Ventricular conduction stability test: a method to identify and quantify changes in whole heart activation patterns during physiological stress

EP Europace ◽  
2019 ◽  
Vol 21 (9) ◽  
pp. 1422-1431
Author(s):  
Matthew J Shun-Shin ◽  
Kevin M W Leong ◽  
Fu Siong Ng ◽  
Nicholas W F Linton ◽  
Zachary I Whinnett ◽  
...  

Abstract Aims Abnormal rate adaptation of the action potential is proarrhythmic but is difficult to measure with current electro-anatomical mapping techniques. We developed a method to rapidly quantify spatial discordance in whole heart activation in response to rate cycle length changes. We test the hypothesis that patients with underlying channelopathies or history of aborted sudden cardiac death (SCD) have a reduced capacity to maintain uniform activation following exercise. Methods and results Electrocardiographical imaging (ECGI) reconstructs >1200 electrograms (EGMs) over the ventricles from a single beat, providing epicardial whole heart activation maps. Thirty-one individuals [11 SCD survivors; 10 Brugada syndrome (BrS) without SCD; and 10 controls] with structurally normal hearts underwent ECGI vest recordings following exercise treadmill. For each patient, we calculated the relative change in EGM local activation times (LATs) between a baseline and post-exertion phase using custom written software. A ventricular conduction stability (V-CoS) score calculated to indicate the percentage of ventricle that showed no significant change in relative LAT (<10 ms). A lower score reflected greater conduction heterogeneity. Mean variability (standard deviation) of V-CoS score over 10 consecutive beats was small (0.9 ± 0.5%), with good inter-operator reproducibility of V-CoS scores. Sudden cardiac death survivors, compared to BrS and controls, had the lowest V-CoS scores post-exertion (P = 0.011) but were no different at baseline (P = 0.50). Conclusion We present a method to rapidly quantify changes in global activation which provides a measure of conduction heterogeneity and proof of concept by demonstrating SCD survivors have a reduced capacity to maintain uniform activation following exercise.

EP Europace ◽  
2020 ◽  
Author(s):  
Kevin Ming Wei Leong ◽  
Fu Siong Ng ◽  
Matthew J Shun-Shin ◽  
Michael Koa-Wing ◽  
Norman Qureshi ◽  
...  

Abstract 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 &lt; 0.01] and 2 min into recovery [95.2% (91.1–97.2%) vs. 98.9% (96.9–99.5%); P &lt; 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.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Sattar ◽  
W Ullah ◽  
S Mamtani ◽  
C Alraies

Abstract Introduction Ventricular tachycardia is a major complication associated with increased risk of sudden cardiac death in arrhythmogenic ventricular cardiomyopathy. Recurrence of VT status post catheter endocardial ablation with conventional mapping is a evolving discussion in management of VT prevention in ARVC. With the evolution of new mapping techniques to locate ectopic foci of VT, a combination of endo- and epicardial catheter ablation have proven to be efficacious in the prevention of frequency of VT recurrence and its duration. Methods Using PubMed, Ovid (MEDLINE) and Cochrane database we searched using the MeSH terms including: “arrhythmogenic right ventricular cardiomyopathy”, “arrhythmogenic right ventricular dysplasia”, “monomorphic ventricular tachycardia”, “polymorphic ventricular Tachycardia”, “endocardial catheter ablation”, “epicardial catheter ablation”. The primary outcomes were to assess VT frequency and duration status post endocardial or epicardial or a combination of both types of ablation. The secondary outcome includes sudden cardiac arrest or sudden cardiac death after procedure. ANOVA with post HOC analysis was performed using SPSS v.26 (IBM Corp, NY, USA) Results A total of 33 studies included 1437 patients with a mean male=67%. The data analysis showed a mean VT prevention for endocardial ablation was 65%, epicardial 78%, and for combined epi-endocardial was 89% (figure-1). The mean procedural mortality rate was 2%. In order to test the hypothesis that combined epi-endocardial ablation was more successful in the prevention of VT recurrence, we performed a one-way analysis of variance (ANOVA). The analysis was statistically significant F(2,14)=5.879, 95% CI, p=0.014. Post Hoc test (Tukey HSD test) with multiple comparisons indicated that patients who underwent combined epi-endocardial ablation experienced a statistically significant difference in VT prevention of 89% (95% CI p=0.01) compared to only endocardial ablation, mean VT prevention of 65% (95% CI, p=0.189) or only epicardial, mean VT prevention of 78% (95% CI, p=0.353). Conclusion With new mapping techniques, use of endocardial, and epicardial ablation is linked to decrease VT frequency, duration, ICD shocks, and sudden cardiac death in patients with ARVC in cohorts with prior failure of antiarrhythmics. Total VT Prevention across target sites Funding Acknowledgement Type of funding source: None


2008 ◽  
Vol 7 ◽  
pp. 109-109
Author(s):  
R BRECKENRIDGE ◽  
Z ZUBERI ◽  
L FELKIN ◽  
E BIRKS ◽  
P BARTON ◽  
...  

2016 ◽  
Vol 73 (12) ◽  
pp. 759-765
Author(s):  
Bettina Muggli ◽  
Christiane Gruner

Zusammenfassung. Die hypertrophe Kardiomyopathie (HCM) ist die häufigste hereditäre Kardiomyopathie und wird definiert durch eine unerklärte linksventrikuläre Hypertrophie mit normal grossen Ventrikeln ohne andere kardiale Ursachen oder systemische Erkrankungen. Die klinische Präsentation ist vielfältig und reicht vom asymptomatischen Familienmitglied bis hin zu Patienten mit Symptomen einer schweren Herzinsuffizienz. Häufige Probleme sind der plötzliche Herztod (’sudden cardiac death’ SCD) und die Risikostratifizierung der Patienten im Hinblick auf eine primärprophylaktische ICD-Implantation. Des Weiteren spielen natürlich die Obstruktion des linksventrikulären Ausflusstrakts und deren Behandlung (medikamentös, kathetertechnisch mittels Septalalkoholablation, chirugische Myektomie), diastolische Dysfunktion, Vorhofflimmern und die Entwicklung einer Herzinsuffizienz mit systolischer linksventrikulärer Dysfunktion eine wichtige Rolle bei der Betreuung von Patienten mit HCM. Beim Vorhofflimmern muss unabhängig vom CHA2DS2Vasc Score eine orale Antikoagulation begonnen werden und aufgrund der diastolischen Dysfunktion sollte wenn möglich wieder ein Sinusrhythmus erreicht werden durch medikamentöse Massnahmen, elektrische Kardioversion und / oder Pulmonalvenenisolation. Kommt es zur Entwicklung einer Herzinsuffizienz ist eine übliche Herzinsuffizienztherapie indiziert. Bei terminaler Herzinsuffizienz sollte frühzeitig eine Herztransplantation evaluiert werden.


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