You are here

Article Text

Article menu
Download PDFPDF
Editorial
The sEROtonergic pathway: a hERO for the brain, a zERO for the valves?
  1. Tine L M De Backer1,2,
  2. Frank Timmermans1
  1. 1 Cardiovascular Diseases, University Hospital Ghent, Ghent, Belgium
  2. 2 Clinical Pharmacology, University Ghent, Ghent, Belgium
  1. Correspondence to Professor Tine L M De Backer, Cardiovascular Diseases, University Hospital Ghent, Gent 9000, Belgium; tine.debacker{at}ugent.be

https://doi.org/10.1136/heartjnl-2018-314551

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    In medical school and ever since, we have been taught with the wisdom that pharmacological agents can heal, but also can harm. Medications or their metabolites that target the serotonergic pathways do not escape form this mantra. The last decades, several reports have suggested an association between serotonergic agents and valvular heart disease that eventually led to their withdrawal from the market. This was the case for the anorectic drugs fenfluramine and dexfenfluramine in the 1990s, and for the dopamine receptor agonist pergolide, a second-line Parkinson disease therapy, withdrawn in 2007 in the USA and in 2011 in Europe.1 2 As a large number of commonly prescribed medications such as antipsychotics, antidepressants, anxiolytics and antimigraine medications act on serotonergic mechanisms, concerns were and are raised that these approved agents might also cause drug-induced valvular heart disease (DIVHD).

    Most reports that have studied an association between serotonergic medications and valvular disease show an inherent risk of bias and confounding due to methodological issues such as study …

    View Full Text

    Footnotes

    • Contributors FT and TLMdB contributed equally to this editorial.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Provenance and peer review Commissioned; internally peer reviewed.

    • Patient consent for publication Not required.

    Linked Articles