Is prolactin involved in the evolution of atherothrombotic disease?

Abstract

Cardiovascular diseases (CVDs) account for approximately 30% of all deaths globally. The most important cause of CVD is atherothrombosis, in other words, narrowing of the arteries as a result of the deposition of cholesterol and other lipoid substances within the arterial wall. Several endocrine disorders have been linked to this pathological state. Recent clinical and experimental studies have suggested that prolactin, a pleiotropic pituitary hormone, may potentially contribute to CVD, either through direct modulation of local cellular processes within atherosclerotic plaques/thrombi and/or through influencing conventional cardiovascular metabolic risk factors. However, the precise role of prolactin in the pathology of CVD remains largely unknown. Here, the authors speculate whether prolactin-lowering treatment may become a future therapeutic approach in patients with elevated prolactin levels and concomitantly presenting with coexisting vascular disease or a significantly elevated risk for premature atherothrombotic vascular disease. Awareness of these new developments may also change our clinical opinions about therapeutic strategies in patients with prolactinomas.

Keywords::

• atherothrombosis
• inflammation
• metabolic syndrome
• prolactin-lowering therapy
• prolactinoma
• prolactin receptor antagonists
• residual cardiovascular risk

Acknowledgements

The authors are grateful to Astrid Sibbes, from the Department of Medical Photography and Illustration of the Academic Medical Center, Amsterdam (The Netherlands), for her help with formatting Figure 1.

Financial & competing interests disclosure

M Hoekstra was supported by The Netherlands Heart Foundation (grant 2008T070) and MThB Twickler by a Veni grant from Dutch Association of Sciences (NWO/ZonMW). V Goffin acknowledges INSERM and University Paris Descartes for recurrent funding. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.