Electrical Remodeling Following Percutaneous Pulmonary Valve Implantation Carla M. Plymen, MRCP a, *, Aidan P. Bolger, MRCP b , Philipp Lurz, MD c , Johannes Nordmeyer, MD c , Twin Yen Lee, RN c , Alamgir Kabir, PhD a , Louise Coats, MRCP a , Seamus Cullen, MBBCh a , Fiona Walker, BM a , John E. Deanfield, FRCP a,d , Andrew M. Taylor, MD c,d , Philipp Bonhoeffer, MD c,d , and Pier D. Lambiase, PhD a Sudden cardiac death in congenital heart disease is related to increased right ventric- ular end-diastolic volume (RVEDV), abnormalities of QRS duration, and QRS, JT, and QT dispersions. Surgical pulmonary valve replacement and percutaneous pulmonary valve implantation (PPVI) decrease RVEDV, but the effects of PPVI on surface electrocardiographic parameters are unknown. PPVI represents a pure model of RV mechanical and electrophysiologic changes after replacement. This prospective study sought to determine the effects of PPVI on surface electrocardiographic parameters: Ninety-nine PPVI procedures in patients with congenital heart disease (23.1  10 years of age) were studied before, after, and 1 year after PPVI with serial electrocardiograms and echocardiogram/magnetic resonance images. Forty-three percent had pulmonary stenosis, 27% pulmonary regurgitation (PR), and 29% mixed lesions. In those with predominantly PR (n  26), QRS duration decreased significantly (135  27 to 128  29 ms, p  0.007). However, in the total cohort no significant change in QRS duration at 1 year was observed (137  29 to 134  29 ms). Corrected QT interval and QRS, QT, and JT dispersions significantly decreased at 1 year (p <0.001). RVEDV correlated with preprocedure QRS duration (r  0.34, p <0.002) but there was no correlation after PPVI. In conclusion, this is the first study reporting electrical remodeling after isolated PPVI and it confirms that decreases in QRS duration occur after PPVI in PR, as reported for equivalent surgical cohorts. Further, increased homogeneity of repolar- ization in combination with improved conduction may decrease arrhythmic events in congenital cardiac patients with pulmonary valvular disease. © 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;107:309 –314) Percutaneous pulmonary valve implantation (PPVI) has been shown to be a safe and feasible treatment option for right ventricular (RV) to pulmonary artery conduit dysfunction 1 and is not subject to the confounding effects of open heart surgery, including cardiopulmonary by- pass. 2,3 PPVI represents a pure model for studying the hemodynamic consequences of RV stretch. It is associ- ated with positive outcomes 4 and avoids incisions in the right ventricle that could promote further conduction block and re-entrant ventricular tachycardia. Follow-up of patients has revealed significant improvements in RV end-diastolic volume (EDV) and RV systolic pressure in patients with pulmonary regurgitation (PR) or outflow tract obstruction. 4,5 In this study, we investigated changes in electrocardiographic parameters (QRS duration, corrected QT interval, and QRS/QT/JT dispersions) after PPVI and their relation, if any, to RVEDV and RV systolic pressure. Methods Ninety-nine patients were included in this prospective study. All had underlying congenital heart disease with hemodynamically significant pulmonary valve lesions and underwent PPVI at Great Ormond Street Hospital, The Heart Hospital, or Harley Street Clinic (London, United Kingdom). PPVI occurred from May 2001 to July 2007, enabling 1-year follow-up in all subjects. Clinical and morphologic inclusion criteria for PPVI have been described previously, 6 but briefly, include RV systolic pressure 2/3 systemic with symptoms, RV systolic pressure 3/4 without symptoms, mod- erate to severe PR with either symptom, severe RV dysfunction or dilatation, or impaired exercise capacity. RV outflow tract diam- eter measurements had to be 22  22 mm and 14  14 mm. a Departments of Adult Congenital Heart Disease and Electrophysiol- ogy, The Heart Hospital, University College London Hospitals NHS Foun- dation Trust, London, United Kingdom; b East Midlands Congenital Heart Centre, Glenfield Hospital, Leicester, United Kingdom; c Great Ormond Street Hospital for Children NHS Trust, London, United Kingdom; d UCL Institute of Child Health, London, United Kingdom. Manuscript received June 11, 2010; revised manuscript received and accepted September 2, 2010. The research was supported by the National Institute of Health Re- search, London and University College London, Comprehensive Biomed- ical Research Centre, London, United Kingdom. Dr. Plymen is funded by a Clinical Research Fellowship grant from the British Heart Foundation. Dr. Taylor and Dr. Lambiase receive funding from the Higher Education Funding Council for England. *Corresponding author: Tel: 0044-207-573-8888; fax: 0044-207-573- 8847. E-mail address: carla.plymen@uclh.nhs.uk (C.M. Plymen). 0002-9149/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved. www.ajconline.org doi:10.1016/j.amjcard.2010.09.017