AIMS: Rate adaptation of the action potential ensures spatial heterogeneities in conduction across the myocardium are minimized at different heart rates providing a protective mechanism against ventricular fibrillation (VF) and sudden cardiac death (SCD), which can be quantified by the ventricular conduction stability (V-CoS) test previously described. We tested the hypothesis that patients with a history of aborted SCD due to an underlying channelopathy or cardiomyopathy have a reduced capacity to maintain uniform activation following exercise. METHODS AND RESULTS: Sixty individuals, with (n = 28) and without (n = 32) previous aborted-SCD event underwent electro-cardiographic imaging recordings following exercise treadmill test. These included 25 Brugada syndrome, 13 hypertrophic cardiomyopathy, 12 idiopathic VF, and 10 healthy controls. Data were inputted into the V-CoS programme to calculate a V-CoS score that indicate the percentage of ventricle that showed no significant change in ventricular activation, with a lower score indicating the development of greater conduction heterogeneity. The SCD group, compared to those without, had a lower median (interquartile range) V-CoS score at peak exertion [92.8% (89.8-96.3%) vs. 97.3% (94.9-99.1%); P < 0.01] and 2 min into recovery [95.2% (91.1-97.2%) vs. 98.9% (96.9-99.5%); P < 0.01]. No significant difference was observable later into recovery at 5 or 10 min. Using the lowest median V-CoS scores obtained during the entire recovery period post-exertion, SCD survivors had a significantly lower score than those without for each of the different underlying aetiologies. CONCLUSION: Data from this pilot study demonstrate the potential use of this technique in risk stratification for the inherited cardiac conditions. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Rate adaptation of the action potential ensures spatial heterogeneities in conduction across the myocardium are minimized at different heart rates providing a protective mechanism against ventricular fibrillation (VF) and sudden cardiac death (SCD), which can be quantified by the ventricular conduction stability (V-CoS) test previously described. We tested the hypothesis that patients with a history of aborted SCD due to an underlying channelopathy or cardiomyopathy have a reduced capacity to maintain uniform activation following exercise. METHODS AND RESULTS: Sixty individuals, with (n = 28) and without (n = 32) previous aborted-SCD event underwent electro-cardiographic imaging recordings following exercise treadmill test. These included 25 Brugada syndrome, 13 hypertrophic cardiomyopathy, 12 idiopathic VF, and 10 healthy controls. Data were inputted into the V-CoS programme to calculate a V-CoS score that indicate the percentage of ventricle that showed no significant change in ventricular activation, with a lower score indicating the development of greater conduction heterogeneity. The SCD group, compared to those without, had a lower median (interquartile range) V-CoS score at peak exertion [92.8% (89.8-96.3%) vs. 97.3% (94.9-99.1%); P < 0.01] and 2 min into recovery [95.2% (91.1-97.2%) vs. 98.9% (96.9-99.5%); P < 0.01]. No significant difference was observable later into recovery at 5 or 10 min. Using the lowest median V-CoS scores obtained during the entire recovery period post-exertion, SCD survivors had a significantly lower score than those without for each of the different underlying aetiologies. CONCLUSION: Data from this pilot study demonstrate the potential use of this technique in risk stratification for the inherited cardiac conditions. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Douglas P Zipes; A John Camm; Martin Borggrefe; Alfred E Buxton; Bernard Chaitman; Martin Fromer; Gabriel Gregoratos; George Klein; Arthur J Moss; Robert J Myerburg; Silvia G Priori; Miguel A Quinones; Dan M Roden; Michael J Silka; Cynthia Tracy; Silvia G Priori; Jean-Jacques Blanc; Andrzej Budaj; A John Camm; Veronica Dean; Jaap W Deckers; Catherine Despres; Kenneth Dickstein; John Lekakis; Keith McGregor; Marco Metra; Joao Morais; Ady Osterspey; Juan Luis Tamargo; José Luis Zamorano; Sidney C Smith; Alice K Jacobs; Cynthia D Adams; Elliott M Antman; Jeffrey L Anderson; Sharon A Hunt; Jonathan L Halperin; Rick Nishimura; Joseph P Ornato; Richard L Page; Barbara Riegel Journal: Europace Date: 2006-08-25 Impact factor: 5.214
Authors: Matthew J Shun-Shin; Kevin M W Leong; Fu Siong Ng; Nicholas W F Linton; Zachary I Whinnett; Michael Koa-Wing; Norman Qureshi; David C Lefroy; Sian E Harding; Phang Boon Lim; Nicholas S Peters; Darrel P Francis; Amanda M Varnava; Prapa Kanagaratnam Journal: Europace Date: 2019-09-01 Impact factor: 5.214
Authors: Perry M Elliott; Aris Anastasakis; Michael A Borger; Martin Borggrefe; Franco Cecchi; Philippe Charron; Albert Alain Hagege; Antoine Lafont; Giuseppe Limongelli; Heiko Mahrholdt; William J McKenna; Jens Mogensen; Petros Nihoyannopoulos; Stefano Nistri; Petronella G Pieper; Burkert Pieske; Claudio Rapezzi; Frans H Rutten; Christoph Tillmanns; Hugh Watkins Journal: Eur Heart J Date: 2014-08-29 Impact factor: 29.983
Authors: R C Saumarez; S Heald; J Gill; A K Slade; M de Belder; F Walczak; E Rowland; D E Ward; A J Camm Journal: Circulation Date: 1995-11-01 Impact factor: 29.690
Authors: Kevin M W Leong; Fu Siong Ng; Caroline Roney; Christopher Cantwell; Matthew J Shun-Shin; Nicholas W F Linton; Zachary I Whinnett; David C Lefroy; D Wyn Davies; Sian E Harding; Phang Boon Lim; Darrel Francis; Nicholas S Peters; Amanda M Varnava; Prapa Kanagaratnam Journal: J Cardiovasc Electrophysiol Date: 2017-12-07