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 nested case-control study of 11 417 subjects aged 40–80 years prescribed antiparkinsonian drugs and listed in the UK General Practice Research Database, Schade et al3 reported an incidence rate ratio of 4.9 with cabergoline and 7.1 with pergolide for new valvular regurgitation. No increased risk was noted with other antiparkinsonian medication (levodopa, selegeline, bromocriptine, lisuride, pramipexole and ropinirole). In an echocardiographic prevalence study, Zanettini et al4 reported that valvular regurgitation was significantly increased in patients taking pergolide or cabergoline but not increased in subjects taking the non-ergot-derived dopamine agonists pramipexole and ropinirole. All 155 patients had Parkinson’s disease, while the 90 controls were selected from relatives of patients, acquaintances of medical staff or from referrals for echocardiography to evaluate fitness before participation in …