Cardiac valvular regurgitation and dopamine agonists (DAs) in Parkinson’s disease (PD)
M Steiger;1 W Jost;2 F Grandas;3 G Van Camp4
1The Walton Centre for Neurology and Neurosurgery, Liverpool, UK; 2German Diagnostic Clinic, Department of Neurology, Wiesbaden, Germany; 3Hospital Gregorio Marañón, Department of Neurology, Madrid, Spain; 4UZ Brussel, Brussels, Belgium.

Objective: A literature review was conducted to assess the risk of cardiac valve regurgitation (CVR) associated with the use of ergot-derived dopamine agonists (EDAs) (potent 5-HT2B–receptor agonists) and non-ergot DAs (non-EDAs), (non- or less-potent 5-HT2B–receptor agonists) in patients with PD.

Methods: A systematic search on PubMed was conducted (March 1 2007) using the terms ‘dopamine agonists’ AND ‘fibrosis’ OR ‘valvulopathy’ OR ‘valvular heart disease’. Inclusion criteria: case-control/observational studies of >10 patients with PD treated with DAs, including a control group and an assessment of the incidence or risk of fibrosis/valvulopathy/valvular heart disease.

Results: In total, 143 publications were identified, ten of which met all inclusion criteria. A total of 1324 patients were included in these ten publications, 769 patients received EDAs (pergolide n=405; cabergoline n=342; bromocriptine n=22), 145 received non-EDAs (ropinirole n=27; pramipexole n=100; unspecified n=18). Controls were defined as patients with and without PD, untreated patients (historical or healthy controls) or, in one study, those receiving non-pergolide treatment (n=410). In eight of the studies, a significant increase in the frequency of CVR of any severity (at the aortic, mitral or tricuspid valve) in the EDA group vs. the non-EDA or control group was described. This increased frequency was reported for both cabergoline (5/6 studies) and pergolide (7/9 studies), despite a shorter duration of treatment with cabergoline (range: cabergoline 24–53 months; pergolide 52–82 months). In five studies, an increased frequency of clinically significant, moderate-to-severe CVR was identified in the EDA group vs the non-EDA or control group (cabergoline three studies; pergolide four studies). A non-significant increased incidence of mild CVR in the EDA group vs. controls was noted in one study; another found no increased risk of CVR with EDAs. No study reported an increased risk of CVR for non-EDAs, compared with controls.

Conclusions: The use of EDAs (pergolide and cabergoline; both drugs that are potent
5-HT2B–receptor agonists) in patients with PD is associated with an increased risk of CVR. In the studies identified in the literature, an increased risk of CVR was not associated with the use of non-EDAs (non- or less-potent 5-HT2B–receptor agonists).