Ventricular Fibrillation Group Research Articles

Abstract Su306: Impact of Ventricular Fibrillation on Myocardial Infarct Size: A Clinical and Experimental Study

Background: Ventricular fibrillation (VF) - induced cardiac arrest is a frequent complication of ST-segment elevation myocardial infarction (STEMI). Although larger infarct sizes (IS) are associated with a higher risk of VF, there has been no investigation into the influence of VF itself on IS. To address this knowledge gap, we analyzed the impact of VF on IS in patients and 2 experimental models. Methods: From the prospective cohort HIBISCUS-STEMI, 30 STEMI patients with VF were matched on common determinants of IS in a 1:2 ratio with patients without VF. The primary endpoint was IS, assessed using the 48-hour area under the curve (AUC) for troponin. We compared IS in pigs with/without spontaneous VF during STEMI (n=15/group), and in an isolated rat heart model of acute myocardial infarction with/without electrically induced VF (n=7/group); IS was assessed using the ratio of the area of necrosis (AN) to the area at risk (AAR). Results: While patient characteristics were similar after matching (including AAR), IS was 33% lower in the VF group than in the control group (troponin AUC 1.6 [0.5-3.3] 10 6 vs. 2.4 [0.9-4.1] 10 6 arbitrary units; p=0.049). In pigs, IS was lower (p<0.01) in the VF group (24% [11-40]) than in controls (71% [48-75]). In the isolated heart model, IS was lower (p<0.05) in the VF group (9% [7-15]) than in controls (42% [38-44]). Conclusion: When common determinants of IS are comparable, the occurrence of VF prior to MI reperfusion is associated with significantly smaller IS.

Ventricular parasystole as a new indicator suggesting ventricular arrhythmias in cardiac sarcoidosis

Abstract Background In cardiac sarcoidosis (CS), it is considered that inflammation occurs in localized areas such as the basal septum. Inflammation has been suggested to be associated with ventricular fibrillation (VF). Meanwhile, ventricular parasystole is strongly associated with VF in non-ischemic cardiomyopathy. However, the relationship between CS and ventricular parasystole remains unclear. Purpose The purpose is to examine the frequency of parasystole in cases of VF and ventricular tachycardia (VT) in CS, and whether there is a correlation between the inflammatory activity of sarcoidosis and the origin of ventricular parasystole. Methods We evaluated ventricular arrhythmias (VA) in a cohort of 213 consecutive cases diagnosed with CS from 1989 to 2021 (median age 69 years, 104 males, median LVEF 36%) in our center. We investigated parasystole in cases that developed VA, using 5,313 electrocardiograms, 94 Holter electrocardiograms, and 3,174 ICD interrogation records. Classic parasystole is defined as three ventricular ectopic beats with the same morphology at a fixed interval but different coupling intervals (CI) in a 10-second continuous ECG. A new definition of parasystole requires two ventricular ectopic beats with a CI difference of more than 120ms. We also investigated the correlation of the inflammation site with ECG morphology. Results VAs were observed in 95 individuals (33.7%), and 22 developed VF (23.2%). In the VF group, parasystole was observed in 12 of 22 individuals (classic: 5, new: 7), and in the VT group observed in 20 of 73 individuals (classic: 5, new: 15), with parasystole being significantly more frequent in the VF group (P=0.018) and classic parasystole (P=0.033). In VF patients with recorded 12-lead ECGs of parasystole, the inflammation site on PET within 3 months of the VA and PVC origin matched in all 4 out of 4 cases, but no VF starting from ventricular parasystole ectopic beats was recorded. Conclusion Ventricular parasystole was detected in 54.5% of CS patients with VF. There is a possibility that the presence of parasystole and the inflammatory activity in the CS can predict the occurrence of VF.

Efficacy of percutaneous stellate ganglion block according to ventricular arrhythmia cycle length: a post-hoc sub-analysis of the STAR study

Abstract Background Percutaneous stellate ganglion block (PSGB) is an effective treatment for patients with electrical storm (ES). However, literature is scarce about a possible relation between ventricular arrhythmias’ cycle length and the effectiveness extent of PSGB. Purpose To assess whether the PSGB efficacy is affected by the arrhythmias’ cycle length prior to the procedure. Methods This is a post-hoc sub-analysis of the STAR study (STellate ganglion block for Arrythmic stoRm), a multicentre observational study aimed to assess PSGB’s effectiveness and safety in ES patients [1]. According to both the type and the median cycle of the latest ventricular arrhythmia before PSGB we considered 3 groups: ventricular fibrillation (VF), fast ventricular tachycardia (VT) and slowVT. The primary outcome is the number of treated arrhythmic episodes (with ATPs and/or DC-shocks) in the hour immediately after the PSGB as compared to the hour immediately before. The secondary outcome was the extent of the reduction of the number of ATPs/DC-shocks delivered from the hour before to the hour immediately after the PSGB. Results The original study included 184 PSGBs performed on 131 patients. We excluded 32 PSGBs with a continuous infusion and 13 PSGBs with an unknown VT cycle. The median VT cycle was 375 msec, so the final dataset of 139 PSGBs from 112 patients was divided as follows: 51 VF; 44 fastVT (VT cycle <375 msec) and 44 slowVT (VT cycle ≥375 msec). The number of treated arrhythmic episodes in the first hour after every PSGB was significantly lower compared to the first hour before in all the three groups [VF: 0 (IQR, 0-1) vs 5 (IQR, 2-8), p<0.001; fastVT: 0 (IQR, 0-0) vs 1 (IQR, 0-6.5), p<0.001; slowVT: 0 (IQR, 0-0) vs 1 (IQR, 0-4.5), p=0.001] (Figure 1). The Hodges-Lehman median difference of treated arrhythmic episodes between the hour after and before the PSGB was significantly higher in VF group [-4 (-3 to -6)] than in the fast-VT [-2 (-1 to -4)] and slow-VT [-1 (0 to -2.5)] (Figure 2). Analysing the reduction (delta less than zero) of the number of ATPs/DC-shocks from the hour before to the hour immediately after the PSGB, a significant trend was observed across the three groups (Jonckheere-Terpstra trend p<0.001) and a significant difference was observed comparing slow-VT vs VF [0 (IQR, -3 to 0) vs -4 (IQR, -7 to -1)] and fast-VT versus VF [-1 (IQR, -4.5 to 0) vs -4 (IQR, -7 to -1)], but not comparing slow-VT versus fast-VT [0 (IQR, -3 to 0) vs -1 (IQR, -4.5 to 0)]. VF was a predictor of the reduction of treated arrhythmic episodes at univariable analysis and after correction for the number of treated arrhythmic episodes in the hour immediately before PSGB and of left ventricular ejection fraction (OR 7.8, 95%CI 2.1-28.6). Conclusion PSGB is an effective treatment for ES in patients with all type of ventricular arrhythmias. However, its effectiveness was more pronounced in patients with VF or rapid ventricular tachycardia.

T-wave Peak-to-End Changes Quantified by Time-Warping Predicts Ventricular Fibrillation in a Porcine Myocardial Infarction Model.

The T-peak-to-T-end ( Tpe) interval has shown potential in predicting ventricular arrhythmic risk. It is an appealing index to be measured during ischemia since it is less influenced by ST-segment changes than the early part of the T wave. A time-warping-based index, derived from a spatially transformed PCA lead, [Formula: see text], quantifying changes in the Tpe morphology, has previously demonstrated utility in tracking repolarization changes induced by a 5-minute ischemia model in humans. The value of [Formula: see text] as a predictor of ventricular fibrillation (VF) episodes is assessed in a porcine model of myocardial ischemia with ischemia maintained for 40 minutes. From 32 pigs undergoing a coronary occlusion, pre-occlusion and occlusion ECG recordings from 10 pigs suffering a VF episode after 10 min of occlusion (Delayed VF) and 16 that did not had any episode during the recording were analyzed. The [Formula: see text] series was measured by comparing Tpe morphologies at different stages of the occlusion relative to the peak-to-end morphology of a baseline T-wave. During baseline, [Formula: see text] remained stationary with an intra-recording median [IQR] value of 1.60 [1.33] ms. During artery occlusion, [Formula: see text] followed a well-marked gradual increasing trend as ischemia progressed, reaching a median of 14.58 [17.72] ms. [Formula: see text] averages were significantly higher ( ) in the VF group than in the Non-VF group at time intervals 0-5, 5-10, 10-15, 15-20, 20-25 min after occlusion onset and at 10-15, 5-10 and 5-0 minutes prior to VF episode, with median values of 12.5, 18.8, 26.8, 24.0, 31.0, 18.6, 25.0 and 28.8 vs 6.3, 7.6, 8.0, 7.8, 7.8, 8.5, 7.2 and 6.0 ms, respectively. The [Formula: see text] interval was also significantly higher in the VF group at all analyzed time periods, but with a lower significance level. Pigs with maximum [Formula: see text] ≥ 20.0 ms and [Formula: see text] ≥ 85.4 ms had significantly higher risk for VF occurring in the early 5-10 minutes interval, with 90.0%/75.0% and 80.0%/69.0% sensitivity/specificity, respectively. Univariate Cox analysis yielded hazard ratios of 12.5 for [Formula: see text] vs 5.5 for [Formula: see text]. The time-warping-based index, [Formula: see text], is a stronger VF predictor than [Formula: see text] during ischemia in a porcine model, advising for further clinical exploration studies in humans.

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.

Abstract 214: A Counterfactual Machine Learning Model Study To Estimate The Impact Of Coronary Angiography For Out Of Hospital Cardiac Arrest

Background: The American Heart Association guidelines for resuscitation 2020 recommends emergency coronary angiography (CAG) in cases of out-of-hospital cardiac arrest (OHCA) after return of spontaneous circulation (ROSC) with ST-segment elevation(STE) and, it is unclear how much CAG actually contributes to improved outcomes in various OHCA patient populations. The aim of this study is to estimate the impact of CAG on OHCA using a counterfactual machine learning model. Methods: We analyzed adult non-traumatic OHCA patients (43,977 cases) from June 2014 to December 2019 from the JAAM (Japan Association for Acute Medicine)-OHCA registry, which includes post-hospitalization data from 140 Japanese hospitals. We defined outcomes as favorable neurological outcomes (Cerebral Performance Categories (CPC) 1-2) and survival at 30 and 90 days. We estimated the outcome assuming that all patients had received CAG using a machine learning and counterfactual hypothetical model, and also estimated the outcome assuming that all patients had not received CAG. An average of each individual difference between the two estimations was calculated as average treatment effect (ATE) (%), which represents the effect of CAG on improving outcomes for the population. In addition, subgroup analysis was performed based on ROSC, STE and initial documented rhythm. Results: The ATE(%, 95% confidence interval) of CAG in all OHCA patients for CPC 1-2 at 30 and 90 days was 3.11% (2.92-3.30) and 1.85% (1.74-1.95), and survival at 30 and 90 days was 6.25%(5.93-6.57) and 2.20%(1.88-2.52), respectively. The subgroup analysis of ATE for CPC 1-2 at 90 days was particularly lower in the no STE group, initial pulseless electrical activity (PEA) group and initial asystole group than in the STE group and initial ventricular fibrillation(VF) group (Figure). Conclusions: In the JAAM-OHCA registry, we used a counterfactual machine learning model to estimate the effect of CAG on OHCA.

Ventricular fibrillation in acute myocardial infarction: 20-year trends in the FAST-MI study.

Sudden cardiac arrest remains a major complication of acute myocardial infarction (AMI) and is frequently related to ventricular fibrillation (VF). Incidence and impact of VF among patients hospitalized for AMI were evaluated. Data from the FAST-MI programme consisting of 5 French nationwide prospective cohort studies between 1995 and 2015 were analysed, totally including 14 423 patients with AMI (66 ± 14 years, 72% males, 59% ST-elevation myocardial infarction). Overall, proportion of patients presenting in-hospital VF decreased from 3.9% in 1995 to 1.8% in 2015 (P < 0.001). One-year mortality decreased from 60.7% to 24.6% (P < 0.001). However, compared with patients who did not develop VF, the over-risk of 1-year mortality associated with VF was stable over time [hazard ratio (HR) 6.78, 95% confidence interval (CI) 5.03-9.14 in 1995 and HR 6.64, 95% CI 4.20-10.49 in 2015, P = 0.52]. This increased mortality in the VF group was mainly related to fatal events occurring prior to hospital discharge, representing 86.2% of 1-year mortality, despite the very low rate of implantable cardioverter defibrillator in the VF group (2.6%). This study demonstrates that in-hospital VF incidence and mortality in the setting of AMI have significantly decreased over the past 20 years. Nevertheless, VF remained steadily associated with approximately a 10-fold increased relative risk of in-hospital mortality, without an impact on post-discharge mortality. Beyond long-term cardiac defibrillation strategy, these results emphasize the need to identify in-hospital interventions to further reduce mortality in VF patients. ClinicalTrials.gov Identifier: NCT00673036, NCT01237418, NCT02566200.

Determinants of venous return in steady-state physiology and asphyxia-induced circulatory shock and arrest: an experimental study

BackgroundMean circulatory filling pressure (Pmcf) provides information on stressed volume and is crucial for maintaining venous return. This study investigated the Pmcf and other determinants of venous return in dysrhythmic and asphyxial circulatory shock and arrest.MethodsTwenty Landrace/Large-White piglets were allocated into two groups of 10 animals each. In the dysrhythmic group, ventricular fibrillation was induced with a 9 V cadmium battery, while in the asphyxia group, cardiac arrest was induced by stopping and disconnecting the ventilator and clamping the tracheal tube at the end of exhalation. Mean circulatory filling pressure was calculated using the equilibrium mean right atrial pressure at 5–7.5 s after the onset of cardiac arrest and then every 10 s until 1 min post-arrest. Successful resuscitation was defined as return of spontaneous circulation (ROSC) with a MAP of at least 60 mmHg for a minimum of 5 min.ResultsAfter the onset of asphyxia, a ΔPmca increase of 0.004 mmHg, 0.01 mmHg, and 1.26 mmHg was observed for each mmHg decrease in PaO2, each mmHg increase in PaCO2, and each unit decrease in pH, respectively. Mean Pmcf value in the ventricular fibrillation and asphyxia group was 14.81 ± 0.5 mmHg and 16.04 ± 0.6 mmHg (p < 0.001) and decreased by 0.031 mmHg and 0.013 mmHg (p < 0.001), respectively, for every additional second passing after the onset of cardiac arrest. With the exception of the 5–7.5 s time interval, post-cardiac arrest right atrial pressure was significantly higher in the asphyxia group. Mean circulatory filling pressure at 5 to 7.5 s after cardiac arrest predicted ROSC in both groups, with a cut-off value of 16 mmHg (AUC = 0.905, p < 0.001).ConclusionMean circulatory filling pressure was higher in hypoxic hypercapnic conditions and decreased at a lower rate after cardiac arrest compared to normoxemic and normocapnic state. A Pmcf cut-off point of 16 mmHg at 5–7.5 s after cardiac arrest can highly predict ROSC.

Incorporating Latent Variables Using Nonnegative Matrix Factorization Improves Risk Stratification in Brugada Syndrome.

BackgroundA combination of clinical and electrocardiographic risk factors is used for risk stratification in Brugada syndrome. In this study, we tested the hypothesis that the incorporation of latent variables between variables using nonnegative matrix factorization can improve risk stratification compared with logistic regression.Methods and ResultsThis was a retrospective cohort study of patients presented with Brugada electrocardiographic patterns between 2000 and 2016 from Hong Kong, China. The primary outcome was spontaneous ventricular tachycardia/ventricular fibrillation. The external validation cohort included patients from 3 countries. A total of 149 patients with Brugada syndrome (84% males, median age of presentation 50 [38–61] years) were included. Compared with the nonarrhythmic group (n=117, 79%), the spontaneous ventricular tachycardia/ ventricular fibrillation group (n=32, 21%) were more likely to suffer from syncope (69% versus 37%, P=0.001) and atrial fibrillation (16% versus 4%, P=0.023) as well as displayed longer QTc intervals (424 [399–449] versus 408 [386–425]; P=0.020). No difference in QRS interval was observed (108 [98–114] versus 102 [95–110], P=0.104). Logistic regression found that syncope (odds ratio, 3.79; 95% CI, 1.64–8.74; P=0.002), atrial fibrillation (odds ratio, 4.15; 95% CI, 1.12–15.36; P=0.033), QRS duration (odds ratio, 1.03; 95% CI, 1.002–1.06; P=0.037) and QTc interval (odds ratio, 1.02; 95% CI, 1.01–1.03; P=0.009) were significant predictors of spontaneous ventricular tachycardia/ventricular fibrillation. Increasing the number of latent variables of these electrocardiographic indices incorporated from n=0 (logistic regression) to n=6 by nonnegative matrix factorization improved the area under the curve of the receiving operating characteristics curve from 0.71 to 0.80. The model improves area under the curve of external validation cohort (n=227) from 0.64 to 0.71.ConclusionsNonnegative matrix factorization improves the predictive performance of arrhythmic outcomes by extracting latent features between different variables.

Coronary angiography findings in patients with refractory vs. non-refractory ventricular fibrillation cardiac arrest

Abstract Introduction Refractory ventricular fibrillation (VF) is usually defined as the need for &amp;gt;3 shocks and poses a therapeutic challenge during cardiac arrest. For these patients, new treatment strategies such as early invasive management are under active investigation, yet the underlying myocardial substrate has poorly been characterised. In search of potential therapeutic targets, we studied coronary angiography findings in refractory vs. non-refractory VF. Methods Out of our prospective cardiac arrest registry (2013–2018), we studied all VF-patients that were transported to our tertiary hospital, and underwent coronary angiography (CAG). CAGs were assessed by interventional cardiologists blinded for clinical outcomes and patient category, being either patients with refractory (&amp;gt;3 shocks) or non-refractory VF (≤3 shocks). CAG images were scored using predefined data-sheets with uniform definitions. Results We studied 301 patients, of which the majority was male (82%) and median age was 63 (53–70) years. Of all patients, 105 (35%) had refractory VF and 196 (66%) had non-refractory VF. We found no differences in baseline and arrest characteristics (i.e. arrest location, witnessed arrest, bystander CPR, EMS response time and AED use) between refractory and non-refractory VF. In both groups, significant coronary artery disease (≥1 stenosis &amp;gt;70%) was highly prevalent (78 vs. 77%, p=0.76). Acute coronary occlusions were more prevalent in the refractory VF group (41% in refractory VF vs. 26% in non-refractory VF, p=0.006). Figure 1 demonstrates that the proportion patients with an coronary occlusion increases with an increasing number of shocks (p for trend=0.003). Chronic total occlusions did not differ between both groups (29% vs. 33%, p=0.47). Refractory VF-patients had lower proportions 24-hour survival (75% vs. 93%, p&amp;lt;0.001) and survival to discharge (61% vs. 78%, p=0.002). Conclusion In this VF-cardiac arrest study on patients transported to the hospital and undergoing coronary angiography, acute coronary occlusions were more prevalent in refractory compared to non-refractory VF. After confirmation of these findings, further studies on the potential benefit of early treatment of acute coronary occlusions in patients with refractory VF are eagerly awaited. Figure 1 Funding Acknowledgement Type of funding source: None

Value of heart rate variability on dynamic electrocardiogram in predicting ventricular fibrillation in elderly acute myocardial infarction patients.

Ventricular fibrillation (VF) is the main cause of sudden death in Acute myocardial infarction (AMI) patients. Identifying arrhythmia as early as possible is of great significance in improving prognosis of AMI patients. The article is aimed at exploring the predictive value of heart rate variability (HRV) of dynamic electrocardiogram (DCG) in VF of elderly AMI patients. A total of 122 elderly AMI patients were enrolled as the research objects. They were divided into VF group and simple AMI group (AMI group). All underwent DCG test after admission. The basic data of patients were compared. HRV of DCG was observed. The predictive value of HRV of DCG in VF of elderly AMI patients was evaluated by receiver operating characteristic (ROC) curves. The ratio of Killip at grade II-III, activity of creatine kinase-MB (CK-MB), standard deviation of all R-R intervals (SDNN), the standard deviation of the R-R intervals (SDANN), root-mean-square of the successive differences of normal RR intervals (rMSSD) and percentage of NN50 in the total number of NN intervals PNN50 (PNN50%)]in VF group were higher than those in AMI group (P<0.05). The area under the ROC curves (AUC)and cut-off values of SDNN, SDANN, rMSSD and PNN50% were (0.773, 0.761, 0.800, 0.819) and (135.675, 106.850, 33.570, 14.080), respectively. HRV of DCG is of certain predictive value for VF in the elderly with AMI, which is expected to be an auxiliary diagnosis method of VF.

Implications of Initial Recorded Rhythm on Cardioverter-Defibrillator Insertion and Subsequent All-Cause Mortality in Sudden Cardiac Arrest Survivors

Sudden cardiac arrest (SCA) rhythms have been traditionally divided into shockable [ventricular tachycardia (VT)/ventricular fibrillation (VF)] and nonshockable [(asystole (ASY)/pulseless electrical activity (PEA)] rhythms. It is unclear if the specific rhythm has implications on patient management and outcomes. We evaluated 1,433 patients who were admitted with SCA from 2000 to 2012 and were discharged alive. Of those, 1,123 patients had a recorded initial SCA rhythm. Subjects included were >18 years of age, and without an implantable cardioverter-defibrillator (ICD) in place at the time of the event. The likelihood of receiving an ICD for each SCA rhythm and the time to death were analyzed. Of the overall cohort of 1,123 SCA survivors (age of 62 ± 15 years; 39.2% women; 56.3% in-hospital SCA; 83% white; 67% coronary artery disease), 355 (31.6%) received an ICD, and 493 (43.9%) died over a mean follow-up of 3.8 ± 3.2 years. Patients with VF (n = 254, 43.6%) or VT (n = 83, 43.9%) were more likely to receive ICD therapy compared with those with ASY (n = 9, 5.3%) or PEA (n = 9, 4.8%; p <0.001). All-cause mortality was lower in VF patients compared with the other groups (p <0.0001). ICD therapy was associated with lower risk of death in the VF group (hazard ratio [HR] 0.61 [0.45 to 0.83]; p = 0.002) and strong trends toward less mortality in patients with VT (HR 0.64 [0.40 to 1.03]; p = 0.07) and ASY (HR 0.39 [0.12 to 1.31]; p = 0.13) but not in those with PEA (HR 0.93 [0.39 to 2.23]; p = 0.88). In conclusion, long-term survival in post-SCA patients is influenced by initial SCA rhythm. Although SCA survivors with shockable rhythms were more likely to receive ICDs, the ICD was associated with lower risk of death in most patients, including those with ASY. In conclusion, our data suggest that a more detailed SCA rhythm classification has important implications to patient management and long-term survival in this population.

Cardiopulmonary resuscitation ameliorates myocardial mitochondrial dysfunction in a cardiac arrest rat model

PurposePrevious studies implicate that the mitochondrial injury may play an important role in the development of post-resuscitation myocardial dysfunction, however few of them are available regarding the ultrastructural alterations of myocardial mitochondria, mitochondrial energy producing and utilization ability in the stage of arrest time (no-low) and resuscitation time (low-flow). This study aimed to observe the dynamic changes of myocardial mitochondrial function and metabolic disorders during cardiac arrest (CA) and following cardiopulmonary resuscitation (CPR). MethodsA total of 30 healthy male Sprague-Dawley rats were randomized into three groups: 1) VF/CPR: Ventricular fibrillation (VF) was electrically induced, and 5 min of CPR was performed after 10 min of untreated VF; 2) Untreated VF: VF was induced and untreated for 15 min; and 3) Sham: Rats were identically prepared without VF/CPR. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 min were calculated from ECG signals. The rats' hearts were quickly removed at the predetermined time of 15 min after beginning the procedure to gather measurements of myocardial mitochondrial function, high-energy phosphate stores, lactate, mitochondrial ultrastructure, and myocardial glycogen. ResultsThe mitochondrial respiratory control ratios significantly decreased after CA compared to sham group. CPR significantly increased respiratory control ratios compared with untreated VF animals. A significant decrease of myocardial glycogen was observed after CA, and a more rapid depletion of myocardial glycogen was observed in CPR animals. CPR significantly reduced the tissue lactate. The mitochondrial ultrastructure abnormalities in CPR animals were less severe than untreated VF animals. AMSA decayed during untreated VF; however, it was significantly greater in CPR group than the untreated VF group. In addition, AMSA was clearly positively correlated with ATP, but negatively correlated with myocardial glycogen. ConclusionImpairment of myocardial mitochondrial function and the incapability of utilizing glycogen were observed after CA. Furthermore, optimal CPR might, in part, preserved mitochondrial function and enhanced utilization of myocardial glycogen.

Abstract 289: Relationship Between Myocardial Glycogen Concentrations and Amplitude Spectrum Area During Ventricular Fibrillation in a Rat Model of Cardiac Arrest and Resuscitation

Introduction: Myocardial high-energy phosphate (ATP) levels has been demonstrated correlating with amplitude spectrum area (AMSA) during ventricular fibrillation (VF) in previous experimental studies. In the present study, we investigated the relationship between AMSA and myocardial glycogen content (MGC),which can be used to reflect the status of myocardial energy metabolism indirectly during VF. Hypothesis: AMSA has a significantly correlation with MGC during VF in a rat model of cardiac arrest and resuscitation. Methods: Twenty male Sprague-Dawley rats weighing 350 to 450 g were utilized and randomized into two groups: VF and cardiopulmonary resuscitation (CPR) (VF/CPR group) or untreated VF (VF group). 5 mins of CPR was performed after 10 mins of untreated VF in VF/CPR animals. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 mins were calculated from ECG signals. The rats’ hearts were quickly removed at the predetermined time of 15 min for determines the glycogen contents by the anthrone reagent method using a glycogen assay kit. Results: AMSA values significantly decreased during untreated VF in both VF and VF/CPR animals. However, much greater AMSA during CPR was achieved by the VF/CPR group in comparison with the VF group. There was a marked and negative relationship between AMSA at VF 15 min and MGC. (Figure). Conclusion: MGC was significantly and negatively correlated with AMSA during VF in this rat model of cardiac arrest and resuscitation. In clinical practice, we can use AMSA to reflect the state of myocardial energy metabolism indirectly. Figure The changes of AMSA and relationship between AMSA and glycogen content:(A) The change of AMSA between VF/CRP group and VF group;(B) The relationship between AMSA and glycogen content. AMSA, amplitude spectrum area; V, time of ventricular fibrillation; # p &lt;0.05 vs. V4.

Quantitative CT assessment of lung injury after successful cardiopulmonary resuscitation in a porcine cardiac arrest model of different downtimes.

Utilize quantitative computed tomography (QCT) to detect and evaluate the severity of lung injury after successful cardiopulmonary resuscitation (CPR) in a porcine cardiac arrest (CA) model with different downtimes. Twenty-one male domestic pigs weighing 38±3 kg were randomized into 3 groups: the sham group (n=5), the ventricular fibrillation (VF) 5 min (VF5) group (n=8), and the VF 10 min (VF10) group (n=8). VF was induced and untreated for 5 (VF5 group) or 10 (VF10 group) min before the commencement of manual CPR. Eight animals (8/8, 100%) in VF5 and 6 (6/8, 75%) in VF10 were successfully resuscitated. Chest QCT scans and arterial blood gas tests were performed at baseline and 6 h post-resuscitation. The QCT score, volume, and weight of ground-glass opacification (GGO), which was defined as poorly aerated regions with a CT value ranging from -500 Hounsfield units (HU) to -100 HU, and intense parenchymal opacification (IPO), which was defined as a non-aerated area with a CT value greater than -100 HU, were quantitatively measured. Significantly shorter durations of CPR and fewer defibrillations were observed in the VF5 group compared with the VF10 group [duration of CPR: VF5 (6±0 minutes) versus VF10 (8.3±1.5 minutes), P<0.05; numbers of defibrillation: VF5 (1±0) versus VF10 (2.2±0.8), P<0.05]. Compared with the baseline or sham animals, declining gas exchanges (end-tidal CO2, PO2, oxygen index) were observed in both VF groups; however, there were no significant differences in gas exchanges between the VF groups. Compared with the VF5 group, the GGO QCT score, volume, and weight were significantly greater in the VF10 group (P=0.002, 0.001, and 0.002 respectively), while no significant differences were found in the IPO QCT score, volume, or weight between two the VF groups (P=0.354, 0.447, and 0.512 respectively). QCT analysis enables unique non-invasive assessments of different lung injuries (IPO and GGO lesions) that can clearly distinguish heterogeneous lesions and allow for early detection and quantitative monitoring of the severity of lung injury following CPR. QCT could provide a basis for clinical early ventilation strategy management after CPR.

Impact of the angiographic burden on the incidence of out-of-hospital ventricular fibrillation in patients with acute myocardial infarction.

Ventricular fibrillation (VF) is a catastrophic complication of spontaneous (type 1) acute myocardial infarction (AMI). This study sought to clarify the angiographic coronary characteristics related to out-of-hospital VF in AMI patients. We retrospectively reviewed 464 consecutive cases of suspicious AMI, including type 1 AMI, with or without out-of-hospital VF. In addition to patient demographics, proximal left coronary artery (LCA) disease, multivessel disease (MVD), and chronic total occlusion (CTO) were assessed via coronary angiography and compared between patients with and without out-of-hospital VF. Coronary angiography was evaluated for 74 patients with out-of-hospital VF and for 237 without. Male sex (93.2 vs. 83.1%; P = 0.036), Killip class ≥ 2 (89.2 vs. 16.5%; P < 0.001), and ST elevation myocardial infarction (83.8 vs. 66.7%; P = 0.003) were more frequent in the out-of-hospital VF group. The culprit lesions located in the proximal left coronary artery (62.2 vs. 29.5%; P < 0.001), MVD (75.7 vs. 41.8%, P < 0.001), and CTO (43.2 vs. 10.5%, P < 0.001) were more frequently observed in patients with out-of-hospital VF. Multivariate logistic regression analysis identified the culprit lesion located in the proximal LCA [odds ratio (OR) 2.86; 95% confidence interval (CI) 1.34-6.08], the presence of CTO (OR 8.52; 95% CI 3.35-21.65), and MVD (OR 3.69; 95% CI 1.57-8.65) as predictors of out-of-hospital VF. For type 1 AMI patients, advanced disease burden including the culprit lesion located in the proximal LCA and coexistence of CTO or MVD might be associated with out-of-hospital VF.

Novel patterns of left ventricular mechanical activity during experimental cardiac arrest in pigs.

We conducted an experimental study to evaluate the presence of coordinated left ventricular mechanical myocardial activity (LVMA) in two types of experimentally induced cardiac arrest: ventricular fibrillation (VF) and pulseless electrical activity (PEA). Twenty anesthetized domestic pigs were randomized 1:1 either to induction of VF or PEA. They were left in nonresuscitated cardiac arrest until the cessation of LVMA and microcirculation. Surface ECG, presence of LVMA by transthoracic echocardiography and sublingual microcirculation were recorded. One minute after induction of cardiac arrest, LVMA was identified in all experimental animals. In the PEA group, rate of LVMA was of 106+/-12/min. In the VF group, we identified two patterns of LVMA. Six animals exhibited contractions of high frequency (VFhigh group), four of low frequency (VFlow group) (334+/-12 vs. 125+/-32/min, p<0.001). A time from cardiac arrest induction to asystole (19.2+/-7.2 vs. 7.3+/-2.2 vs. 8.3+/-5.5 min, p=0.003), cessation of LVMA (11.3+/-5.6 vs. 4.4+/-0.4 vs. 7.4+/-2.9 min, p=0.027) and cessation of microcirculation (25.3+/-12.6 vs. 13.4+/-2.4 vs. 23.2+/-8.7 min, p=0.050) was significantly longer in VFlow group than in VFhigh and PEA group, respectively. Thus, LVMA is present in both VF and PEA type of induced cardiac arrest and moreover, VF may exhibit various patterns of LVMA.

Prehospital intravenous access for survival from out-of-hospital cardiac arrest: propensity score matched analyses from a population-based cohort study in Osaka, Japan

ObjectivesPrehospital intravenous access is a common intervention for patients with out-of-hospital cardiac arrest (OHCA). We aimed to assess the effectiveness of prehospital intravenous access and subsequent epinephrine administration on outcomes...

Establishment of porcine model of prolonged cardiac arrest and cardiopulmonary resuscitation electrically induced by ventricular fibrillation

To investigate the optimal injury time point of cardiac arrest (CA) induced electrically, and establish a reproducible prolonged CA and cardiopulmonary resuscitation (CPR) model in pigs. Forty healthy domestic male pigs were randomly divided into four groups, which were ventricular fibrillation (VF) 8, 10, 11, and 12 minutes groups, each group for 10 animals. In these groups, VF was induced by alternating current delivered to right ventricular endocardium and untreated for 8, 10, 11, and 12 minutes, respectively, followed by 6 minutes of CPR procedure. The resuscitation and survival outcomes were recorded. Hemodynamic parameters and arterial blood gases of animals after successful resuscitation were measured and recorded for 6 hours. Those successful resuscitation animals were regularly evaluated for the neurological deficit score (NDS) and survival outcomes every 24 hours till 96 hours after resuscitation. The shortest duration of CPR (minute: 6.9±1.3) and the highest successful ratio of the first defibrillation (7/10) were observed in group VF 8 minutes, and the ratio of successful resuscitation was 100%. The best coronary perfusion pressure (CPP) during the CPR, less neurological impairment, longer survival time, more stable hemodynamics, and shorter time for arterial pH and lactate level restoring to the original state after CPR were also observed in group VF 8 minutes, and no severe damage was found in those animals. The longest duration of CPR (minute: 10.3±2.9) and the lowest successful ratio of the first defibrillation (1/10) were observed in group VF 12 minutes, and only 4 animals achieved restoration of spontaneous circulation (ROSC), and no animal survived to CPR 96 hours. The worst CPP during CPR and the highest NDS after resuscitation were also found in VF 12 minutes animals compared to those animals in the other groups. The injuries caused by ischemia and hypoxia in groups VF 10 minutes and VF 11 minutes were in between those of the groups VF 8 minutes and VF 12 minutes, and the duration of CPR were (7.0±2.1) minutes and (8.2±2.6) minutes. There were 9 and 7 animals achieved ROSC in groups VF 10 minutes and VF 11 minutes correspondingly, and 6 and 4 animals survived to 96 hours respectively. Obviously unstable hemodynamics was observed during the period of CPR 2 hours in the two groups. At CPR 1 hour, the heart rates (HR, beats/min) in groups VF 10 minutes and VF 11 minutes increased to 172 (155, 201) and 168 (136, 196) respectively, and the mean arterial pressures (MAP, mmHg, 1 mmHg = 0.133 kPa) declined to 97 (92, 100) and 81 (77, 100), the cardiac output (CO, L/min) decreased to 5.0 (4.0, 5.8), 3.7 (3.0, 5.4) correspondingly. Distinct injuries were found in the two groups [CPR 24-96 hours NDS in groups VF 10 minutes and VF 11 minutes: 180 (110, 255)-20 (0, 400) and 275 (223, 350)-240 (110, 400)], and the arterial pH of the two group decreased to 7.26±0.09 and 7.23±0.09 respectively, and the level of lactate (mmol/L) increased to 9.17±1.48 and 12.80±2.71 correspondingly at CPR 0.5 hour. Significantly lower pH was observed in group VF 11 minutes compared to group VF 8 minutes at CPR 0.5 hour (7.23±0.09 vs. 7.33±0.04, P < 0.05). The highest level of lactate (mmol/L) was also found at the same time point in group VF 11 minutes, which recovered to normal slowly, and was still significantly higher than groups VF 8, 10, 12 minutes (7.58±3.99 vs. 2.55±1.53, 2.13±2.00, 3.40±2.30, all P < 0.05) at CPR 4 hours. The longer duration of CA was, the more severe damage would be, the longer CPR time would be required, and the harder of the animals to achieve ROSC. In this prolonged CA and CPR porcine model, 10-11 minutes for untreated VF, was an optimal time point with appropriate successful rate of resuscitation, survival outcomes, and post-resuscitation injuries. Therefore, we recommended 10-11 minutes might be the rational length of no-flow time in this model.

Progressive increase of the Tpeak-Tend interval is associated with ischaemia-induced ventricular fibrillation in a porcine myocardial infarction model.

Repolarization indices of ECG have been widely assessed as predictors of ventricular arrhythmias. However, little is known of the dynamic changes of these parameters during continuous monitoring in acute ischaemic episodes. The objective of the study was to evaluate repolarization-related predictors of ventricular fibrillation (VF) during progression of experimental myocardial infarction. Myocardial infarction was induced in 27 pigs by 40-min balloon inflation in the left anterior descending coronary artery, and 12-lead ECG was continuously recorded. Rate-corrected durations of the total Tpeak-Tend intervals measured from the earliest T-wave peak to the latest T-wave end in any lead were determined at baseline and at minute 1, 2, 5, and then every 5th minute of occlusion. There were 7 early (1-3 min) and 10 delayed (15-30 min) VFs in 16 pigs. Baseline Tpeak-Tend did not differ between animals with and without VF. Tpeak-Tend interval rapidly increased immediately after balloon inflation and was greater in VF-susceptible animals at 2-15 min compared with the animals that never developed VF (P < 0.05). Tpeak-Tend was tested as a predictor of delayed VFs. Median Tpeak-Tend at 10th min of occlusion was higher in delayed VF group (n = 10) than in animals without VF (n = 11): 138 [IQR 121-148] ms vs. 111 [IQR 106-127] ms, P = 0.02. Tpeak-Tend ≥123 ms (10th min) predicted delayed VF episodes with HR = 4.5 95% CI 1.1-17.8, P = 0.031. Tpeak-Tend prolongation during ischaemia progression predicts VF in the experimental porcine myocardial infarction model and warrants further testing in clinical settings of acute coronary syndromes.