Onset Of Ventricular Fibrillation Research Articles

Prediction and Detection of Ventricular Fibrillation Using Complex Features and AI-Based Classification

We analyzed the possibility of detecting and predicting ventricular fibrillation (VF), a medical emergency that may put people’s lives at risk, as the medical prognosis depends on the time in which medical personnel intervene. Therefore, besides immediate detection of VF, the possibility of predicting VF 40 or even 50 min in advance was analyzed. For testing the proposed algorithm, we used ECG signals taken from the MIT-BIH database, namely, Malignant Ventricular Ectopy Database, Sudden Cardiac Death Holter Database and Normal Sinus Rhythm Database. The presented method is based on features extracted from the ECG signals in the time domain, frequency domain and complexity measures. For VF detection, the possibility of identifying the VF episode in the first 3 s after its occurrence was tested. For this, the first 3 s immediately after the appearance of VF were cut out and the features were computed on these sections. For VF prediction, 3 min of the ECG signal clipped 40 or 50 min before VF onset was used. Then, on these pieces of ECG signal, the specific features were calculated for 1 s segments. For the normal signal situation, 3 min was randomly selected from the database with normal ECGs. For the classification or detection stage, both an MLP-type neural network and the classifiers from the Machine Learning toolbox of the MATLAB® environment were used. The results obtained for both detection and classification are over 94% in both cases. The novelty of our results compared to those previously obtained is the time interval with which the possibility of prediction was analyzed, namely, 50 min in advance of the VF installation date. This means that the patient will be informed that it is possible to suffer a VF and has time to take the necessary measures to overcome a possible medical emergency.

The significance of early-onset malignant arrhythmias in ST-elevation myocardial infarction patients treated with primary percutaneous coronary intervention and their relationship with biomarkers

Background/Aim. Patients who were treated with primary percutaneous coronary intervention (pPCI) and survived ventricular tachycardia (VT) and ventricular fibrillation (VF) in the first 48 hrs after ST-elevation myocardial infarction (STEMI) had, in most investigations, a similar long-term prognosis of the outcome, compared to those patients who did not have VT and VF during the first 48 hrs after STEMI. The aim of the study was to determine the association of myocardial infarction markers: creatine kinase-MB fraction (CK-MB), heart failure marker ? B-type natriuretic peptide (BNP), and systemic inflammation factor ? C-reactive protein (CRP) with early VT and VF onset, in relation to patient mortality during the first six months after STEMI. Methods. The retrospective study included 971 patients with STEMI treated with pPCI for ten years. VF and sustained VT (sVT) were detected outside of the hospital and during the first 48 hrs of hospitalization. Results. During the first 4 8 hrs from admission, 1 08 ( 11.1%) patients had life-threatening arrhythmias, of which 75 (69.4%) had VF, and 33 (30.6%) had sVT and were treated with direct current ? DC shock and intravenous amiodarone. Intrahospital mortality was significantly higher in patients with VF/sVT in the first 48 hrs compared to patients without VF/sVT (14.8% vs. 5.7%, p = 0.001). BNP level had higher accuracy in the prediction of six-month death than the maximum blood level of CRP in patients without VF/sVT after 48 hrs. However, in patients with early-onset malignant arrhythmias, BNP showed a lower level of accuracy in predicting the six-month mortality, a s did the CRP values, which had almost the same level of accuracy. Admission glycemia had a much lower predictive value in both groups of patients compared to BNP and C RP [ 0.705 ( 0.628? 0.781), p < 0.001 and 0.662 (0.521?0.803), p = 0.046, respectively]. In either of the groups, maximum CK-MB levels were not significant in predicting the six-month all-cause mortality. Conclusion. Our study indicates that STEMI patients with early onset of VF and sVT, treated with pPCI, with a high BNP level, have a statistically significantly higher mortality rate compared to patients with a lower BNP level.

Network representations of attractors for change point detection

A common approach to monitoring the status of physical and biological systems is through the regular measurement of various system parameters. Changes in a system’s underlying dynamics manifest as changes in the behaviour of the observed time series. For example, the transition from healthy cardiac activity to ventricular fibrillation results in erratic dynamics in measured electrocardiogram (ECG) signals. Identifying these transitions—change point detection—can be valuable in preparing responses to mitigate the effects of undesirable system changes. Here, we present a data-driven method of detecting change points using a phase space approach. Delay embedded trajectories are used to construct an ‘attractor network’, a discrete Markov-chain representation of the system’s attractor. Once constructed, the attractor network is used to assess the level of surprise of future observations where unusual movements in phase space are assigned high surprise scores. Persistent high surprise scores indicate deviations from the attractor and are used to infer change points. Using our approach, we find that the attractor network is effective in automatically detecting the onset of ventricular fibrillation (VF) from observed ECG data. We also test the flexibility of our method on artificial data sets and demonstrate its ability to distinguish between normal and surrogate time series.

Electropharmacological Characterization of Licorice Using the Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes Sheets and the Chronic Atrioventricular Block Dogs.

Licorice has been traditionally prescribed for palpitation, whereas its overdose has caused lethal arrhythmias including torsade de pointes. Licorice contains glycyrrhizic acid of ≥ 2% (w/w), which is hydrolyzed to glycyrrhetinic acid (GRA) in the intestine. Since their cardiac electropharmacological properties are not fully understood, we assessed them to ask mechanism of licorice-induced torsade de pointes. GRA at 0.1, 1 and 10μg/mL was cumulatively applied to the human induced pluripotent stem cell-derived cardiomyocytes sheets (n = 6). GRA shortened spontaneous activation interval and repolarization period, and decreased maximum contraction velocity, indicating Ca2+ channel blockade. It prolonged effective refractory period and post-repolarization refractoriness with a steep frequency-dependency, whereas it delayed conduction with a modest use-dependency, resembling lidocaine in the mode of Na+ channel-blocking action. Meanwhile, Kanzoto containing a decoction of licorice alone in a dose of 2 or 6g/body/day was orally administered to the conscious chronic atrioventricular block dogs for 3days (n = 4). Kanzoto prolonged QT interval with increasing its temporal dispersion, suggesting K+ channel suppression, and slightly decreased the plasma K+ concentration without inducing torsade de pointes. Moreover, it significantly suppressed atrial and idioventricular rates, leading to sinus arrest along with the onset of ventricular fibrillation in one animal, possibly due to Na+ channel blockade. These results indicate that electropharmacological profile of licorice can be explained by Na+, Ca2+ and K+ channels blockade, which may be associated with low torsadogenic risk, but might contribute to the onset of other types of lethal ventricular arrhythmias.

C2 DIFFERENT CLINICAL PREDICTORS OF EARLY AND LATE PRIMARY VENTRICULAR FIBRILLATION: RESULTS OF THE PREDESTINATION STUDY

Abstract Introduction Few studies evaluated risk factors for primary ventricular fibrillation (VF) before reperfusion during a first acute myocardial infarction (AMI). Important parameters such as kalemia, blood pressure (BP) and heart rate (HR) at presentation were rarely considered. Furthermore, potential differences according to the time elapsed between symptoms onset and VF onset have never been investigated. Objectives to evaluate predictors of primary VF in the PREDESTINATION (PRImary vEntricular fibrillation and suDden dEath during a firST myocardIal iNfArcTION) study cohort also differentiating between early (<60 min from symptoms onset) and late (>60 min) VF. Early VF is more likely to cause sudden death (SD) before medical services arrival. Patients and Methods PREDESTINATION is a prospective, multicenter, case–control (1:2 age– and sex–matched) study enrolling patients aged 18–80 years with a first AMI, either complicated (cases) or not (controls) by primary VF before reperfusion. Results 1478 patients were analysed: mean age was 59 years, 83% were male, 36% cases. The multivariate analysis (logistic regression) on the whole population (c–statistic= 0.74) identified 8 independent predictors of primary VF: atrial fibrillation as presenting rhythm (OR 4.61), kalemia ≤3.5 mEq/L (OR 2.8), HR at presentation ≥90 bpm (OR 2.25), first–degree family history of SD (OR 2.08), anterior infarct site (OR 1.54), physical inactivity (OR 1.59), systolic BP at presentation (OR 0.98 for each mmHg), and first–degree family history of coronary artery disease/myocardial infarction (OR 0.71). The time elapsed between symptoms onset and VF was known for 405 cases (184 early and 221 late VF). There were 6 predictors of early VF, with loss of significance of physical inactivity and of family history of coronary artery disease/infarction, and an increase in the OR of family history of SD to 2.85 (95% CI: 1.6–5.08), and in the c–statistic of the model to 0.80. Among the 6 predictors of late VF, on the other hand, anterior site of AMI and family history of SD were not confirmed (c–statistic of the model 0.7). Conclusions The present study identified 8 independent predictors of primary VF. First–degree family history of SD is a powerful independent predictor of early VF, but not of late VF, suggesting that genetic predisposition plays a determining role only in early–onset VF cases and therefore the advisability of a specific genetic investigation in these patients.

RESPIRATORY MECHANICS AND NEURAL RESPIRATORY DRIVE OF UNTREATED GASPING DURING CARDIAC ARREST IN A PORCINE MODEL.

Introduction: Although the effects on hemodynamics of gasping during cardiac arrest (CA) have received a lot of attention, less is known about the respiratory mechanics and physiology of respiration in gasping. This study aimed to investigate the respiratory mechanics and neural respiratory drive of gasping during CA in a porcine model. Method: Pigs weighing 34.9 ± 5.7 kg were anesthetized intravenously. Ventricular fibrillation (VF) was electrically induced and untreated for 10 min. Mechanical ventilation (MV) was ceased immediately after the onset of VF. Hemodynamic and respiratory parameters, pressure signals, diaphragmatic electromyogram data, and blood gas analysis data were recorded. Results: Gasping was observed in all the animals at a significantly lower rate (2-5 gaps/min), with higher tidal volume ( VT ; 0.62 ± 0.19 L, P < 0.01), and with lower expired minute volume (2.51 ± 1.49 L/min, P < 0.001) in comparison with the baseline. The total respiratory cycle time and the expiratory time tended to be lengthened. Statistically significant elevations in transdiaphragmatic pressure, the pressure-time product of diaphragmatic pressure, and the mean of root mean square diaphragmatic electromyogram values (RMSmean) were observed ( P < 0.05, P < 0.05, and P < 0.001, respectively); however, VT /RMSmean and transdiaphragmatic pressure/RMSmean were reduced at all time points. The partial pressure of oxygen showed a continuous decline after VF to reach statistical significance in the 10th minute (9.46 ± 0.96 kPa, P < 0.001), whereas the partial pressure of carbon dioxide tended to first rise and then fall. Conclusions: Gasping during CA was characterized by high VT , extremely low frequency, and prolonged expiratory time, which may improve hypercapnia. During gasping, increased work of breathing and insufficient neuromechanical efficacy of neural respiratory drive suggested the necessity of MV and appropriate management strategies for MV during resuscitation after CA.

Incidence, Characteristics, and Outcomes of Ventricular Fibrillation Complicating Acute Myocardial Infarction in Women Admitted Alive in the Hospital.

BackgroundLittle data are available in women presenting with ventricular fibrillation (VF) in the setting of acute myocardial infarction (AMI). We assessed frequency, predictors of VF, and outcomes, with a special focus on women compared with men.Methods and ResultsData were analyzed from the FAST‐MI (French Registry of Acute ST‐Elevation or Non‐ST‐Elevation Myocardial Infarction) program, which prospectively included 14 406 patients admitted to French cardiac intensive care units ≤48 hours from AMI onset between 1995 and 2015 (mean age, 66±14 years; 72% men; mean left ventricular ejection fraction, 52±12%; 59% with ST‐segment–elevation myocardial infarction). A total of 359 patients developed VF during AMI, including 81 women (2.0% of 4091 women) and 278 men (2.7% of 10 315 men, P=0.02). ST‐segment–elevation myocardial infarction (odds ratio [OR], 2.29 [95% CI, 1.75–2.99]; P<0.001) was independently associated with the onset of VF during AMI. In contrast, female sex (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 myocardial infarction (OR, 0.69 [95% CI, 0.50–0.96]; P=0.03) were protective factors. Women were less likely to have cardiac intervention than men (percutaneous coronary intervention during hospitalization 48.1% versus 66.9%, respectively; P=0.04) with a higher 1‐year mortality in women compared with men (50.6% versus 37.4%, respectively; P=0.03), including increased in‐hospital mortality (42.0% versus 32.7%, respectively; P=0.12). After adjustment, female sex was no longer associated with a worse 1‐year mortality (adjusted hazard ratio, 1.10 [95% CI, 0.75–1.61]; P=0.63).ConclusionsWomen have lower risk of developing VF during AMI compared with men. However, they are less likely to receive cardiac interventions than men, possibly contributing to missed opportunities of improved outcomes.

AUTOMATIC EMS ALERT WITH REAL-TIME PATIENT LOCATION AFTER WCD SHOCK DELIVERY: IMPROVING THE CHAIN OF SURVIVAL

BackgroundVentricular fibrillation (VF) commonly occurs at home and is unwitnessed. Wearable cardioverter defibrillators (WCD) are effective in terminating VF, but patients may need assistance afterwards.ObjectiveTo evaluate feasibility of a novel shock alert system linking a WCD (ASSURE® WCD system, Kestra Medical Technologies) to Emergency Medical Services (EMS).MethodsWCD shock delivery triggers creation of a shock event message via patient app including location derived from GPS, cellular and WiFi networks. The message is transferred to an emergency response data platform (ERDP) which determines physical address and associated local EMS, and displays this information to a public safety call center via web portal (Figure 1).Simulations of message transfer were performed to evaluate compliance with applicable standards for time to alarm (UL 1635 Digital Alarm Communicator System Units) and reliability of triggering devices (UL 1637 Home Health Care Signaling Equipment). A waveform generator was used to input VF into the WCD. An automated test system recorded total shocks and shock event messages received by the ERDP. Throughput was compared to the standard for rate (max missed messages 38/100,000) and time (max delay <90s).Simulated complete shock alert process duration was measured over repeated tests using a waveform generator and WCD at a remote test location.ResultsWCD delivered 8,680 shocks and transferred 8,680 (100%) shock event messages to the ERDP. Mean time to transfer was 5.2 ± 3.4 s exceeding compliance standard throughput requirements with 95% confidence.For the simulated complete shock alert process, mean time from VF onset to dispatch operator call was 57 ± 3 s in three tests.Conclusions BackgroundVentricular fibrillation (VF) commonly occurs at home and is unwitnessed. Wearable cardioverter defibrillators (WCD) are effective in terminating VF, but patients may need assistance afterwards. Ventricular fibrillation (VF) commonly occurs at home and is unwitnessed. Wearable cardioverter defibrillators (WCD) are effective in terminating VF, but patients may need assistance afterwards. ObjectiveTo evaluate feasibility of a novel shock alert system linking a WCD (ASSURE® WCD system, Kestra Medical Technologies) to Emergency Medical Services (EMS). To evaluate feasibility of a novel shock alert system linking a WCD (ASSURE® WCD system, Kestra Medical Technologies) to Emergency Medical Services (EMS). MethodsWCD shock delivery triggers creation of a shock event message via patient app including location derived from GPS, cellular and WiFi networks. The message is transferred to an emergency response data platform (ERDP) which determines physical address and associated local EMS, and displays this information to a public safety call center via web portal (Figure 1).Simulations of message transfer were performed to evaluate compliance with applicable standards for time to alarm (UL 1635 Digital Alarm Communicator System Units) and reliability of triggering devices (UL 1637 Home Health Care Signaling Equipment). A waveform generator was used to input VF into the WCD. An automated test system recorded total shocks and shock event messages received by the ERDP. Throughput was compared to the standard for rate (max missed messages 38/100,000) and time (max delay <90s).Simulated complete shock alert process duration was measured over repeated tests using a waveform generator and WCD at a remote test location. WCD shock delivery triggers creation of a shock event message via patient app including location derived from GPS, cellular and WiFi networks. The message is transferred to an emergency response data platform (ERDP) which determines physical address and associated local EMS, and displays this information to a public safety call center via web portal (Figure 1). Simulations of message transfer were performed to evaluate compliance with applicable standards for time to alarm (UL 1635 Digital Alarm Communicator System Units) and reliability of triggering devices (UL 1637 Home Health Care Signaling Equipment). A waveform generator was used to input VF into the WCD. An automated test system recorded total shocks and shock event messages received by the ERDP. Throughput was compared to the standard for rate (max missed messages 38/100,000) and time (max delay <90s). Simulated complete shock alert process duration was measured over repeated tests using a waveform generator and WCD at a remote test location. ResultsWCD delivered 8,680 shocks and transferred 8,680 (100%) shock event messages to the ERDP. Mean time to transfer was 5.2 ± 3.4 s exceeding compliance standard throughput requirements with 95% confidence.For the simulated complete shock alert process, mean time from VF onset to dispatch operator call was 57 ± 3 s in three tests. WCD delivered 8,680 shocks and transferred 8,680 (100%) shock event messages to the ERDP. Mean time to transfer was 5.2 ± 3.4 s exceeding compliance standard throughput requirements with 95% confidence. For the simulated complete shock alert process, mean time from VF onset to dispatch operator call was 57 ± 3 s in three tests. Conclusions

Role of Purkinje-muscle junction in early ventricular fibrillation in a porcine model: Beyond the trigger concept.

The role of the Purkinje network in triggering ventricular fibrillation (VF) has been studied; however, its involvement after onset and in early maintenance of VF is controversial. We studied the role of the Purkinje-muscle junctions (PMJ) on epicardial-endocardial activation gradients during early VF. In a healthy, porcine, beating-heart Langendorff model [control, n = 5; ablation, n = 5], simultaneous epicardial-endocardial dominant frequent mapping was used (224 unipolar electrograms) to calculate activation rate gradients during the onset and early phase of VF. Selective Purkinje ablation was performed using Lugol's solution, followed by VF re-induction and mapping and finally, histological evaluation. Epicardial activation rates were faster than endocardial rates for both onset and early VF. After PMJ ablation, activation rates decreased epicardially and endocardially for both onset and early VF [Epi: 9.7 ± 0.2 to 8.3 ± 0.2 Hz (p <.0001) and 10.9 ± 0.4 to 8.8 ± 0.3 Hz (p < .0001), respectively; Endo: 8.2 ± 0.3 Hz to 7.4 ± 0.2 Hz (p < .0001) and 7.0 ± 0.4 Hz to 6.6 ± 0.3 Hz (p = .0002), respectively]. In controls, epicardial-endocardial activation rate gradients during onset and early VF were 1.7 ± 0.3 Hz and 4.5 ± 0.4 Hz (p < .001), respectively. After endocardial ablation of PMJs, these gradients were reduced to 0.9 ± 0.3 Hz (onset VF, p < .001) and to 2.2 ± 0.3Hz (early VF, p <.001). Endocardial-epicardial Purkinje fiber arborization and selective Purkinje fiber extinction after only endocardial ablation (not with epicardial ablation) was confirmed on histological analysis. Beyond the trigger paradigm, PMJs determine activation rate gradients during onset and during early maintenance of VF.

Ventricular fibrillation during carotid endarterectomy and bailout stenting: a case report

BackgroundCarotid artery manipulation is not a special technique but reports of intraoperative ventricular fibrillation are rare. The risk of fatal arrhythmias may be hidden behind routine surgical techniques and anesthetic management. We focused on QT prolongation and QT dispersion.Case presentationA 77-year-old man underwent carotid endarterectomy and bailout stenting. Although there were no obvious preoperative risk factors for intraoperative ventricular tachyarrhythmia, ventricular fibrillation (VF) had occurred during a maneuver of the carotid artery under hypercapnia. QTc was prolonged from 317 ms before surgery to 458 ms before the onset of VF. QTc dispersion between leads II and III was also increased to 50 ms. Hypomagnesemia was noted after resuscitation by electrical defibrillation, adrenaline, and noradrenaline.ConclusionsWe considered that the combination of multiple risk factors led to the development of ventricular fibrillation. It should be noted that carotid artery manipulation has the potential to cause arrhythmias.

Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation.

AimsMapping data of human ventricular fibrillation (VF) are limited. We performed detailed mapping of the activities underlying the onset of VF and targeted ablation in patients with structural cardiac abnormalities.Methods and resultsWe evaluated 54 patients (50 ± 16 years) with VF in the setting of ischaemic (n = 15), hypertrophic (n = 8) or dilated cardiomyopathy (n = 12), or Brugada syndrome (n = 19). Ventricular fibrillation was mapped using body-surface mapping to identify driver (reentrant and focal) areas and invasive Purkinje mapping. Purkinje drivers were defined as Purkinje activities faster than the local ventricular rate. Structural substrate was delineated by electrogram criteria and by imaging. Catheter ablation was performed in 41 patients with recurrent VF. Sixty-one episodes of spontaneous (n = 10) or induced (n = 51) VF were mapped. Ventricular fibrillation was organized for the initial 5.0 ± 3.4 s, exhibiting large wavefronts with similar cycle lengths (CLs) across both ventricles (197 ± 23 vs. 196 ± 22 ms, P = 0.9). Most drivers (81%) originated from areas associated with the structural substrate. The Purkinje system was implicated as a trigger or driver in 43% of patients with cardiomyopathy. The transition to disorganized VF was associated with the acceleration of initial reentrant activities (CL shortening from 187 ± 17 to 175 ± 20 ms, P < 0.001), then spatial dissemination of drivers. Purkinje and substrate ablation resulted in the reduction of VF recurrences from a pre-procedural median of seven episodes [interquartile range (IQR) 4–16] to 0 episode (IQR 0–2) (P < 0.001) at 56 ± 30 months.ConclusionsThe onset of human VF is sustained by activities originating from Purkinje and structural substrate, before spreading throughout the ventricles to establish disorganized VF. Targeted ablation results in effective reduction of VF burden.Key questionThe initial phase of human ventricular fibrillation (VF) is critical as it involves the primary activities leading to sustained VF and arrhythmic sudden death. The origin of such activities is unknown.Key findingBody-surface mapping shows that most drivers (≈80%) during the initial VF phase originate from electrophysiologically defined structural substrates. Repetitive Purkinje activities can be elicited by programmed stimulation and are implicated as drivers in 37% of cardiomyopathy patients.Take-home messageThe onset of human VF is mostly associated with activities from the Purkinje network and structural substrate, before spreading throughout the ventricles to establish sustained VF. Targeted ablation reduces or eliminates VF recurrence.

Human Plasma Metabolomics Identify 9-cis-retinoic Acid and Dehydrophytosphingosine Levels as Novel biomarkers for Early Ventricular Fibrillation after ST-elevated Myocardial Infarction

ABSTRACT The relevant metabolite biomarkers for risk prediction of early onset of ventricular fibrillation (VF) after ST-segment elevation myocardial infarction (STEMI) remain unstudied. Here, we aimed to identify these imetabolites and the important metabolic pathways involved, and explore whether these metabolites could be used as predictors for the phenotype. Plasma samples were obtained retrospectively from a propensity-score matched cohort including 42 STEMI patients (21 consecutive VF and 21 non-VF). Ultra-performance liquid chromatography and mass spectrometry in combination with a comprehensive analysis of metabolomic data using Metaboanalyst 5.0 version were performed. As a result, the retinal metabolism pathway proved to be the most discriminative for the VF phenotype. Furthermore, 9-cis-Retinoic acid (9cRA) and dehydrophytosphingosine proved to be the most discriminative biomarkers. Biomarker analysis through receiver operating characteristic (ROC) curve showed the 2-metabolite biomarker panel yielding an area under the curve (AUC) of 0.836. The model based on Monte Carlo cross-validation found that 9cRA had the greatest probability of appearing in the predictive panel of biomarkers in the model. Validation of model efficiency based on an ROC curve showed that the combination model constructed by 9cRA and dehydrophytosphingosine had a good predictive value for early-onset VF after STEMI, and the AUC was 0.884 (95% CI 0.714–1). Conclusively, the retinol metabolism pathway was the most powerful pathway for differentiating the post-STEMI VF phenotype. 9cRA was the most important predictive biomarker of VF, and a plasma biomarker panel made up of two metabolites, may help to build a potent predictive model for VF.

Autoimmune Myocarditis and Arrhythmogenic Mitral Valve Prolapse: An Unexpected Overlap Syndrome

Background: both myocarditis and mitral valve prolapse (MVP) are known uncommon causes of ventricular arrhythmias in young patients. Aim: to report the first clinical case of endomyocardial biopsy (EMB)-proven autoimmune myocarditis and associated arrhythmogenic MVP in a patient with recurrent ventricular fibrillation (VF) episodes. Methods: myocarditis was diagnosed both by cardiac magnetic resonance (CMR) and EMB. Arrhythmogenic MVP was documented by transthoracic echocardiogram, CMR, and electroanatomical mapping of the trigger premature ventricular contractions (PVCs). Results: a 22-year-old woman underwent immunosuppressive therapy after EMB-proven diagnosis of autoimmune myocarditis with VF onset and early implantable cardioverter defibrillator (ICD) placement. Three years later, she experienced two VF recurrences and persistent PVCs, despite no signs of myocarditis recurrence. An echocardiogram revealed bileaflet MVP with high arrhythmic risk features. Finally, electroanatomical mapping and ablation of the trigger PVC were successfully performed. Conclusion: in patients with recurrent VF episodes despite evidence-based medical treatment for myocarditis, MVP should be considered as an alternative arrhythmogenic substrate, and warrants early ICD implant and PVC-targeted therapy.

The development of L-type Ca2+ current mediated alternans does not depend on the restitution slope in canine ventricular myocardium

Cardiac alternans have crucial importance in the onset of ventricular fibrillation. The early explanation for alternans development was the voltage-driven mechanism, where the action potential (AP) restitution steepness was considered as crucial determining factor. Recent results suggest that restitution slope is an inadequate predictor for alternans development, but several studies still claim the role of membrane potential as underlying mechanism of alternans. These controversial data indicate that the relationship of restitution and alternans development is not completely understood. APs were measured by conventional microelectrode technique from canine right ventricular papillary muscles. Ionic currents combined with fluorescent measurements were recorded by patch-clamp technique. APs combined with fluorescent measurements were monitored by sharp microelectrodes. Rapid pacing evoked restitution-independent AP duration (APD) alternans. When non-alternating AP voltage command was used, Ca2+i-transient (CaT) alternans were not observed. When alternating rectangular voltage pulses were applied, CaT alternans were proportional to ICaL amplitude alternans. Selective ICaL inhibition did not influence the fast phase of APD restitution. In this study we found that ICaL has minor contribution in shaping the fast phase of restitution curve suggesting that ICaL—if it plays important role in the alternans mechanism—could be an additional factor that attenuates the reliability of APD restitution slope to predict alternans.

Prevalence of mitral annulus disjunction and mitral valve prolapse in a multicenter cohort of idiopathic ventricular fibrillation patients

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dutch Heart Foundation Background Idiopathic ventricular fibrillation (IVF) is diagnosed in patients with sudden onset of ventricular fibrillation of which the origin is not identified after extensive evaluations. Recent studies suggest an association between mitral annulus disjunction (MAD), mitral valve prolapse (MVP) and ventricular arrhythmias[1,2]. The prevalence of MAD and MVP in IVF patients in this regard, is not well established. Purpose To explore prevalence of MAD and MVP in IVF patients. Methods In this retrospective multicenter cohort study, Cardiac Magnetic Resonance images from IVF patients (i.e., negative for ischemia, cardiomyopathy and channelopathies) and matched control subjects were analyzed for MAD (≥2mm) and MVP (&amp;gt;2mm). Results In total, 71 IVF patients (mean age 39, 59% male) and 71 controls (mean age 41, 58% male) were included. MAD in the inferolateral wall was more prevalent in IVF patients versus healthy controls (6 [10%] vs. 1 [1%], p = 0.035). MVP was only seen in IVF patients and not in controls (4 [7%] vs. 0 [0%], p = 0.037). MVP was observed both in IVF patients with (n = 3) and without (n = 1) MAD. Patients with MAD did not show papillary muscle fibrosis. Four (67%) patients with MAD showed frequent ventricular ectopy from the basal myocardial region. Conclusion Inferolateral MAD and MVP were significantly more prevalent in IVF patients compared to healthy controls (figure). This is in line with previous studies suggesting a correlation between mitral valve disease and IVF. Our findings support further exploration of the pathophysiological mechanisms underlying a subset of IVF that associates with MAD and MVP.

Echocardiographic deformation imaging unmasks global and regional mechanical dysfunction in patients with idiopathic ventricular fibrillation: A multicenter case-control study

Idiopathic ventricular fibrillation (IVF) is diagnosed in patients with sudden onset of ventricular fibrillation of unidentified origin. New diagnostic tools that can detect subtle abnormalities are needed to diagnose and treat patients with an underlying substrate. The purpose of this study was to explore echocardiographic deformation characteristics in IVF patients. Echocardiograms were analyzed with deformation imaging by 2-dimensional speckle tracking. Global and regional measurements of the left ventricle (LV) and right ventricle (RV) were performed. Regional LV deformation patterns were evaluated for the presence of postsystolic shortening. Regional RV deformation patterns were classified as type I (normal) or type II/III (abnormal). In total, 47 IVF patients (mean age 45 years; left ventricular ejection fraction [LVEF] 56%) and 47 healthy controls (mean age 41 years; LVEF 60%) were included. IVF patients showed more global deformation abnormalities as indicated by lower LV global longitudinal strain (18.5% ± 2.6% vs 21.6% ± 1.8%; P <.001) and higher LV mechanical dispersion (41 ± 12 ms vs 26 ± 6 ms; P <.001). In addition, IVF patients showed more regional LV postsystolic shortening compared to healthy controls (50% vs 11%; P <.001). Abnormal RV deformation patterns were observed in 16% of IVF patients and in none of the control subjects (P <.001). We were able to show both regional and global echocardiographic deformation abnormalities in IVF patients. This study provides evidence that localized myocardial disease is present in a subset of IVF patients.

Short-coupled ventricular fibrillation represents a distinct phenotype among latent causes of unexplained cardiac arrest: a report from the CASPER registry.

The term idiopathic ventricular fibrillation (IVF) describes survivors of unexplained cardiac arrest (UCA) without a specific diagnosis after clinical and genetic testing. Previous reports have described a subset of IVF individuals with ventricular arrhythmia initiated by short-coupled trigger premature ventricular contractions (PVCs) for which the term short-coupled ventricular fibrillation (SCVF) has been proposed. The aim of this article is to establish the phenotype and frequency of SCVF in a large cohort of UCA survivors. We performed a multicentre study including consecutive UCA survivors from the CASPER registry. Short-coupled ventricular fibrillation was defined as otherwise unexplained ventricular fibrillation initiated by a trigger PVC with a coupling interval of <350 ms. Among 364 UCA survivors, 24/364 (6.6%) met diagnostic criteria for SCVF. The diagnosis of SCVF was obtained in 19/24 (79%) individuals by documented ventricular fibrillation during follow-up. Ventricular arrhythmia was initiated by a mean PVC coupling interval of 274 ± 32 ms. Electrical storm occurred in 21% of SCVF probands but not in any UCA proband (P < 0.001). The median time to recurrent ventricular arrhythmia in SCVF was 31 months. Recurrent ventricular fibrillation resulted in quinidine administration in 12/24 SCVF (50%) with excellent arrhythmia control. Short-coupled ventricular fibrillation is a distinct primary arrhythmia syndrome accounting for at least 6.6% of UCA. As documentation of ventricular fibrillation onset is necessary for the diagnosis, most cases are diagnosed at the time of recurrent arrhythmia, thus the true prevalence of SCVF remains still unknown. Quinidine is effective in SCVF and should be considered as first-line treatment for patients with recurrent episodes.

Optimal Length of Heart Rate Variability Data and Forecasting Time for Ventricular Fibrillation Prediction Using Machine Learning.

Ventricular fibrillation (VF) is a cardiovascular disease that is one of the major causes of mortality worldwide, according to the World Health Organization. Heart rate variability (HRV) is a biomarker that is used for detecting and predicting life-threatening arrhythmias. Predicting the occurrence of VF in advance is important for saving patients from sudden death. We extracted features from seven HRV data lengths to predict the onset of VF before nine different forecast times and observed the prediction accuracies. By using only five features, an artificial neural network classifier was trained and validated based on 10-fold cross-validation. Maximum prediction accuracies of 88.18% and 88.64% were observed at HRV data lengths of 10 and 20 s, respectively, at a forecast time of 0 s. The worst prediction accuracy was recorded at an HRV data length of 70 s and a forecast time of 80 s. Our results showed that features extracted from HRV signals near the VF onset could yield relatively high VF prediction accuracies.

241 Delayed onset of ventricular fibrillation after electrical injury in a young patient with asymptomatic mitral valve prolapse

Abstract Aims The most frequent cardiovascular effects induced by electrical injury (EI) are arrhythmias, which occur mostly early after the electrical shock. A few cases of delayed malignant arrhythmias have been described, raising doubts about the helpfulness of heart monitoring after an EI. Methods and results A 46-year-old man experienced an out-of-hospital cardiac arrest four hours after receiving an electrical shock with an alternating voltage of 380 volts from high-pressure water jet cleaner. The out-of-hospital ECG displayed ventricular fibrillation, eight DC shocks were delivered, and return of spontaneous circulation was obtained after 15 minutes. ECG on admission showed bradycardia, HR 55 b.p.m., no clear P waves and prominent T waves in the precordial leads (Figure A). No coronary lesions were detected at the urgent PCI. An ABG on admission revealed lactic acidosis (LAC 18 mmol/L), mild hyperkalaemia (5.19 mmol/L) and mild renal dysfunction (serum creatinine 1.71 mg/dL). Toxicology screen was negative. During the hospital stay, the patient developed a voluminous hematoma and swelling on the right arm, site of the EI. In the following days, blood tests revealed an increase in serum creatinine (peak 4.99 mg/dL), creatine kinase (peak 46186 U/L), liver enzymes (AST peak 2859 U/L and ALT peak 1365 U/L), LDH (peak 2718 U/L) and troponin T (peak 2757 ng/L); these alterations were probably linked to rhabdomyolysis provoked by EI and acute kidney injury was secondary to myoglobinuria. The patient received fluid therapy and furosemide bolus injections. On echocardiography a myxomatous mitral valve with prolapse of both leaflets, mitral annular disjunction and severe mitral regurgitation were displayed (Figure B). Left ventricle was severely dilated with ejection fraction 69%. After improvement in renal function, a cardiac MRI was performed, which ruled out myocardial oedema and displayed subendocardial LGE at the base of the posteromedial papillary muscle (Figure C). The Heart Team opted for mitral valve surgery with P2 resection and mitral valve annuloplasty with 36 mm Carpentier-Edwards Physio II Ring. An ICD was not implanted because the electrical shock and the alteration in electrolytes were considered the primary reasons for cardiac arrest. The patient underwent a cycle of rehabilitation after the intervention and now he does not report any relevant symptom. Conclusion Our patient had bileaflet mitral valve prolapse, mitral annular disjunction and myocardial fibrosis of the papillary muscles, all of which are associated with higher risk of sudden cardiac death. This case highlights that patients with an underlying heart condition predisposing to arrhythmias should promptly seek medical care even after a mild EI for appropriate management.

Atrial natriuretic peptide accelerates onset and dynamics of ventricular fibrillation during hypokalemia in isolated rabbit hearts

BackgroundAtrial natriuretic peptide (ANP), which is released by the heart in response to acute cardiac stretch, possesses cardiac electrophysiological properties that include modulation of ion channel function and repolarization. However, data regarding whether ANP can directly modulate electrical instability or arrhythmias are largely lacking. ObjectiveThis study sought to determine whether ANP modifies onset or electrophysiological characteristics of ventricular fibrillation (VF) induced by severe hypokalemia in an isolated heart model. MethodsLangendorff-perfused rabbit hearts in the absence and presence of 10 nM ANP (n = 9 in each group) were subjected to a low potassium (K+) perfusate (1.2 mM K+). Left ventricular (LV) epicardial monophasic action potential (MAP) and pressure were monitored continuously. Incidence and time to onset of VF and dominant frequency during VF determined by spectral analysis were evaluated. ResultsANP did not alter ventricular repolarization (MAP duration) or LV pressure during perfusion with physiologic, K+-containing solution. Within the first 30 s after low K+ perfusion, ANP accelerated the onset of beat-to-beat repolarization alternans (100% vs. 33% in ANP-treated vs. non-treated hearts, p < 0.01). During low K+ perfusion, the incidence of VF did not differ between ANP-treated and non-treated hearts (8 of 9 [89%] in each group). However, VF occurred sooner (3.75 ± 0.33 vs. 5.78 ± 0.70 min, P < 0.05) and immediately after VF onset, peak dominant frequency was higher (24.1 ± 7.3 vs. 14.2 ± 2.3 Hz, P = 0.01) in ANP-treated than in non-treated hearts. ConclusionsANP accelerates initiation of VF and increases maximum dominant frequency during VF in isolated hearts subjected to severe hypokalemia.