The Wolff–Parkinson–White Syndrome

Abstract

A mong patients with a Wolff-Parkinson-White (WPW) syndrome, approximately half will experience arrhythmia during their lifetime. Radiofrequency catheter ablation of the accessory atrioventricular pathway is the treatment of choice for this condition and is associated with a high success rate. Electrophysiology study is indeed the key procedure for identifying the target of radiofrequency ablation. The present prospective study, published in this issue of Circulation: Cardiovascular Imaging by Ishizu et al, investigated the ability of a new imaging technology based on 3-dimensional speckle-tracking (ST) strain echocardiography in localizing AP in WPW syndrome.1 This tool, named isochrone activation imaging (AI), was accurate enough to assess synchronized activation in the normal heart and to detect contractile abnormalities, which approximately matched ablation site in WPW patients with left-or right-sided AP. See Article by Ishizu et al Localization of Accessory Pathways With Echocardiography, a 40-Year-Old StoryHistorically, motion-mode (M-mode) echocardiography was the first effective modality for the ultrasonic detection of early pre-ejection events, concomitant with the delta wave in WPW syndrome. Because of its high temporal resolution (1000-3000 Hz), M-mode echocardiography can display the reduced amplitude of left ventricle (LV) posterior systolic wall motion for AP, emerging from LV basal free wall. This modality can also display rapid pre-ejection posterior septal motion associated with a slow anterior motion of the septum for AP, emerging from the right ventricular (RV) free wall.2 Twenty years later, pulsed-wave tissue doppler imaging (TDI) and high frame-rate tissue velocity imaging enabled AP-accurate localization in 50% more patients, when compared with the M-mode method.2 High temporal resolution (at least 150 Hz) is a potential advantage of TDI; however, clinical use was limited by artifacts, caused by myocardial translational motion, nonoptimal Doppler alignment, and poor reproducibility.Approximately 10 years ago, 2-dimensional speckletracking echocardiography gained popularity in quantification of amplitude and timing of myocardial deformation, with a lower influence of cardiac motion as compared with TDI. Optimal frame rate for speckle-tracking echocardiography is 50 to 90 Hz, a much lower rate than that of M-mode or TDI. Nevertheless, using customized software, De Boeck's team demonstrated that speckle-tracking echocardiography mapping matched the electrophysiology localization (with a tolerance of 1 contiguous segment) of the AP in 28 patients (85%) with a WPW syndrome. 4 Importantly, early deformation associated with the AP was subsequently followed by reduced local deformation during systole, especially in patients with AP involving the interventricular septum (IVS). In a cohort of 40 patients with WPW syndrome referred for radiofrequency ablation, longitudinal speckle-tracking echocardiography strain accurately identified early basal pre-ejection LV deformation in 38 patients (95%), 5 w...

Ablation of Ventricular Preexcitation to Cure Preexcitation-Induced Dilated Cardiomyopathy in Infants: Diagnosis and Outcome

“…The inclusion criteria were as follows: (1) 12-lead electrocardiography (ECG) showing ventricular preexcitation of the right AP; (2) echocardiography showing dyssynchrony of LV wall, left ventricular dilation and cardiac dysfunction; (3) normal cardiac anatomical structure; and (4) normalization or improvement of the ventricular size and cardiac function after successful blocking of pathway anterograde conduction via catheter ablation. 1,2 The exclusion criteria included intermittent preexcitation, tachycardiomyopathy, congenital heart disease, endocardial fibroelastosis, hypertrophic cardiomyopathy, primary hereditary dilated cardiomyopathy, noncompaction of the ventricular myocardium, and a positive family history of cardiomyopathy.…”

“…Preexcitation-induced dilated cardiomyopathy (DCM) presents with left ventricle (LV) remodeling, progressive dilation, and cardiac dysfunction which are caused by ventricular preexcitation-related ventricular systolic dyssynchrony. 1–3 The prevalence of preexcitation-induced DCM is unknown due to absence of epidemiologic data. The incidence, clinical features, and severity of cardiac dysfunction in infantile preexcitation-induced DCM are uncertain due to the limited number of case reports.…”