Occurrence Of Ventricular Fibrillation Research Articles

High-resolution repolarization changes preceding short-coupled ectopy in idiopathic ventricular fibrillation, and effects of quinidine

Abstract Background Idiopathic ventricular fibrillation (VF) is linked to early repolarization, increased repolarization heterogeneity, and (short-coupled) premature ventricular complexes (PVCs). Quinidine, an antiarrhythmic drug with class-IA and -III effects, reduces the occurrence of PVCs and VF, but its effects on repolarization have not yet been studied at the whole-heart level in idiopathic-VF patients. Purpose To study dynamic changes in repolarization preceding short-coupled PVCs using noninvasive electrocardiographic imaging (ECGI) in a patient with idiopathic VF, and the antiarrhythmic effects of quinidine. Methods ECGI was performed during sinus rhythm in a 61-year-old male with an ICD (secondary prevention; 2.5 mg nebivolol daily) two days after recurrent idiopathic VF (Fig. A). This was done 1) at baseline, 2 minutes before short-coupled ectopy ("baseline"); 2) at baseline, 10 seconds before the short-coupled PVC ("pre PVC"); and 3) at 2 hours after start of quinidine 200 mg ("on-quinidine"). The ECGI procedure consisted of a 224-electrode body surface potential map and a contrast-enhanced CT scan to obtain torso and heart geometries. After reconstruction of epicardial unipolar electrograms (UEGs), local activation and repolarization times (ATs and RTs) were derived from UEGs by assessing the steepest downslope of the QRS complex and steepest upslope of the T waves, respectively, of 10-second signal-averaged beats. AT and RT duration (first to last AT or RT) were assessed. Results At baseline, QRS duration and QT interval measured 107 ms and 343 ms, respectively, on the standard 12-lead ECG. ECGI-derived epicardial AT duration was 72 ms, and RT histogram span 92 ms. The coupling interval of the PVC that triggered VF in the ICD readout was 340 ms (Fig. A). During 44 minutes of ECGI, 157 short-coupled PVCs from the moderator-band region were recorded (Fig. B; no tachycardia or VF). Just prior to a PVC, epicardial early repolarization at the PVC origin decreased by 26 ms (star in Figs. C-E), and the RT histogram broadened to 109 ms (Fig. E). While on-quinidine, (25 minutes; QRS duration 107 ms, QT interval 419 ms), epicardial repolarization was prolonged (Fig. C/D), also at the site of abnormal impulse formation. Quinidine had increased the epicardial AT duration to 79 ms, and RT histogram span to 133 ms. PVCs were completely suppressed. The patient remained free of sustained arrhythmias while on-quinidine. Conclusion(s) In this case of short-coupled idiopathic VF, epicardial early repolarization shortened momentarily prior to abnormal impulse formation. We found dynamic substrate-trigger characteristics that likely facilitate reentrant excitation. Quinidine prolonged the duration of epicardial activation and repolarization, suppressing the ectopy and VF recurrence.

Blood cardioplegia reduces intraoperative ventricular fibrillation and transfusion requirements compared to crystalloid cardioplegia in canine mitral valve repair.

Cardioplegic solutions are indispensable for open-heart surgeries, including mitral valve repair (MVR), a potentially curative treatment for myxomatous mitral valve disease in dogs. However, procedural methodologies are not fully established, and complications are yet to be comprehensively understood. Cardioplegic solutions contain various substances to protect the myocardium under temporal cardiac arrest. Nevertheless, ventricular fibrillation (VF) occurs as a common complication after releasing the crossclamp. Based on these backgrounds, the search for optimal cardioplegic solutions in dogs undergoing MVR is an urgent issue. This study aims to evaluate the occurrence of VF in dogs treated with blood cardioplegia (BCP) versus crystalloid cardioplegia (CCP) during MVR. A total of 251 client-owned dogs who underwent MVR from November 2015 to November 2017 were included. We retrospectively assessed the relationship between VF and type of cardioplegia (CCP or BCP) based on surgical records, including VF incidence, transfusion use, crossclamp time, and echocardiographic measurements. Logistic regression analysis showed that the CCP group was associated with the occurrence of VF (OR, 2.378; CI, 1.133-4.992; P = .022). In addition, the CCP group was associated with transfusion use (OR, 2.586; CI, 1.232-5.428, P = .022). There was no difference between the groups for the pre- and postoperative echocardiographic measurements. The BCP group had a lower incidence of VF and less transfusion use than the CCP group. This finding indicates that BCP may be a superior cardioplegic technique for MVR in dogs.

Complete Left Bundle Branch Block in Acute Coronary Syndrome with ST Segment Elevation: Epidemiological Features

Background: Complete left bundle branch in acute coronary syndrome with ST segment elevation is not common, but known as a sign of poor prognosis. Several international studies had reported its incidence and related mortality, but its epidemiological data is lacking in Algeria. Aims: The main objective of our study is the determination of the frequency of complete left bundle branch block in acute coronary syndrome with ST segment elevation, the secondary objective was the analysis of its predictive factors and related mortality. Methods and materials: In this prospective study, conducted in the cardiology department of Hussein Dey hospital (Algiers-Algeria), 467 patients with acute coronary syndrome with elevated ST segment (87 women and 380 men) were enrolled between 28 February 2014 and 16 July 2015. The average age is 60 ± 13 years; at admission, a Holter recorder was attached for continuous ECG monitoring during 48 hours. Kruskal’s ANNOVA or H tests were used for comparison of quantitative variables, χ2 test or Fisher’s exact test, were used for qualitative variables, all tests were performed with 1st species risk of 5%. Results: The frequency of complete left bundle brunch block is 1.7 % (8 patients), CI 95%: [0.5%-2.9%], multivariate analysis identified the two independent predictors: diabetes type 1, and Angiotensin Receptor-Blockers as current treatment. Despite the risk of mortality expressed by Hazard Ration (HR) is 4.7, but remains not significant: CI95%: [0.62-36], p = 0.134; however, the risk of ventricular fibrillation occurrence is high, with relative risk (RR) at 7.17, CI 95 %: [2.70-19.03], p = 0.007. Conclusion: Complete left bundle brunch block is not common in acute coronary syndrome with elevated ST segment, its predictive factors according to our study are: Diabetes type 1 and Angiotensin Receptor-Blockers as current treatment. The high-risk mortality in the left bundle brunch block group isn’t significant; however the risk of ventricular fibrillation occurrence is high.

Sustained Ventricular Tachycardia in Acute Coronary Syndrome with ST Segment Elevation: Incidence, Predictive Factors and Related Mortality.

Background: Sustained Ventricular Tachycardia is the most serious complication; in acute coronary syndrome with ST segment elevation, several international studies have reported incidence and predictive factors of severe ventricular arrhythmias, without identifying sustained ventricular tachycardia separately; also, its epidemiological data is lacking in Algeria. Aims: The main objective of our study is the determination of the frequency of sustained ventricular tachycardia in acute coronary syndrome with ST segment elevation, the secondary objective was the analysis of predictive factors of this arrhythmia, and related mortality. Methods and materials: In this prospective study, conducted in the cardiology department of Hussein Dey hospital (Algiers-Algeria), 467 patients with acute coronary syndrome with elevated ST segment (87 women and 380 men) were enrolled between 28 February 2014 and 16 July 2015. The average age is 60 ± 13 years; at admission, a Holter recorder was attached for continuous ECG monitoring during 48 hours Kruskal’s ANNOVA or H tests were used for comparison of quantitative variables, χ2 test or Fisher’s exact test, were used for qualitative variables, all tests were performed with 1st species risk of 5%. Results: The frequency of Sustained Ventricular Tachycardia is 3.6 % (17 patients), CI 95%: [1.9%-5.3%], multivariate analysis identified the following independent predictors: low diastolic blood pressure, severe coronary artery lesions, Elevated high sensitive troponin concentrations more than 5ng/ml. The risk of mortality expressed by Hazard Ration (HR) is 6. (CI95%: [1.7-21], p = 0.005); the predictors of mortality are: occurrence of ventricular fibrillation and low diastolic blood pressure. Conclusion: Sustained Ventricular tachycardia is the most serious complication during acute coronary syndrome with elevated ST segment, its predictive factors according to our study are: low diastolic blood pressure, severe coronary lesions, Elevated high sensitive troponin concentrations more than 5ng/ml, its occurrence increases the risk of hospital mortality.

Age and genetics are associated with ventricular fibrillation but not with monomorphic ventricular tachycardia in Brugada syndrome

Abstract Funding Acknowledgements Type of funding sources: None. Background/introduction Brugada syndrome (BrS) is associated with ventricular arrhythmias (VA) in macroscopically normal hearts. VA in BrS can be classified as ventricular fibrillation (VF) and monomorphic ventricular tachycardia (MVT). Although BrS has been initially described in association with VF, MVT is not rare, as it occurs in ≈30% of BrS patients. Purpose The aim of this study is to correlate VF or MVT with the genetic background and other clinical variables. Methods All BrS patients, were prospectively enrolled in a monocentric registry between 1992 and 2022. Inclusion criteria for the study were: 1) BrS diagnosis; 2) Genetic analysis performed for SCN5A; 3) Classification of variants following ACMG guidelines. Patients with a pathogenic/likely pathogenic (P/LP) variant in SCN5A were defined as (P+). Patients without a P/LP variant were defined as (P-). Primary endpoint was VA occurrence, defined as: documented arrhythmic SCD, documented arrhythmic aborted SCD, VF, sustained MVT or appropriate ICD intervention. All VA events were adjudicated as VF or MVT. Results A total of 500 BrS patients were analyzed. A P/LP variant in SCN5A was found in 104 patients (20.8%). After a mean follow-up of 110.9 months, 48 patients (9.6%) experienced a VA, adjudicated as MVT in 18 patients (37.5%) and VF in 30 patients (62.5%). At survival analysis, P- patients had higher VF free survival, compared with P+ patients (96.5% vs 84.6%, Log-Rank p<0.001) with no difference in MVT free survival (Log-Rank p=0.61), Figure 1. BrS patients > 30 years at diagnosis had higher VF free survival, compared with patients ≤ 30 years at diagnosis (95.5% vs 90.3%, Log-Rank p=0.041), with no difference in MVT free survival (Log-Rank p=0.9), Figure 2. Patients > 50 years at index event had higher VF free survival, compared with patients ≤ 50 years at index event (Log-Rank p=0.002), with no significant difference in MVT free survival (Log-Rank p=0.81). At Cox multivariate analysis independent predictors of VF occurrence were as follows: Age at index event ≤ 50 years (HR=2.57, CI 95% 1.01-6.6, p=0.04), P/LP variant in SCN5A (HR= 2.35, CI 95% 1.12-4.92, p=0.02), SND (HR= 2.67, CI 95% 1.01-7.04, p=0.044), history of syncope (HR= 2.14, CI 95% 1.02-4.51, p=0.047) and history of aborted SCD (HR= 18.66, CI 95% 8.87-39.27, p<0.001). Independent predictors of MVT occurrence were the following: history of syncope (HR= 2.71, CI 95% 1.26-5.80, p=0.01), history of aborted SCD (HR= 4.82, CI 95% 2.14-10.85, p<0.001), VA inducibility at EPS (HR= 3.71, CI 95% 1.66-8.31, p=0.001). Conclusion In a large BrS cohort undergoing genetic analysis MVT occurred in 37.5% of patients and VF in 62.5% of patients. P/LP SCN5A carriers and younger BrS population had a higher incidence of VF with no difference in MVT incidence.

Association between new-onset right bundle branch block and primary or secondary ventricular fibrillation in ST-segment elevation myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: None. Background New-onset right bundle branch block (RBBB) in myocardial infarction (MI) is often associated with ventricular fibrillation (VF) but the nature of this relationship has not been determined. Aims To investigate the association between new-onset RBBB and VF in ST-segment elevation MI (STEMI) as well as its peculiarities attending to the permanent or transient character of RBBB and the distinction of VF as primary or secondary. Methods and results Between 1998 and 2014, among other data, incidence and duration of RBBB and VF occurrence were prospectively collected in 5301 patients with ST-segment elevation MI (STEMI) admitted to two Coronary Care Units. Multinomial adjusted logistic regression analyses were used to examine the association between RBBB, attending to its duration, and VF according to its primary VF (PVF) (<24h from symptom-onset and Killip I) or secondary VF (SVF) (>24h from symptom-onset and/or Killip>I) character. Among 284 (5.4%) patients with new-onset RBBB, 158 were transient and 126 permanent. VF occurred in 339 (6.4%) patients, 201 PVF and 138 SVF, documented within the first 2 h of symptoms-onset in 78% and 60%, respectively. Newonset RBBB was more frequent in PVF (11.4%) and SVF (20.3%), than in non-VF (4.7%). Transient RBBB incidence was higher in PVF (9.0%) and SVF (9.4) than in non-VF (2.6%), whereas permanent RBBB was higher in SVF (10.9%) than PVF (2.5%) and non-VF (2.1%). New-onset RBBB 1.83 [95% confidence interval (CI): 1.07–3.11] and new-onset transient RBBB 2.39 (95% CI: 1.32–4.32) were independently associated with PVF. New-onset 3.03 (95% CI: 1.83–5.02), transient 2.40 (95% CI: 1.27–4.55), and permanent 2.99 (95% CI: 1.52–5.86) RBBB were independently associated with SVF. Conclusion New-onset RBBB and VF in STEMI are independently associated and show particularities based on the duration of the conduction disturbance and/or the primary or secondary character of the arrhythmia.

PO-03-232 PROGNOSTIC IMPACT OF NON-SUSTAINED VENTRICULAR TACHYCARDIA IN WILD-TYPE TRANSTHYRETIN CARDIAC AMYLOIDOSIS

Non-sustained ventricular tachycardia (NSVT) detected on rhythm monitoring is common in AL amyloidosis, but data on its prevalence and prognostic impact in patients with wild-type transthyretin cardiac amyloidosis (ATTRwt-CA) are sparse. To investigate the prevalence of NSVT detected during clinically-indicated ambulatory Holter monitoring and its association with incident sustained VT and ventricular fibrillation (VF) in ATTRwt-CA patients. A single-center retrospective cohort of ATTRwt-CA patients without known history of sustained VT/VF was included (2011-2022). The presence and characteristics of NSVT (≥3 beats) at the first Holter after the ATTRwt-CA diagnosis at our institution were documented. The endpoint was the first occurrence of sustained VT or VF recorded by an implantable cardioverter-defibrillator (ICD) or other methods (in patients without ICD), and it was comparatively assessed in patients with and without NSVT with Kaplan-Meier analysis. Multivariate Cox regression analyses using stepwise variable selection were also performed to identify predictors of incident VT/VF. A total of 219 patients with ATTRwt-CA were included (mean age 74.9 years; 95% males; mean LVEF 52%). Of them, 8 had an ICD at baseline while 14 underwent ICD implantation within a 6-month window from baseline. Mean Holter monitoring duration was 25.6 hours and 53% of patients had at least one NSVT run at index Holter monitor with mean total ventricular ectopy burden 3.8%. After mean follow up 35.2 months, 17 patients experienced the primary outcome. Patients with NSVT had a lower survival free of VT/VF compared to those without NSVT (log-rank p=0.01; figure). In multivariable analysis, the presence of NSVT (HR 3.95, 95% CI 1.10-14.0) and the number of NSVT runs (HR 1.003, 95% 1.00-1.01, per run) were significant predictors of future VT/VF. NSVT is highly prevalent among patients with ATTRwt-CA and confers an increased risk of incident sustained ventricular arrhythmias. This finding has implications in the risk stratification and decision-making for the prevention of sudden cardiac death in these patients.

Vagal response is involved in the occurrence of ventricular fibrillation in patients with early repolarization syndrome

Patients with early repolarization syndrome (ERS) and Brugada syndrome (BruS) have comparable clinical symptoms. In both conditions, ventricular fibrillation (VF) is experienced often near midnight or in the early morning hours when the parasympathetic tone is augmented. However, differences between ERS and BruS regarding the risk of VF occurrence have recently been reported. The role of vagal activity remains especially unclear. The study's goal was to determine the relationship between VF occurrence and autonomic nervous activity in patients with ERS and BruS. We enrolled 50 patients with ERS (n = 16) and BruS (n = 34) who received implantable cardioverter-defibrillators. Of these, 20 patients (5 ERS and 15 BruS) experienced VF recurrence (recurrent-VF group). We investigated baroreflex sensitivity (BaReS) with the phenylephrine method and heart rate variability (HRV) using a Holter ECG in all patients to estimate autonomic nervous function. In both patients with ERS and BruS, there was no significant difference in HRV between the recurrent-VF and the non-recurrent-VF groups. However, in patients with ERS, BaReS was significantly higher in the recurrent-VF group than in the non-recurrent-VF group (p = 0.03); this difference was not evident in BruS patients. High BaReS was independently associated with VF recurrence in patients with ERS, according to Cox proportional hazards regression analyses (HR: 1.52; 95% CI: 1.031-3.061; p = 0.032). Our findings suggest that in patients with ERS, an exaggerated vagal response, as represented by increased BaReS indices, may be involved in the risk of VF occurrence.

Risk stratification of ventricular fibrillation in patients with symptomatic Brugada syndrome using pharmacological tests.

Brugada syndrome (BrS), which is characterized by J-point elevation in right precordial leads of a 12-lead electrocardiogram, is associated with the occurrence of ventricular fibrillation (VF). However, risk stratification of VF in patients with BrS remains challenging. The aim of this study was to identify a risk predictor of VF in patients with BrS using pharmacological tests. Twenty-one consecutive patients with BrS and a history of documented spontaneous VF (n = 16) or syncope presumed to be caused by lethal ventricular arrhythmia (n = 5) were enrolled. J-wave changes in response to intravenous verapamil, propranolol, and pilsicainide were separately assessed. During the median follow-up period of 86.0 months, 8 patients had VF recurrence (recurrence group) and 13 patients did not have VF recurrence (non-recurrence group). Intravenous propranolol injection induced significant J-wave augmentation (i.e., increase in amplitude >0.1 mV) in the inferior and/or lateral leads in the recurrence group compared to the non-recurrence group (p = .048 and p = .015, respectively). Kaplan-Meier analysis revealed that VF recurrence is significantly higher in patients with BrS and J-wave augmentation due to intravenous propranolol than in patients without J-wave augmentation (p = .014). The study results show that propranolol-induced J-wave augmentation is involved in the risk of VF in patients with BrS. The results suggest that early repolarization patterns in response to pharmacological tests may be useful for risk stratification of VF in patients with symptomatic BrS.

Ventricular fibrillation complicating acute myocardial infarction in women

Abstract Background Very little data is available in women presenting with ventricular fibrillation in the setting of acute myocardial infarction. Purpose To investigate sex-discrepancies in the incidence, characteristics and outcomes of acute myocardial infarction complicated by ventricular fibrillation. Methods Data were analyzed from the FAST-MI registry, which prospectively included 14,406 patients with acute myocardial infarction (mean age 66±14 years, 72% male, mean left ventricular ejection fraction 52±12%, 59% with ST elevation myocardial infarction). All consecutive patients admitted to French cardiac intensive care units ≤48 hours from acute myocardial infarction onset during a 1-month period every five years during 1995 and 2015 were included. This analysis focused on ventricular fibrillation occurring during the initial in-hospital stay for acute myocardial infarction in women compared to men. Results A total of 359 patients developed ventricular fibrillation during acute myocardial infarction, including 81 women (2.0% of 4,091 women overall) and 278 men (2.7% of 10,315) (p=0.02). ST-elevation myocardial infarction (OR 2.29, 95% CI 1.75–2.99, p<0.001) was independently associated with occurrence of ventricular fibrillation, while female gender (OR 0.73, 95% CI 0.56–0.95, p=0.02), hypertension (OR 0.75, 95% CI 0.60–0.94, p=0.01) and prior MI (OR 0.69, 95% CI 0.50–0.96, p=0.03) were protective factors. Women were less likely to have percutaneous coronary intervention during hospitalization than men (48.1% vs. 69.1%, OR 0.48, 95% CI 0.29–0.80, p<0.001). One-year mortality was higher in women compared to men (23.1% vs. 7.0%, HR 5.5, 95% CI 1.7–17.2, p=0.001). However, after adjustment for age, type of myocardial infarction and percutaneous coronary intervention, female gender was no longer associated with a worse one-year mortality (adjusted HR 1.04, 95% CI 0.71–1.51, p=0.85). Conclusion and relevance Women have lower risk of developing ventricular fibrillation during acute myocardial infarction compared to men. However, they are less likely to receive early coronary interventions than men, possibly contributing to worse outcomes. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): French Society of Cardiology

(-)-Carvone Modulates Intracellular Calcium Signaling with Antiarrhythmic Action in Rat Hearts.

ResumoFundamento:A (-)-carvona é um monoterpeno encontrado em óleos essenciais com atividade antioxidante e anti-inflamátoria.Objetivos:O objetivo deste estudo foi analisar a propriedade antiarrítmica da (-)-carvona no coração de rato e seus efeitos sobre a sinalização de Ca+2 intracelular.Métodos:Os efeitos da (-)-carvona foram avaliados sobre a contratilidade atrial (0,01 – 4 mM) e ventricular (0,5 mM), e no eletrocardiograma (0,5mM). A fração de encurtamento, a corrente de cálcio do tipo L (ICa,L) e a sinalização de Ca+2 foram medidas no cardiomiócito isolado (0,5 mM). O efeito antiarrítmico foi avaliado no modelo de arritmia induzida por sobrecarga de cálcio (0,5 mM) (n = 5). Um p < 0,05 foi adotado como nível de significância estatística.Resultados:No átrio, a (-)-carvona causou inotropismo negativo de maneira concentração-dependente (EC50 0,44 ± 0,11 mM) e diminuiu o inotropismo positivo induzido pelo CaCl2 (0,1 – 8,0 mM) e BAY K8644 (5 - 500 nM), um agonista de canal de cálcio do tipo L. Em coração isolado, a (-)-carvona (0,5mM) reduziu a contratilidade ventricular em 73% e a frequência cardíaca (em 46%), aumentou o Pri (30,7%, tempo desde o início da onda P até a onda R) e o QTc (9,2%, uma medida de despolarização e repolarização dos ventrículos), sem mudar a duração do complexo QRS. A (-)-carvona diminuiu a fração de encurtamento (61%), a (ICa,L) (79%) e o transiente intracelular de Ca+2 (38%). Além disso, a (-)-carvona apresentou ação antiarrítmica, identificada pela redução do escore de arritmia (85%) e ocorrência de fibrilação ventricular.Conclusão:A (-)-carvona reduz a entrada de Ca+2 através de canais de Ca+2 do tipo L e, assim, diminui a contratilidade cardíaca e o Ca+2 intracelular e apresenta promissora atividade antiarrítmica no coração de ratos.

Incidence of life-threatening events in children with Wolff-Parkinson-White syndrome: Analysis of a large claims database.

Previous estimates of life-threatening event (LTE) risk in Wolff-Parkinson-White (WPW) syndrome are limited by selection bias inherent to tertiary care referral-based cohorts. This analysis sought to measure LTE incidence in children with WPW syndrome in a large contemporary representative population. A retrospective cohort study was conducted using claims data from the IBM MarketScan Research Databases, evaluating subjects with WPW syndrome (age 1-18 years) from any encounter between January 1, 2013, and December 31, 2018. Subjects with congenital heart disease and cardiomyopathy were excluded. The primary outcome was diagnosis of ventricular fibrillation (VF); a composite outcome, LTE, was defined as occurrence of VF and/or cardiac arrest. VF and LTE rates were compared to matched representative controls without WPW syndrome (3:1 ratio). The prevalence of WPW syndrome was 0.03% (8733/26,684,581) over a median follow-up of 1.6 years (interquartile range 0.7-2.9 years). Excluding congenital heart disease/cardiomyopathy, 6946 subjects were analyzed. An LTE occurred in 49 subjects (0.7%), including VF in 20 (0.3%). The incidence of VF was 0.8 events per 1000 person-years, and the incidence of LTE was 1.9 events per 1000 person-years. There were no occurrences of VF in controls; the rate of LTE was 70 times higher in subjects with WPW syndrome (0.7%; 95% confidence interval 0.5%-0.9%) than in controls (0.01%; 95% confidence interval 0%-0.02%). The use of a large claims data setallowed for an evaluation of VF and LTE risk in an unselected pediatric population with WPW syndrome. The observed range of 0.8-1.9 events per 1000 person-years is consistent with prior reports from selected populations. A comparison of event rates to matched controls confirms and quantifies the significant elevation in VF and LTE risk in pediatric WPW syndrome.

Fragmented QRS as a risk marker for the occurrence of ventricular fibrillation in patients with variant angina.

BackgroundVariant angina (VA) is caused by reversible coronary artery spasm, which is characterized by chest pain with ST‐segment elevations on standard 12‐lead electrocardiogram (ECG) at rest. Ventricular fibrillation (VF) is often caused by VA attack, but the risk stratification is not well understood. The purpose of this study was to evaluate the impact of fragmented QRS (fQRS) on VF occurrence in VA patients.MethodsNinety‐four patients who showed ST elevation on 12‐lead ECGs with total or nearly total occlusion in response to coronary spasm provocation test were enrolled. Among them, 16 patients had documented VF before hospital admission (n = 12) or experienced VF during provocation test (n = 4) (VF occurrence group). The fQRS was defined as the presence of spikes within the QRS complex of two or more consecutive leads.ResultsThe prevalence of fQRS was more often observed in the VF occurrence group than in the non‐VF occurrence group (63% [10/16] vs. 27% [21/78], p = 0.009). Univariate analyses revealed that age, history of syncope, QTc, and the presence of fQRS were associated with VF occurrence (p = 0.004, 0.005, 0.029, and 0.008, respectively). Furthermore, upon multivariate analyses using those risk factors, age, QTc, and fQRS predicted VF occurrence independently (p = 0.007, 0.041, and 0.014, respectively).ConclusionsThe present study demonstrated that fQRS in VA patients is a risk factor for VF. The fQRS may be a useful factor for the risk stratification of VF occurrence in VA patients.

Effect of Dexmedetomidine on Tachyarrhythmias After Cardiac Surgery: A Systematic Review and Meta-Analysis.

Tachyarrhythmias after cardiac surgery is a common occurrence in clinical practice, which can be life threatening. We searched 6 databases, including Embase, PubMed, Cochrane, CNKI, Wanfang, and Sinomed, to evaluate the effect of dexmedetomidine on tachyarrhythmias after adult cardiac surgery. The primary end point was the number of patients with atrial fibrillation (AF) after cardiac surgery. The secondary end points included the number of patients with supraventricular tachycardia or with ventricular tachycardia or with ventricular fibrillation or with myocardial infarction or deceased patients, the duration of mechanical ventilation, the intensive care unit stay, hospital stay, and the number of patients with bradycardia and those with hypotension. Among the 1388 retrieved studies, 18 studies (n = 3171 participants) met our inclusion criteria. Dexmedetomidine reduced the incidence of AF by 17% [relative risk (RR) = 0.83; 95% confidence interval (CI), 0.73-0.93; P = 0.002]. Through subgroup analysis, we found that when the maintenance dose of dexmedetomidine was >0.7 µg·kg-1·h-1, the effect of preventing AF was obvious (RR = 0.58; 95%CI 0.43-0.78; P = 0.0003). Dexmedetomidine also reduced the incidence of supraventricular tachycardia by approximately 70% (RR = 0.29; 95% CI, 0.11-0.77; P = 0.01) and the incidence of ventricular tachycardia by approximately 80% (RR = 0.23; 95% CI, 0.08-0.63; P = 0.004) but had no effect on ventricular fibrillation (RR = 1.02; 95% CI, 0.14-7.31; P = 0.99). The major side effect of dexmedetomidine was bradycardia. Dexmedetomidine can reduce the incidence of AF (especially high dosages), supraventricular tachycardia, and ventricular tachycardia after cardiac surgery in adults, but it does not affect the occurrence of ventricular fibrillation.

Relationship Between an Ischaemic J Wave Pattern and Ventricular Fibrillation in ST-Elevation Myocardial Infarction Patients.

BackgroundThis study determined the ischaemic J wave pattern associated with ventricular fibrillation (VF).MethodsA total of 262 patients diagnosed with ST-elevation myocardial infarction (STEMI) were recruited from October 2017 to September 2020. All data were collected and analysed, including baseline characteristics, electrocardiogram (ECG), coronary angiography (CAG), and examination outcomes.ResultsThere were 193 STEMI patients with J wave elevation but without an ischaemic J wave (NJ group) and 69 patients with an ischaemic J wave; the latter were then subgrouped into early repolarization pattern (ERP; n=62) and Brugada pattern groups (BrP [anteroseptal ERP]; n=7). Univariate and multivariate logistic regression analyses were used to clarify high-risk factors and characteristics of ischaemic J waves. Multivariate logistic regression analysis revealed that an ischaemic J wave (odds ratio [OR], 9.708; 95% CI, 2.570–36.664; P=0.01) independently predicted VF. In the subgroup analysis, BrP (OR, 31.214; 95% CI, 3.949–246.742; P=0.001), slur morphology of the ERP (OR, 8.15; 95% CI, 1.563–42.558; P<0.05), and the number of leads with an ischaemic J wave > 3 (OR, 16.174; 95% CI, 3.064–85.375; P=0.001) were significantly associated with VF occurrence after adjusting for multiple variables.ConclusionAn ischaemic J wave is an independent risk factor for VF in STEMI patients. BrP, slur morphology, and > 3 leads with an ischaemic J wave could increase the incidence of VF.

Frequency and distribution of J waves in survivors of ventricular fibrillation relationship with presence of myocardial fibrotic and or fat change and coronary arterial stenosis on cardiac CT

Abstract Background The presence and distribution of J waves, the occurrence of ventricular fibrillation (VF), and the presence of left ventricular (LV) myocardial fibrotic or fat change or coronary stenosis may be related. Purpose To determine the relationship of frequency and distribution of J waves with presence of myocardial fibrotic or fat change and coronary arterial stenosis on cardiac computed tomography (CT) in survivors of VF. Methods We conducted a retrospective analysis of 21 survivors of VF (17 males; mean age, 61±14 years) that were implanted with a cardioverter defibrillator and underwent cardiac CT. Results On ECG, four subjects had atrial fibrillation. The mean corrected QT interval was 442±39 msec. On CT, two subjects had significant coronary artery stenosis and 12 had LV myocardial fibrotic and/or fat change. The distribution of J waves were as follows: five subjects had J waves in II, III and aVF leads (three had myocardial fibrotic and/or fat change); and 2 had J waves in III lead (one had myocardial fibrotic and/or fat change). One subject each had J waves in V1 lead; V1, 2 leads; II, III, aVF and V1 leads; II, III, aVF and V1–3 leads; II, III, aVF, aVL and V1–6 leads; II, III, aVF and V1–6 leads; II, III, aVF and V4,5 leads; II, III, aVF and V2–5 leads; and III and aVF leads, respectively. The first two subjects did not have LV myocardial fibrotic and/or fat change and the remaining six subjects had myocardial fibrotic and/or fat change (Figure). Conclusions Survivors of VF with organized LV myocardial fibrotic and/or fat change showed more frequent J waves with a wider distribution (reached LV inferior wall leads) than survivors without these changes. Monitoring these characteristics on CT may be useful to predict VF. Funding Acknowledgement Type of funding sources: None. CT images of fat in a VF survivorJ waves and fibrotic and/or fat change

Presence of myocardial fibrotic or fat change on cardiac CT influences the width of distribution range of J waves in survivors of ventricular fibrillation

Abstract Background The distribution of J waves may correlate with left ventricular (LV) myocardial damage in survivors of ventricular fibrillation (VF). Purpose To determine the relationship of the distribution of J waves with presence of myocardial damage such as fibrotic or fat change on cardiac computed tomography (CT) in survivors of VF. Methods We conducted a retrospective analysis of 21 survivors of VF (17 males; mean age, 61±14 years) that were implanted with a cardioverter defibrillator and underwent cardiac CT. Results On ECG, 4 patients had atrial fibrillation and 15 had J waves. On CT, 13 patients had organized LV myocardial fibrotic and/or fat change in myocardium. The mean corrected QT interval was 453±30 and 429±48 msec in patients with and without myocardial fibrotic and/or fat change, respectively (P=0.182). The distribution of J waves was as follows: 5 had J waves in II, III and aVF leads (one had myocardial fibrotic and/or fat change) and 2 had J waves in III lead (one had myocardial fibrotic and/or fat change). One patient each had J waves in V1 lead; V1,2 leads; II, III, aVF and V1–3 leads; I, III, aVF and V1 leads; II, III, aVF, aVL and V1–6 leads; II, III, aVF and V4,5 leads; II, III, aVF and V2–5 leads; and III and aVF leads. The first one did not have myocardial fibrotic and/or fat change and the remaining 6 had myocardial fibrotic and/or fat change (Figure). If the J waves reached to ≥1 of 3 LV inferior wall leads (II, III, aVF leads) (N=13), 10 (77%) had LV myocardial fibrotic and/or fat change. If not (N=8), 3 (38%) had LV myocardial fibrotic and/or fat change (P=0.071). If the J waves reached ≥2 of 3 LV inferior wall leads (N=11), 9 (82%) had LV myocardial fibrotic and/or fat change. If not (N=10), 4 (40%) had LV myocardial fibrotic and/or fat change (P=0.049). If the J waves reached all three LV inferior wall leads (N=10), 8 (80%) had LV myocardial fibrotic and/or fat change. If not (N=11), 5 (46%) had LV myocardial fibrotic and/or fat change (P=0.104). Conclusions In survivors of VF, organized LV myocardial fibrotic and/or fat changes on cardiac CT correlate with a wider distribution range of J waves (reached to LV inferior wall leads). The distribution of J waves and the presence of myocardial fibrotic and/or fat change on CT may be useful to predict the occurrence of VF. Funding Acknowledgement Type of funding sources: None. CT fibrosis in VF survivorsJ waves and fibrotic and/or fat change

Atrial fibrillation is associated with increased risk of lethal ventricular arrhythmias

Atrial fibrillation (AF) is associated with various major adverse cardiac events such as ischemic stroke, heart failure, and increased overall mortality. However, its association with lethal ventricular arrhythmias such as ventricular tachycardia (VT), ventricular flutter (VFL), and ventricular fibrillation (VF) is controversial. We conducted this study to determine whether AF can increase the risk of VT, VFL, and VF. We utilized the Korean National Health Insurance Service database for this nationwide population-based study. This study enrolled people who underwent a nationwide health screen in 2009 for whom clinical follow-up data were available until December 2018. Primary outcome endpoint was the occurrence of VT, VFL, or VF in people who were and were not diagnosed with new-onset AF in 2009. We analyzed a total of 9,751,705 people. In 2009, 12,689 people were diagnosed with new-onset AF (AF group). The incidence (events per 1000 person-years of follow-up) of VT, VFL, and VF was 2.472 and 0.282 in the AF and non-AF groups, respectively. After adjustment for covariates, new-onset AF was associated with 4.6-fold increased risk (p < 0.001) of VT, VFL, and VF over 10 years of follow-up. The risk of VT, VFL, and VF was even higher if identification of AF was based on intensified criteria (≥ 2 outpatient records or ≥ 1 inpatient record; hazard ratio = 5.221; p < 0.001). In conclusion, the incidence of VT, VFL, and VF was significantly increased in people with new-onset AF. The potential risk of suffering lethal ventricular arrhythmia in people with AF should be considered in clinical practice.

Association between new-onset right bundle branch block and primary or secondary ventricular fibrillation in ST-segment elevation myocardial infarction.

New-onset right bundle branch block (RBBB) in myocardial infarction (MI) is often associated with ventricular fibrillation (VF) but the nature of this relationship has not been determined. Between 1998 and 2014, among other data, incidence and duration of RBBB and VF occurrence were prospectively collected in 5301 patients with ST-segment elevation MI (STEMI) admitted to two University Hospitals in Murcia (Spain). Multinomial adjusted logistic regression analyses were used to examine the association between RBBB, attending to its duration, and VF according to its primary VF (PVF) or secondary VF (SVF) character. Among 284 (5.4%) patients with new-onset RBBB, 158 were transient and 126 permanent. VF occurred in 339 (6.4%) patients, 201 PVF and 138 SVF, documented within the first 2 h of symptoms-onset in 78% and 60%, respectively. New-onset RBBB was more frequent in PVF (11.4%) and SVF (20.3%), than in non-VF (4.7%). Transient RBBB incidence was higher in PVF (9.0%) and SVF (9.4) than in non-VF (2.6%), whereas permanent RBBB was higher in SVF (10.9%) than PVF (2.5%) and non-VF (2.1%). New-onset RBBB 1.83 [95% confidence interval (CI): 1.07-3.11] and new-onset transient RBBB 2.39 (95% CI: 1.32-4.32) were independently associated with PVF. New-onset 3.03 (95% CI: 1.83-5.02), transient 2.40 (95% CI: 1.27-4.55), and permanent 2.99 (95% CI: 1.52-5.86) RBBB were independently associated with SVF. New-onset RBBB and VF in STEMI are independently associated and show particularities based on the duration of the conduction disturbance and/or the primary or secondary character of the arrhythmia.

Progressive increase in activation delay during premature stimulation is related to ventricular fibrillation in Brugada syndrome.

The local conduction delay has been deemed to play an important role in the perpetuation of ventricular fibrillation (VF) in Brugada syndrome (BrS). We evaluated the relationship between the activation delay during programmed stimulation and cardiac events in BrS patients. This study included 47 consecutive BrS patients who underwent an electrophysiological study and received implantable cardiac defibrillator therapy. We divided the patients into two groups based on whether they had developed VF (11 patients) or not (36 patients) during the follow-up period of 89 ± 53 months. The activation delay was assessed using the interval between the stimulus and the QRS onset during programmed stimulation. The mean increase in delay (MID) was used to characterize the conduction curves. The MID at the right ventricular outflow tract (RVOT) was significantly greater in patients with VF (4.5 ± 1.2 ms) than in those without VF (2.2 ± 0.9 ms) (p < .001). A receiver operating characteristics curve analysis indicated that the optimal cut-off point for discriminating VF occurrence was 3.3 with 88.9% sensitivity and 91.3% specificity. Furthermore, patients with an MID at the RVOT ≥ 3.3 ms showed significantly higher rates of VF recurrence than those with an MID at the RVOT < 3.3 ms (p < .001). The clinical characteristics, including the signal-averaged electrocardiogram measurement and VF inducibility were similar between the two groups. A prolonged MID at the RVOT was associated with VF and maybe an additional electrophysiological risk factor for VF in BrS patients.