Kevin Ming Wei Leong

Visualizing Localized Reentry With Ultra–High Density Mapping in Iatrogenic Atrial Tachycardia: Beware Pseudo-Reentry

Background— The activation pattern of localized reentry (LR) in atrial tachycardia remains incompletely understood. We used the ultra–high density Rhythmia mapping system to study activation patterns in LR. Methods and Results— LR was suggested by small rotatory activations (carousels) containing the full spectrum of the color-coded map. Twenty-three left-sided atrial tachycardias were mapped in 15 patients (age: 64±11 years). 16 253±9192 points were displayed per map, collected over 26±14 minutes. A total of 50 carousels were identified (median 2; quartiles 1–3 per map), although this represented LR in only n=7 out of 50 (14%): here, rotation occurred around a small area of scar (<0.03 mV; 12±6 mm diameter). In LR, electrograms along the carousel encompassed the full tachycardia cycle length, and surrounding activation moved away from the carousel in all directions. Ablating fractionated electrograms (117±18 ms; 44±13% of tachycardia cycle length) within the carousel interrupted the tachycardia in every LR case. All remaining carousels were pseudo-reentrant (n=43/50 [86%]) occurring in areas of wavefront collision (n=21; median 0.5; quartiles 0–2 per map) or as artifact because of annotation of noise or interpolation in areas of incomplete mapping (n=22; median 1, quartiles 0–2 per map). Pseudo-reentrant carousels were incorrectly ablated in 5 cases having been misinterpreted as LR. Conclusions— The activation pattern of LR is of small stable rotational activations (carousels), and this drove 30% (7/23) of our postablation atrial tachycardias. However, this appearance is most often pseudo-reentrant and must be differentiated by interpretation of electrograms in the candidate circuit and activation in the wider surrounding region.

ST-Elevation Magnitude Correlates With Right Ventricular Outflow Tract Conduction Delay in Type I Brugada ECG

Background: The substrate location and underlying electrophysiological mechanisms that contribute to the characteristic ECG pattern of Brugada syndrome (BrS) are still debated. Using noninvasive electrocardiographical imaging, we studied whole heart conduction and repolarization patterns during ajmaline challenge in BrS individuals. Methods and Results: A total of 13 participants (mean age, 44±12 years; 8 men), 11 concealed patients with type I BrS and 2 healthy controls, underwent an ajmaline infusion with electrocardiographical imaging and ECG recordings. Electrocardiographical imaging activation recovery intervals and activation timings across the right ventricle (RV) body, outflow tract (RVOT), and left ventricle were calculated and analyzed at baseline and when type I BrS pattern manifested after ajmaline infusion. Peak J-ST point elevation was calculated from the surface ECG and compared with the electrocardiographical imaging–derived parameters at the same time point. After ajmaline infusion, the RVOT had the greatest increase in conduction delay (5.4±2.8 versus 2.0±2.8 versus 1.1±1.6 ms; P=0.007) and activation recovery intervals prolongation (69±32 versus 39±29 versus 21±12 ms; P=0.0005) compared with RV or left ventricle. In controls, there was minimal change in J-ST point elevation, conduction delay, or activation recovery intervals at all sites with ajmaline. In patients with BrS, conduction delay in RVOT, but not RV or left ventricle, correlated to the degree of J-ST point elevation (Pearson R, 0.81; P<0.001). No correlation was found between J-ST point elevation and activation recovery intervals prolongation in the RVOT, RV, or left ventricle. Conclusions: Magnitude of ST (J point) elevation in the type I BrS pattern is attributed to degree of conduction delay in the RVOT and not prolongation in repolarization time.

Repolarization abnormalities unmasked with exercise in sudden cardiac death survivors with structurally normal hearts

Models of cardiac arrhythmogenesis predict that nonuniformity in repolarization and/or depolarization promotes ventricular fibrillation and is modulated by autonomic tone, but this is difficult to evaluate in patients. We hypothesize that such spatial heterogeneities would be detected by noninvasive ECG imaging (ECGi) in sudden cardiac death (SCD) survivors with structurally normal hearts under physiological stress.

Comparison of the Prognostic Usefulness of the European Society of Cardiology and American Heart Association/American College of Cardiology Foundation Risk Stratification Systems for Patients with Hypertrophic Cardiomyopathy

Implantable cardiodefibrillators (ICDs) have proven benefit in preventing sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HC), making risk stratification essential. Data on the predictive accuracy on the European Society of Cardiology (ESC) risk scoring system have been conflicting. We independently evaluated the ESC risk scoring system in our cohort of patients with HC from a large tertiary center and compared this with previous guidance by the American College of Cardiology Foundation and Heart Association (ACCF/AHA). Risk factor profiles, 5-year SCD risk estimates, and ICD recommendations, as defined by the ACCF/AHA and ESC guidelines, were retrospectively ascertained for 288 HC patients with and without SCD or equivalent events at our center. In the SCD group (n = 14), a significantly higher proportion of patients would not have met the criteria for an ICD implant using the ESC scoring algorithm compared with ACCF/AHA guidance (43% vs 7%, p = 0.029). In those without SCD events (n = 274), a larger proportion of individuals not requiring an ICD was identified using the ESC risk score model compared with the ACCF/AHA model (82% vs 57%; p < 0.0001). Based on risk stratification criteria alone, 5 more individuals with a previously aborted SCD event would not have received an ICD with the ESC risk model compared with the ACCF/AHA risk model. In conclusion, we found that the current ESC scoring system potentially leaves more high-risk patients unprotected from sudden death in our cohort of patients.

Recurrent blackouts in a 36-year-old woman

A 36-year-old woman was referred to our neurological and cardiological services with recurrent blackouts. She was diagnosed at age 6 with nocturnal generalised tonic-clonic seizures, which settled by age 13 with Carbamazepine. During adulthood, her seizures were thought to have recurred, but now occurred upon rising up from bed and were preceded by palpitations, breathlessness and light-headedness. Having passed out, she would often bite her cheek, lose urinary continence and was seen to convulse. Upon termination, she would recover rapidly without a clear postictal phase. Our patients grandmother died suddenly of an unknown cause at age 44. Neurological investigations showed a …

Effectiveness of the 2014 European Society of Cardiology guideline on sudden cardiac death in hypertrophic cardiomyopathy: a systematic review and meta-analysis

Objective In 2014, the European Society of Cardiology (ESC) recommended the use of a novel risk prediction model (HCM Risk-SCD) to guide use of implantable cardioverter defibrillators (ICD) for the primary prevention of sudden cardiac death (SCD) in patients with hypertrophic cardiomyopathy (HCM). We sought to determine the performance of HCM Risk-SCD by conducting a systematic review and meta-analysis of articles reporting on the prevalence of SCD within 5 years of evaluation in low, intermediate and high-risk patients as defined by the 2014 guidelines (predicted risk <4%, 4%–<6% and ≥6%, respectively). Methods The protocol was registered with PROSPERO (registration number: CRD42017064203). MEDLINE and manual searches for papers published from October 2014 to December 2017 were performed. Longitudinal, observational cohorts of unselected adult patients, without history of cardiac arrest were considered. The original HCM Risk-SCD development study was included a priori. Data were pooled using a random effects model. Results Six (0.9%) out of 653 independent publications identified by the initial search were included. The calculated 5-year risk of SCD was reported in 7291 individuals (70% low, 15% intermediate; 15% high risk) with 184 (2.5%) SCD endpoints within 5 years of baseline evaluation. Most SCD endpoints (68%) occurred in patients with an estimated 5-year risk of ≥4% who formed 30% of the total study cohort. Using the random effects method, the pooled prevalence of SCD endpoints was 1.01% (95% CI 0.52 to 1.61) in low-risk patients, 2.43% (95% CI 1.23 to 3.92) in intermediate and 8.4% (95% CI 6.68 to 10.25) in high-risk patients. Conclusions This meta-analysis demonstrates that HCM Risk-SCD provides accurate risk estimations that can be used to guide ICD therapy in accordance with the 2014 ESC guidelines. Registration number PROSPERO CRD42017064203;Pre-results.

Proarrhythmogenic effects of lamotrigine during ajmaline testing for Brugada syndrome

Introduction Sodium channel blockade (SCB) with a class Ia or Ic antiarrhythmic agent (eg, ajmaline or procainamide, respectively) is used in the unmasking and diagnosis of Brugada syndrome (BrS). SCB is performed frequently as part of family screening or in symptomatic patients with a suggestive electrocardiogram (ECG), and concurrent medications known to potentiate arrhythmias or contraindicated in BrS are withheld prior to testing. Lamotrigine (LTG) is currently not contraindicated in BrS or known to be potentially arrhythmic during testing with SCB agents. We report a case illustrating its arrhythmogenic potential and the implications of its concurrent usage during such testing in clinical practice.

An electrocardiogram opinion from an National Health Service walk-in centre

A previously fit and well 28-year-old man was referred by his general practitioner to a nearby NHS walk-in centre for an ECG. He presented with a 1-day history of mild pleuritic chest discomfort and dyspnoea while at work. Simple analgesics alleviated the discomfort and improved the dyspnoea slightly. He had a BP of 121/78, a HR of 66 bpm and had an oxygen saturation of 98%. The ECG was electronically sent to a cardiologist based at …

146 Contribution of Conduction and Repolarisation Abnormalities to the Type i Brugada Pattern: A Study Using Non-Invasive Electrocardiographic Imaging

Introduction In Brugada Syndrome (BrS), the substrate location and underlying electrophysiological mechanisms that contribute to the characteristic ECG pattern are still debated. Using non-invasive electrocardiographical imaging (ECGi), we study whole heart conduction and repolarisation patterns following an ajmaline challenge in individuals with concealed Type I BrS. Methods 13 participants (mean age 44 ± 12 yrs; 8 males), 11 concealed Type I BrS and 2 controls, underwent an Ajmaline infusion with ECGI and ECG recordings for a research study. ECGi technology reconstructs >1000 electrograms (EGMs) from 252 surface electrode vest and projects this mathematically onto a 3D cardiac image created using a CT scan. Activation time points were determined as the QRS (dP/dtmin) and repolarisation time as (dP/dtmax) for positive T waves and (dp/dtmin) for negative or biphasic T waves, annotated using a custom built semi-automated software off-line. From these data, the local activation recovery interval (ARI), a surrogate of action potential duration, and activation timings across the right ventricle (RV) body, out flow tract (RVOT), and left ventricle (LV) were computed for all participants (Figure 1a). Changes in AT timings and ARI across the RVOT, RV and LV with ajmaline were calculated, and correlated with peak ST elevation (STE) derived from the ECG at the same time point. Results Following ajmaline administration, the greatest median increase in conduction delay was noted in the RVOT than in the RV or LV (5[3–8] ms vs 1[0–4]ms vs 1[0–2] ms; p < 0.0001) (FigURE 1b). Prolongation of ARI was also observed to have increased the most in the RVOT (68[53–99] ms vs 35[23–46] ms vs 25[9–30] ms; p < 0.01). In the two control patients, no STE was noted with minimal rise in conduction delay or ARI prolongation noted in the RVOT, RV and LV. Only conduction delay in RVOT with ajamaline correlated to amount of STE (Pearson R 0.8, p < 0.001) (Figure 1c), but not in the RV or LV (Pearson 0.3 and 0.2 respectively; p=ns). No significant correlation was also seen between STE and ARI prolongation in the RVOT, RV or LV (Pearson 0.5, 0.4, 0.1 respectively; p=ns). Conclusion Magnitude of STE in the Type I BrS pattern is attributed to degree of conduction delay in the RVOT and not prolongation in repolarisation time.Abstract 146 Figure 1 a) Isochronal crowding seen RVOT following ajmailne, and measurement of activation times across region b) Activation time (AT) delay across the different regions. c) Correlation of RVOT conduction delay with ST elevation on ECG. Black denotes control and red denotes Brugada participants

145 Risk Stratification in Hypertrophic Cardiomyopathy: Evaluation of the European Society of Cardiology Sudden Cardiac Death Risk Scoring System

Introduction Implantable cardio-defibrillators (ICDs) have proven benefit in treating lethal ventricular arrhythmias and preventing sudden death (SD) in hypertrophic cardiomyopathy (HCM), making risk stratification essential. We retrospectively evaluate the effectiveness of the 2014 European Society of Cardiology (ESC) risk scoring system in our cohort of HCM patients. Methods We evaluated the ESC risk scoring system which employs mathematical and statistical modelling of 7 disease variables to predict SD risk over 5 years, with a recommendation for ICD implant if SD risk ≥6%. From our cohort of HCM patients previously evaluated at our centre, we retrospectively calculated the ESC 5 year SD risk score at point of implant and measured it against ICD outcome. Decision of ICD implant, prior to the introduction of the ESC scoring system, was based on clinical history and number of conventional risk markers as defined by the American College of Cardiology and Heart Association. Results 52 out of 199 HCM patients (mean age 51 ± 13 yrs) underwent ICD implantation for primary prevention, with 8 (15%) having appropriate therapy for sustained ventricular tachycardia/fibrillation (VT/VF) over an average follow up period of 6.2 ± 4.9 yrs. There was no difference in the ESC risk scores between patients with or without device therapy (4.79% ± 1.5 vs 5.37% ± 3.3, p = 0.68) (Table 1). 5 of 8 (62%) patients with appropriate therapies for VT/VF had scores ranging from 3.08–5.05% and would not have reached the threshold for an ICD recommendation. In two an ICD would not be recommended and may be considered in the other three.Abstract 145 Table 1 Summary of risk factors in (primary prevention) patients with and without ICD therapy. Mean ± SD and proportion shown ESC -– European Society of cardiology; ACC – American college of cardiology; AHA – American Heart Association; LVH – Left Ventricular Hypertrophy; LVOT – Left Ventricular Outflow Obstruction; LA – left atrium; VT – ventricular tachycardia; SD – sudden death; BP – blood pressure; AF – atrial fibrillation) Conclusion The current ESC scoring system potentially leaves many high-risk patients unprotected or with ambiguous ICD implant guidance. Lowering the current threshold may improve accuracy.