Ventricular Fibrillation Events Research Articles

Ventricular Fibrillation Prediction and Detection: A Comprehensive Review of Modern Techniques

This review offers a detailed examination of modern ECG signal processing techniques employed in the prediction and detection of ventricular fibrillation (VF). It contains a thorough analysis of recent advancements in the field, exploring the strengths, limitations, and real-world applications of these techniques. By evaluating the current state of research, the review seeks to identify the most effective approaches and highlight key areas where further investigation is needed, ultimately guiding future research efforts toward improving VF prediction and detection. Overall, AI has shown significant potential in a range of VF-related tasks. However, real-world implementation encounters several challenges, including difficulties in accurately interpreting ECG signals, the variability in individual physiological responses, and the infrequency of ventricular fibrillation events. Additionally, there are issues related to the critical timing required for detecting VF, the presence of similar arrhythmias, the need for adaptation to new ECG devices, energy consumption concerns, and the complex process of obtaining regulatory and legislative approvals for integrating software components into medical equipment. We consider that the present work might be useful in approaching the above challenges.

Relationship between epicardial adipose tissue and ventricular fibrillation in Brugada syndrome by cardiac computed tomography analysis

Abstract Background Fibrofatty changes in the myocardium of the right ventricular (RV) to right ventricular outflow tract (RVOT) in patients with Brugada syndrome (BrS) may contribute to ventricular conduction delay and ultimately in the development of ventricular fibrillation (VF). In patients with atrial fibrillation (AF), inflammatory infiltration of epicardial adipose tissue (EAT) into the atrial muscle, along with reduced quantity and quality of EAT, has been demonstrated to be associated with the development of AF. We hypothesized that EAT in the RVOT from the RV in patients with BrS may lead to organic abnormalities in the ventricular muscle, resulting in VF. Purpose The purpose of this study was to evaluate the quantity and quality of EAT in patients with BrS using cardiac computed tomography (CT) and to determine the relationship with the occurrence of VF. Methods We retrospectively evaluated 61 of 82 patients with BrS regularly followed in our outpatient clinic from January 2000 to December 2023, who underwent cardiac CT scans. Patients were divided into two groups: those with VF events during follow-up (VF event group) and those without events (VF non-event group). Patient background, various parameters, volume of epicardial adipose tissue (EAT), and CT values from cardiac CT scans were compared between the two groups. EAT volume and CT values were measured for the entire heart and four specific regions: right ventricle (RV-EAT), right ventricular outflow tract (RVOT) to pulmonary artery bifurcation (RVOT-EAT), left ventricle (LV-EAT), and the left coronary artery main trunk circumference (LV summit-EAT) were measured for four specific sites. Results Median age at first diagnosis of BrS was 43 years, 98% were male patients, 41 patients (71%) had symptomatic BrS, and 18 patients (31%) had a family history. During a median follow-up of 72 months (30-136 months), 22 patients (38%) had VF events, including 2 arrhythmic sudden deaths. The median time from diagnosis to the first VF event was 14.3 months (4.3-24.5 months). The VF event group had more overall EAT volume (98.3 cm3 [range: 77.4 to 120.3 cm3] vs. 70.1 cm3 [range: 53.8 to 98.0 cm3], P=0.02) and significantly more RV-EAT volume (18.4 cm3 [range: 11.5 to 28.0 cm3] vs. 11.0 cm3 [range: 7.9 to 18.3 cm3], P=0.008). The CT value of RV-EAT was significantly lower in the VF event group (-83.1±6.1 vs -78.0±6.2, P=0.003), although the RV-EAT/LV-EAT density ratio was not different between the two groups (1.01±0.05 vs 0.99±0.07, P=0.14). On the other hand, the density ratio of RVOT-EAT/LV-EAT was significantly lower in the VF event group (0.95±0.08 vs. 1.00±0.08, P=0.03). Conclusions EAT analysis via CT in patients with BrS revealed that those experiencing VF events during follow-up tended to exhibit greater RV-EAT volume, lower CT values of RV-EAT, and higher CT values of RVOT-EAT density. These findings suggest EAT involvement in VF occurrence in patients with BrS.

Validation of novel risk prediction models in patients with Brugada syndrome: A multicenter study in Japan

BackgroundRisk stratification in patients with Brugada syndrome (BrS) is challenging, especially in those at intermediate risk. The Predicting Arrhythmic evenT (PAT) score has recently been demonstrated to be excellent for predicting future arrhythmic events in patients without prior ventricular fibrillation (VF). However, validation studies are lacking. ObjectiveThis study aimed to assess the performance of a novel risk stratification model in predicting future VF events in patients with BrS in a Japanese multicenter cohort. MethodsThe PAT score was calculated for 413 patients with BrS (mean age, 50.9 ± 13.6 years; 395 men) from 59 hospitals in Japan, including 314 patients without prior VF. The incidence of developing VF during the follow-up period was investigated. ResultsDuring the 106.8-month follow-up period, 54 patients (13.1%) experienced VF events. Of the 314 patients without prior VF at enrollment, 14 (4.5%) experienced VF events. The incidence of VF events during the follow-up period was significantly higher in patients with PAT scores ≥ 10 than in those with scores < 10 (41/173 [23.7%] vs 13/240 [5.4%]; P < .0001) in the total cohort. No difference was observed in the incidence of VF events between patients with PAT scores ≥ 10 and < 10 among the 314 patients without prior VF (6/86 [7.0%] vs 8/228 [3.5%]; P = .22). PAT scores ≥ 10 predicted future VF events with a sensitivity and specificity of 42.9% and 73.3%, respectively. ConclusionThis Japanese multicenter registry demonstrated that the novel risk stratification model could not accurately predict future VF events in patients with BrS but without prior VF.

Ertugliflozin to Reduce Arrhythmic Burden in Patients with ICDs/CRT-Ds

BackgroundSodium–glucose cotransporter 2 inhibitors (SGLT2is) have beneficial pleiotropic effects, contributing to improved cardiovascular and renal outcomes for patients with and without diabetes. The impact of SGLT2is on arrhythmic burden remains largely unexplored through randomized trials.MethodsIn this multicenter, double-blind, randomized, placebo-controlled trial, we investigated the effects of ertugliflozin on arrhythmic burden among patients with heart failure with an ejection fraction less than 50%. All patients had an implantable cardioverter–defibrillator (ICD) with or without a cardiac resynchronization therapy device (CRT-D) and were randomized (1:1) to receive either ertugliflozin 5 mg once daily or placebo. The primary end point was the number of incident sustained (>30 seconds) ventricular tachycardia or ventricular fibrillation events from baseline to week 52. Secondary end points included the total number of non-sustained ventricular tachycardias, appropriate ICD therapies, changes in N-terminal pro-brain–type natriuretic peptide (NTproBNP) levels, and the number of heart failure hospitalizations.ResultsRandomization was prematurely terminated, after class IA guideline recommendations were published for SGLT2is in patients with heart failure regardless of the ejection fraction. The final analysis included 46 patients (11% of the originally planned sample size). The yearly rate of the primary end point was 3.5 (95% confidence interval [CI] 2.8 to 4.4) with ertugliflozin compared with 13.3 with placebo (95% CI 11.8 to 14.8; rate ratio 0.16, 95% CI 0.04 to 0.61; P<0.001). There were no apparent differences in appropriate ICD therapies, hospitalizations, NTproBNP levels, or predefined adverse and serious adverse events.ConclusionsErtugliflozin reduced sustained ventricular tachycardia or ventricular fibrillation events in adults with heart failure and an ICD compared with placebo; however, our trial ended early and thus results should be interpreted with caution. (Funded by Investigator-initiated Studies Program of Merck Sharp & Dohme Corp and Pfizer; EudraCT number, 2020-002581-14; ClinicalTrials.gov number NCT04600921.)

Machine learning for prediction of ventricular arrhythmia episodes from intracardiac electrograms of automatic implantable cardioverter-defibrillators

BackgroundDespite effectiveness of the implantable cardioverter-defibrillator (ICD) in saving patients with life-threatening ventricular arrhythmias (VAs), the temporal occurrence of VA after ICD implantation is unpredictable. ObjectiveThe study aimed to apply machine learning (ML) to intracardiac electrograms (IEGMs) recorded by ICDs as a unique biomarker for predicting impending VAs. MethodsThe study included 13,516 patients who received Biotronik ICDs and enrolled in the CERTITUDE registry between January 1, 2010, and December 31, 2020. Database extraction included IEGMs from standard quarterly transmissions and VA event episodes. The processed IEGM data were pulled from device transmissions stored in a centralized Home Monitoring Service Center and reformatted into an analyzable format. Long-range (baseline or first scheduled remote recording), mid-range (scheduled remote recording every 90 days), or short-range predictions (IEGM within 5 seconds before the VA onset) were used to determine whether ML-processed IEGMs predicted impending VA events. Convolutional neural network classifiers using ResNet architecture were employed. ResultsOf 13,516 patients (male, 72%; age, 67.5 ± 11.9 years), 301,647 IEGM recordings were collected; 27,845 episodes of sustained ventricular tachycardia or ventricular fibrillation were observed in 4467 patients (33.0%). Neural networks based on convolutional neural networks using ResNet-like architectures on far-field IEGMs yielded an area under the curve of 0.83 with a 95% confidence interval of 0.79–0.87 in the short term, whereas the long-range and mid-range analyses had minimal predictive value for VA events. ConclusionIn this study, applying ML to ICD-acquired IEGMs predicted impending ventricular tachycardia or ventricular fibrillation events seconds before they occurred, whereas midterm to long-term predictions were not successful. This could have important implications for future device therapies.

Ventricular Arrhythmias After Primary Percutaneous Coronary Intervention for STEMI

Currently, mortality risk for patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) with an uncomplicated postprocedure course is low. Less is known regarding the risk of in-hospital ventricular tachycardia (VT) and ventricular fibrillation (VF). To evaluate the risk of late VT and VF after primary PCI for STEMI. This cohort study included adults aged 18 years or older with STEMI treated with primary PCI between January 1, 2015, and December 31, 2018, identified in the US National Cardiovascular Data Registry Chest Pain-MI Registry. Data were analyzed from April to December 2020. Multivariable logistic regression was used to evaluate the risk of late VT (≥7 beat run of VT during STEMI hospitalization ≥1 day after PCI) or VF (any episode of VF≥1 day after PCI) associated with cardiac arrest and associations between late VT or VF and in-hospital mortality in the overall cohort and a cohort with uncomplicated STEMI without prior myocardial infarction or heart failure, systolic blood pressure less than 90 mm Hg, cardiogenic shock, cardiac arrest, reinfarction, or left ventricular ejection fraction (LVEF) less than 40%. A total of 174 126 eligible patients with STEMI were treated with primary PCI at 814 sites in the study; 15 460 (8.9%) had VT or VF after primary PCI, and 4156 (2.4%) had late VT or VF. Among the eligible patients, 99 905 (57.4%) at 807 sites had uncomplicated STEMI. The median age for patients with late VT or VF overall was 63 years (IQR, 55-73 years), and 75.5% were men; the median age for patients with late VT or VF with uncomplicated STEMI was 60 years (IQR, 53-69 years), and 77.7% were men. The median length of stay was 3 days (IQR, 2-7 days) for the overall cohort with late VT or VF and 3 days (IQR, 2-4 days) for the cohort with uncomplicated STEMI with late VT or VF. The risk of late VT or VF was 2.4% (overall) and 1.7% (uncomplicated STEMI). Late VT or VF with cardiac arrest occurred in 674 patients overall (0.4%) and in 117 with uncomplicated STEMI (0.1%). LVEF was the most significant factor associated with late VT or VF with cardiac arrest (adjusted odds ratio [AOR] for every 5-unit decrease ≤40%: 1.67; 95% CI, 1.54-1.85). Late VT or VF events were associated with increased odds of in-hospital mortality in the overall cohort (AOR, 6.40; 95% CI, 5.63-7.29) and the cohort with uncomplicated STEMI (AOR, 8.74; 95% CI, 6.53-11.70). In this study, a small proportion of patients with STEMI treated with primary PCI had late VT or VF. However, late VT or VF with cardiac arrest was rare, particularly in the cohort with uncomplicated STEMI. This information may be useful when determining the optimal timing for hospital discharge after STEMI.

Risk stratification for the occurrence of ventricular fibrillation in patients with early repolarization syndrome

BackgroundSeveral signs of malignant early repolarizations have been proposed in patients with early repolarization syndrome (ERS). However, reports have challenged the efficacy of these signs in predicting future ventricular fibrillation (VF) in patients with ERS. ObjectiveThis study aimed to assess the predictive value of various electrocardiogram (ECG) markers for future VF events in patients with ERS. MethodsWe retrospectively evaluated the clinical characteristics of 44 patients with ERS to identify risk factors for VF during follow-up. ResultsAfter the initial event, 16 patients experienced VF (VF group), whereas 28 did not (non-VF group). The VF group had a longer QRS interval, more fragmented QRS (fQRS), and a higher T/R voltage ratio than the non-VF group. Wide J waves were more prevalent in the VF group; however, other J-wave markers did not differ between the groups. Positive late potentials recorded on signal-averaged ECGs were more frequent in the VF group. Whereas none of the patients showed spontaneous Brugada syndrome on ECG, the VF group frequently exhibited pilsicainide-induced ST-segment elevation. These ECG markers were significantly associated with the occurrence of VF during follow-up. Patients with multiple ECG factors, including QRS abnormalities (wide QRS or fQRS), wide J waves, and a high T/R ratio, had a worse prognosis than patients without multiple factors, effectively stratifying patient risk. ConclusionThe occurrence of VF in patients with ERS may be associated with conduction abnormalities such as QRS widening, fQRS, high T/R ratio, positive late potentials, and pilsicainide test results. Therefore, ECG factors could be useful in identifying high-risk patients.

High-risk Brugada syndrome: factors associated with arrhythmia recurrence and benefits of epicardial ablation in addition to implantable cardioverter defibrillator implantation.

This study aims to evaluate the prognostic impact of the arrhythmogenic substrate size in symptomatic Brugada syndrome (BrS) as well as to validate the long-term safety and effectiveness of epicardial radiofrequency ablation (RFA) compared with no-RFA group. In this prospective investigational long-term registry study, 257 selected symptomatic BrS patients with implantable cardioverter defibrillator (ICD) implantation were included. Among them, 206 patients underwent epicardial RFA and were monitored for over 5 years post-ablation (RFA group), while 51 patients received only ICD implantation declining RFA. Primary endpoints included risk factors for ventricular fibrillation (VF) events pre-ablation and freedom from VF events post-ablation. In the RFA group, BrS substrates were identified in the epicardial surface of the right ventricle. During the pre-RFA follow-up period (median 27 months), VF episodes and VF storms were experienced by 53 patients. Independent risk factors included substrate size [hazard ratio (HR), 1.13; 95% confidence interval (CI), 1.08-1.18; P < 0.001], aborted cardiac arrest (HR, 2.98; 95% CI, 1.68-5.28; P < 0.001), and SCN5A variants (HR, 2.22; 95% CI, 1.15-4.27; P = 0.017). In the post-RFA follow-up (median 40 months), the RFA group demonstrated superior outcomes compared with no-RFA (P < 0.001) without major procedure-related complications. Our study underscores the role of BrS substrate extent as a crucial prognostic factor for recurrent VF and validates the safety and efficacy of RFA when compared with a no-RFA group. Our findings highlight the importance of ajmaline in guiding epicardial mapping/ablation in symptomatic BrS patients, laying the groundwork for further exploration of non-invasive methods to guide informed clinical decision-making.

Hands-free continuous carotid Doppler ultrasound for detection of the pulse during cardiac arrest in a porcine model

Background/PurposePulse palpation is an unreliable method for diagnosing cardiac arrest. To address this limitation, continuous hemodynamic monitoring may be a viable solution. Therefore, we developed a novel, hands-free Doppler system, RescueDoppler, to detect the pulse continuously in the carotid artery. MethodsIn twelve pigs, we evaluated RescueDoppleŕs potential to measure blood flow velocity in three situations where pulse palpation of the carotid artery was insufficient: (1) systolic blood pressure below 60 mmHg, (2) ventricular fibrillation (VF) and (3) pulseless electrical activity (PEA). (1) Low blood pressure was induced using a Fogarty balloon catheter to occlude the inferior vena cava. (2) An implantable cardioverter-defibrillator induced VF. (3) Myocardial infarction after microembolization of the left coronary artery caused True-PEA. Invasive blood pressure was measured in the contralateral carotid artery. Time-averaged blood flow velocity (TAV) in the carotid artery was related to mean arterial pressure (MAP) in a linear mixed model. ResultsRescueDoppler identified pulsatile blood flow in 41/41 events with systolic blood pressure below 60 mmHg, with lowest blood pressure of 19 mmHg. In addition the absence of spontaneous circulation was identified in 21/21 VF events and true PEA in 2/2 events. The intraclass correlation coefficient within animals for TAV and MAP was 0.94 (95% CI. 0.85–0.98). ConclusionsIn a porcine model, RescueDoppler reliably identified pulsative blood flow with blood pressures below 60 mmHg. During VF and PEA, circulatory arrest was rapidly and accurately demonstrated. RescueDoppler could potentially replace unreliable pulse palpation during cardiac arrest and cardiopulmonary resuscitation.

Sympathetic nervous stimulation promotes complex rotational ventricular fibrillation events in guinea pig hearts

Sympathetic nervous stimulation promotes complex rotational ventricular fibrillation events in guinea pig hearts

Sex differences in the origin of Purkinje ectopy-initiated idiopathic ventricular fibrillation.

Purkinje ectopics (PurkEs) are major triggers of idiopathic ventricular fibrillation (VF). Identifying clinical factors associated with specific PurkE characteristics could yield insights into the mechanisms of Purkinje-mediated arrhythmogenicity. The purpose of this study was to examine the associations of clinical, environmental, and genetic factors with PurkE origin in patients with PurkE-initiated idiopathic VF. Consecutive patients with PurkE-initiated idiopathic VF from 4 arrhythmia referral centers were included. We evaluated demographic characteristics, medical history, clinical circumstances associated with index VF events, and electrophysiological characteristics of PurkEs. An electrophysiology study was performed in most patients to confirm the Purkinje origin. Eighty-three patients were included (mean age 38 ± 14 years; 44 [53%] women), of whom 32 had a history of syncope. Forty-four patients had VF at rest. PurkEs originated from the right ventricle (RV) in 41 patients (49%), from the left ventricle (LV) in 36 (44%), and from both ventricles in 6 (7%). Seasonal and circadian distributions of VF episodes were similar according to PurkE origin. The clinical characteristics of patients with RV vs LV PurkE origins were similar, except for sex. RV PurkEs were more frequent in men than in women (76% vs 24%), whereas LV and biventricular PurkEs were more frequent in women (81% vs 19% and 83% vs 17%, respectively) (P < .0001). PurkEs triggering idiopathic VF originate dominantly from the RV in men and from the LV or both ventricles in women, adding to other sex-related arrhythmias such as Brugada syndrome or long QT syndrome. Sex-based factors influencing Purkinje arrhythmogenicity warrant investigation.

The association of galectin-3 level with ventricular arrhythmias and left ventricular strain in heart failure patients with implantable cardioverter defibrillator

Background Ventricular arrhythmias are life-threatening complications of heart failure (HF). Galectin-3, an indicator of fibrosis, is associated with incident HF and was found to be related to poor prognosis in these patients. We aimed to investigate the association of galectin-3 level with left ventricular (LV) arrhythmias in HF. Methods A total of 92 non-ischaemic HF patients who had implantable cardioverter-defibrillator were included in this study. Patients were divided into two groups based on the galectin-3 level. Ventricular arrhythmic events and LV strain indices were compared between the two groups. Negative binomial regression was used to detect the independent predictors of total arrhythmic events in HF patients. Results The median age was 65 (54–71) in the high galectin-3 group (HGAL) and 62 (52–68) in the low galectin-3 group (LGAL). Ventricular arrhythmic events were more frequent in HGAL than in LGAL, including non-sustained ventricular tachycardia (VTnon), sustained-VT (VTs), and ventricular fibrillation (VF) (p < 0.0001, p = 0.002, and p = 0.026, respectively). There were no statistically significant differences between HGAL and LGAL in terms of LV strain measurements. Galectin-3 level was positively significantly correlated with total arrhythmic events (r = 0.58, p < 0.001), but no correlation was found between galectin-3 and LV global longitudinal strain (r = 0.15, p = 0.16). Galectin-3 was an independent predictor of total ventricular arrhythmic events in HF patients (p < 0.0001). Conclusion VTnon, VTs, and VF events were higher in HGAL compared to LGAL. Galectin-3 was an independent predictor of total ventricular arrhythmic events in HF patients and might be used to detect high-risk HF patients for arrhythmic events.

A Robust Percutaneous Myocardial Infarction Model in Pigs and Its Effect on Left Ventricular Function.

In this study, we created a reproducible myocardial infarction (MI) model in pigs characterized by a low mortality rate and significant changes in left ventricular function. After administering an arrhythmia prevention regimen, we created a 90-min balloon-induced percutaneous MI in 42 pigs below the first diagonal branch (D1) of the left anterior descending artery. Echocardiograms were performed before and 14 days after MI induction. Pigs with a > 30% decrease in left ventricular ejection fraction (LVEF) underwent electrophysiological mapping by the NOGA system. Our mortality rate was 4.8%. The incidence of ventricular fibrillation (VF) was 28.6%; all VF events were successfully resuscitated. At day 14, echocardiography and NOGA mapping confirmed transmural scar. LVEF decreased 41% from baseline. Radial and circumferential strain significantly decreased in the LAD distal to D1, and the LV showed dyssynchrony. An anti-arrhythmia regimen decreased mortality significantly, and our model induced dramatic functional changes. The basic procedures of the model included an arrhythmia prevention protocol and myocardial infarction creation, which effectively decreased mortality and provided a robust change in left ventricular (LV) function after 14 days.

Parenteral Antiplatelet Agents in Three Patients Receiving VA-ECMO Support to Maintain Drug-Eluting Stent Patency

Introduction The following cases summarize three patients administered intravenous (IV) antiplatelet therapy during their venoarterial-extracorporeal membrane oxygenation (VA-ECMO) support with successful maintenance of drug-eluting stent (DES) patency. Case Report A 36-year-old male was cannulated for VA-ECMO following a cardiac arrest. Subsequently, a DES to the left anterior descending (LAD) artery was placed with Impella CP® support. The patient was started on bivalirudin and eptifibatide 1 mcg/kg/min while awaiting advanced therapy decisions. The following day he was emergently evaluated for in-stent thrombosis due to rising troponin levels. The eptifibatide was changed to cangrelor 4 mcg/kg/min; however the stent was patent. Six units of packed red blood cells (PRBC) were administered prior to discontinuation of cangrelor and successful decannulation from ECMO on day 3. A 62-year-old male presented with an ST-segment elevation myocardial infarction. An Impella CP® was placed in the setting of cardiogenic shock, followed by peripheral VA-ECMO. Three DES were placed and he was initiated on ticagrelor. With a decrease in platelet and hemoglobin levels, he was switched to cangrelor 0.75 mcg/kg/min due to potential procedural intervention. The Impella CP® device was removed as platelets continued to drop. A right lower extremity compartment fasciotomy was performed. ECMO weaning was not possible, and the patient expired on hospital day 5 secondary to multisystem organ failure. A 49-year-old male with ST-segment elevations underwent percutaneous coronary intervention (PCI) with placement of two DES to the LAD. After a ventricular fibrillation event, the patient was taken back to the catheterization lab. During the procedure the patient suffered two cardiac arrests, intra-aortic balloon pump (IABP) placement, and PCI to the RCA. The patient remained unstable and was subsequently cannulated for peripheral VA-ECMO. Bivalirudin and cangrelor 0.75 mcg/kg/min were initiated while oral antiplatelet therapy was held. The following day the patient received 2 units of PRBC and the IABP was removed. On hospital day 5, bivalirudin and cangrelor infusions were stopped and ECMO was weaned successfully. Summary Eptifibatide and cangrelor appear to prevent in-stent thrombosis but may increase bleeding in patients on ECMO.

Genetic Variants and Post-Translational Modifications of Cardiac Troponin C: Insights from the Public Databases

Familial cardiomyopathy is a disease of the sarcomere that affects the structure and function in the heart and has an extreme range of phenotypes. Among the millions of affected individuals, patients with hypertrophic (HCM), dilated (DCM) or left ventricular non-compaction (LVNC) cardiomyopathy can experience functional and morphologic changes of the heart, which lead to sudden death in the most detrimental cases. TNNC1, which codes for cardiac troponin C (cTnC), is a sarcomere gene associated with cardiomyopathies in which probands exhibit young age of presentation and high death, transplant or ventricular fibrillation events relative to TNNT2 and TNNI3 probands.

Significance of Exercise-Related Ventricular Arrhythmias in Patients With Brugada Syndrome.

BackgroundSinus tachycardia during exercise attenuates ST‐segment elevation in patients with Brugada syndrome, whereas ST‐segment augmentation after an exercise test is a high‐risk sign. Some patients have premature ventricular contractions (PVCs) related to exercise, but the significance of exercise‐related PVCs in patients with Brugada syndrome is still unknown. The objective of this study was to determine the significance of exercise‐related PVCs for predicting occurrence of ventricular fibrillation (VF) in patients with Brugada syndrome.Methods and ResultsThe subjects were 307 patients with Brugada syndrome who performed a treadmill exercise test. We evaluated the occurrence of PVCs at rest, during exercise and at the peak of exercise, and during recovery after exercise (0–5 minutes). We followed the patients for 92±68 months and evaluated the occurrence of VF. PVCs occurred in 82 patients (27%) at the time of treadmill exercise test: PVCs appeared at rest in 14 patients (4%), during exercise in 60 patients (20%), immediately after exercise (0–1.5 minutes) in 28 patients (9%), early after exercise (1.5–3 minutes) in 18 patients (6%), and late after exercise (3–5 minutes) in 12 patients (4%). Thirty patients experienced VF during follow‐up. Multivariable analysis including symptoms, spontaneous type 1 ECG, and PVCs in the early recovery phase showed that these factors were independently associated with VF events during follow‐up.ConclusionsPVCs early after an exercise test are associated with future occurrence of VF events. Rebound of vagal nerve activity at the early recovery phase would promote ST‐segment augmentation and PVCs in high‐risk patients with Brugada syndrome.

A comprehensive guide to genetic variants and post-translational modifications of cardiac troponin C.

Familial cardiomyopathy is an inherited disease that affectsthe structure and function of heartmuscle and has an extreme range of phenotypes. Among the millions of affected individuals, patients with hypertrophic (HCM), dilated (DCM), or left ventricular non-compaction (LVNC) cardiomyopathy can experience morphologic changes of the heart which lead to sudden death in the most detrimental cases. TNNC1, the gene that codes for cardiac troponin C (cTnC), is a sarcomere gene associated with cardiomyopathies in which probands exhibit young age of presentation and high death, transplant or ventricular fibrillation events relative to TNNT2 and TNNI3 probands. Using GnomAD, ClinVar, UniProt and PhosphoSitePlus databases and published literature, an extensive list to date of identified genetic variants in TNNC1 and post-translational modifications (PTMs) in cTnC was compiled. Additionally, a recent cryo-EM structure of the cardiac thin filament regulatory unit was used to localize each functionally studied amino acid variant and each PTM (acetylation, glycation, s-nitrosylation, phosphorylation) in the structure of cTnC. TNNC1 has a large number of variants (> 100) relative to other genes of the same transcript size. Surprisingly, the mapped variant amino acids and PTMs are distributed throughout the cTnC structure. While many cardiomyopathy-associated variants are localized in α-helical regions of cTnC, this was not statistically significant χ2 (p = 0.72). Exploring the variants in TNNC1 and PTMs of cTnC in the contexts of cardiomyopathy association, physiological modulation and potential non-canonical roles provides insights into the normal function of cTnC along with the many facets of TNNC1 as a cardiomyopathic gene.

Mechanism of spontaneous initiation of ventricular fibrillation in patients with implantable defibrillators.

To improve the mechanistic understanding of spontaneous initiation of ventricular fibrillation (VF), we characterized the patterns of premature ventricular complex (PVC) preceding spontaneous VF in primary and secondary implantable cardioverter-defibrillator (ICD) recipients. A single-center, cross-sectional analysis of 1209 patients with primary and secondary prevention ICD identified 190 patients who received ICD therapy (firing or antitachycardia pacing) for VF or monomorphic ventricular tachycardia (MMVT). Initiation was quantified by the coupling interval (CI), the cycle length immediately preceding the CI (CL(-1)), the CI corrected by CL(-1) using Fridericia's formula (CIc), and the prematurity index (PI). In both VF (n = 44; 23%) and MMVT (n = 134; 71%), the most common pattern of initiation was late-coupled PVC, followed by the short-long-short pattern. The parameters such as pre-initiation median CL, CL(-1), CI, and PI were not significantly different between VF and MMVT for any patterns. At least some events (45% of VF and 63% of MMVT) had extremely long CIs beyond the QTc cut-off estimated from the CL(-1), suggestive of initiation by a train of multiple PVCs or nonsustained VT instead of a single PVC. Some spontaneous VF events in ICD recipients appear to be initiated by a train of multiple PVC or nonsustained VT rather than a single PVC. This finding indicates that patterns of a single PVC are not an important determinant of VF initiation and thus account for conflicting results in previous studies.

Intra-day change in occurrence of out-of-hospital ventricular fibrillation in Japan: The JCS-ReSS study

BackgroundReal-world evidence of out-of-hospital ventricular fibrillation (VF), especially regarding intra-day change, remains unclear. We aimed to investigate that age- and gender-dependent difference of intra-day change of VF occurrence. MethodWe enrolled 71,692 patients (males: 56,419 [78.7%], females: 15,273 [21.3%]) in whom cardiac VF had been documented from the 2005–2015 All-Japan Utstein Registry data. Subjects were divided into four groups: group-I (<18 years old), group-II (18–39), group-III (40–69), and group-IV (≥70). Among four groups in each of male and female, we compared the intra-day change of VF occurrence, and evaluated the risk factors of the unfavorable neurologic outcomes at 1 month after VF. ResultsRegardless of age, the incidence of VF was significantly greater in male than in female subjects. In male subjects, VF in group-I, III and IV occurred higher at daytime, however, group-II had no intra-day difference because group-II had a higher VF events at midnight~ early morning compared with other aged groups (Poisson regression analysis, p = .03). While in female, each group showed similar intra-day pattern of VF occurrence. Logistic regression analysis revealed that some of the clinical parameters such as time periods from call receipt to first shock and the presence of bystander cardiopulmonary resuscitation were important for risk of 30-day neurologically unfavorable outcomes. ConclusionsThe intra-day change of VF occurrence was age-dependently different in males but not in females, suggesting age- and gender-dependent differences in underlying cardiac diseases. These might affect the significant difference in unfavorable neurologic outcome.

Veno-arterial extracorporeal membrane oxygenation for electrical injury induced cardiogenic shock support: a case report

BackgroundHigh voltage electrical injury (HVEI) of more than 1000 V is a potentially devastating form of a multisystem injury associated with high morbidity and mortality.We present the first case of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) as a life saving device for treating a patient with severe cardiogenic shock after a high voltage electrical injury.Case presentationA 26-year-old male sustained HVEI while working with a concrete mixer pump that came in contact with a high voltage cable of 10,000 V. He was immediately disconnected from the mixer pump, underwent cardiopulmonary resuscitation and was transported to the nearest medical centre with severe cardiogenic shock with an ejection fraction (EF) of < 10%.Upon arrival, he was in critical condition, sedated and mechanically ventilated, haemodynamically unstable and supported by intravenous (IV) inotropes after a few events of ventricular fibrillation, with an electrical entry point on the left hand and an exit point located on his right leg. Blood pH was 6.8, PCO2 53 mmHg, PaO2 of 57 mmHg, lactate 8 mmol/L, and Troponin 38,000 ng/dl. The EF was 10% with global severe left ventricular dysfunction. During cardiopulmonary resuscitation (CPR), including cardiac massage and few electrical shocks, he was immediately connected to the VA-ECMO via open right femoral approach with distal arterial leg perfusion.He was treated with IV broad spectrum antibiotics, and high volume fluids to prevent rhabdomyolysis-induced acute kidney injury, total parenteral nutrition, topical silver sulfadiazine cream, and Granuflex for severe electrical burns. He was gradually weaned from inotropes over the next 3 days, during which his clinical condition and bloodwork improved tremendously. His EF gradually increased to 50% and he was weaned from the VA-ECMO, and underwent decannulation 86 h after initialization. He was discharged on day 27 without any sequelae.ConclusionThe VA-ECMO treatment can be a lifesaving device for treating severe cardiogenic shock caused by high voltage electrical injury, and should be considered while treating these “high-mortality risk” patients.