associated with a 1.5-2.5-fold and 2.3-4.6-fold increase risk of ATEs, respectively. Risk factors for ATEs while on VSP inhibitor therapy include age older than 65 years, previous thromboembolic events, history of atherosclerotic disease, and duration of VSP inhibitor therapy. In clinical practice, hypertension remains the most commonly noted vascular manifestation of VSP inhibition. Optimal blood pressure goals and preferred therapeutic strategies toward reaching these goals are not defined at present. This review summarizes current data on this topic and proposes a more intensive management approach to patients undergoing VSP inhibitor therapy including Systolic Blood PRessure Intervention Trial (SPRINT) blood pressure goals, pleiotropic vasoprotective agents such as angiotensin converting enzyme inhibitors, amlodipine, and carvedilol, high-dose statin therapy, and aspirin.

Indexed as

Angiogenesis inhibitorscardiovascular eventschemotherapyhypertension

Identifiers

PMID29703600
PMCPMC6168784

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.