Heart 2009;95:522-523
EDITORIALS
Dopamine agonist therapy for hyperprolactinaemia and cardiac valve dysfunction; a lot done but much more to do
1 Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
2 Department of Cardiology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
Dr Richard Steeds, Department of Cardiology, Queen Elizabeth Hospital, University Hospital Birmingham NHS Foundation Trust, Edgbaston, Birmingham B15 2TH, UK; Richard.Steeds@uhb.nhs.uk
| The first 150 words of the full text of this article appear below. |
In 2004, van Camp et al1 published the first large observational study describing cardiac valve dysfunction in patients receiving the dopamine agonist (DA) pergolide for Parkinson’s disease. Non-calcific restrictive valvular heart disease was seen in 33/78 patients treated with pergolide but in none of the 18 control patients (who had never received ergot-derived DAs). In most cases, only mild valvular regurgitation (grade 2/4 or less) was detected but one patient required mitral and aortic valve replacement with repair of the tricuspid valve. Valve lesions were assessed using two-dimensional echocardiographic measurement of tenting distance and tenting area, which are methods of estimating the degree of tethering and restriction of valve leaflets previously validated in patients with ischaemic mitral regurgitation.2 Change in tenting distance correlated with cumulative dose of pergolide.1 Subsequent evidence further increased the strength of association between the DA agonists pergolide and cabergoline with restrictive valve dysfunction. In a large
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