The first definitive electronic pacemaker was implanted by Senning and Elmqvist in Sweden in 1958 using a thoracotomy to suture two epicardial electrodes. While the device only fired for 3 h and was followed by numerous surgical pacemaker interventions, the therapy was life saving.1 Since that initial implantation, chronic pacing therapy has rapidly and impressively advanced, first with the development of a totally endocardial device, followed by defibrillator and cardiac-resynchronisation capability and sophisticated diagnostics, all within the last two decades. Despite innovation and progress, complications of device implantation, although relatively infrequent, adversely affect morbidity and, rarely, mortality.2 ,3 Among these is RV lead-associated tricuspid regurgitation,4–7 first described by Gould and colleagues in 1974 with a case of tricuspid valve leaflet perforation found at autopsy.8 Since then numerous studies have reported on pacemaker-associated tricuspid valve dysfunction with a prevalence somewhere between 11% and 29%.9

Hoke et al provide us with more data, obtained retrospectively, on RV lead-associated tricuspid regurgitation from 239 patients who underwent de novo device implantation (191 implantable cardioverter-defibrillators and 28 pacemakers) between January 2002 and January 2009 at a single centre.10 In their study, grade 1 or 2 tricuspid regurgitation was present in 64% (153 patients), grade 3 tricuspid regurgitation in 2% …