Onset Of Spontaneous Ventricular Fibrillation Research Articles

Circadian Variations in ST‐Segment Elevation Surrounding the Spontaneous Onset of Ventricular Fibrillation in Brugada Syndrome

Circadian Variations in ST‐Segment Elevation Surrounding the Spontaneous Onset of Ventricular Fibrillation in Brugada Syndrome

Markers of Progenitor Cell Recruitment and Differentiation Rise Early During Ischemia and Continue During Resuscitation in a Porcine Acute Ischemia Model

Clinical administration of bone marrow-derived stem cells in the setting of acute myocardial infarction (AMI) leads to improved left ventricular ejection fraction. Thymosin beta-4 (TB4) and vascular endothelial growth factor (VEGF) are linked to adult epicardial progenitor cell mobilization and neovascularization and is cardioprotective after myocardial ischemia. This study investigated the time course of TB4 and VEGF during AMI, cardiac arrest, and resuscitation. Fifteen anesthetized and instrumented domestic swine underwent balloon occlusion of the proximal left anterior descending coronary artery. During occlusion, venous blood samples were collected from the right atrium at 5-min intervals until 15 min after the onset of cardiopulmonary resuscitation (CPR). Plasma levels of TB4, VEGF, and matrix metalloproteinase-9 (MMP-9, selected as a marker for remodeling and repair) were measured by ELISA. Generalized linear mixed models were employed to model the time-dependent change in plasma concentration. All variables were natural log transformed, except TB4 values, to normalize distributions. Fifteen animals successfully underwent balloon occlusion of the left anterior descending coronary artery and samples were collected from these subjects. The average onset of spontaneous ventricular fibrillation was 28 min. TB4, VEGF, and MMP-9 demonstrated a statistically significant, time-dependent increase in concentration during ischemia. Following arrest and throughout the first 15 min of resuscitation, MMP-9 had an unchanged rate of rise when compared with the prearrest, ischemic period, with VEGF showing a deceleration in its time-dependent concentration trajectory and TB4 demonstrating an acceleration. Endogenous TB4 and VEGF increase shortly after the onset of AMI and increase through cardiac arrest and resuscitation in parallel to remodeling proteases. These markers continue to rise during successful resuscitation and may represent an endogenous mechanism to recruit undifferentiated stem cells to areas of myocardial injury.

Transesophageal Echocardiography During Ventricular Fibrillation

Sudden cardiac death is most frequently caused by spontaneous onset of ventricular fibrillation (VF), during which the rhythmic heart contractions transform into chaotic, vermiform, and inefficient activity of the myocardium while the pulsatile pulmonary and systemic blood flow circuits stop. Little information is available on the anatomical and hemodynamic changes that occur during VF. These changes could be seen in humans with transesophageal echocardiography (TEE). In the present report, we describe an 81-year-old man with a history of hypertension and upper gastrointestinal bleeding who was admitted with paroxysmal atrial fibrillation with high ventricular response (160 bpm) and heart failure. Given the impossibility of anticoagulation and to control hemodynamic compromise, TEE …

Spontaneous Onset of Ventricular Fibrillation during Atrioventricular Nodal Reentrant Tachycardia

Spontaneous Onset of Ventricular Fibrillation during Atrioventricular Nodal Reentrant Tachycardia

Application of normothermic cardiac arrest algorithms to hypothermic cardiac arrest in a canine model

International guidelines (2000) do not recommend vasopressor and antiarrhythmic medications during ventricular fibrillation (VF) with a core temperature below 30 degrees C. The efficacy of normothermic AHA algorithms using standard doses of epinephrine (EPI) (adrenaline) followed by amiodarone (AMIO) in hypothermic VF is uncertain. To determine the effects of EPI followed by the combination of EPI/AMIO in the treatment of VF in a canine model of severe hypothermia. An un-blinded, placebo controlled experiment using 21 mechanically ventilated dogs. Coronary perfusion pressure (CPP), temperature, and electrocardiogram (ECG) were monitored. Animals were cooled to 22 degrees C or the onset of spontaneous VF. VF was induced if necessary. Animals in the treatment group received EPI (0.01 mg/kg IV) and defibrillation. This was followed by EPI (0.01 mg/kg IV), AMIO (10 mg/kg IV) and defibrillation if there was no sustained return of spontaneous circulation (ROSC) for 15 min. Mean CPP in the treatment group increased after the administration of EPI/AMIO (24.7+/-13.3 mmHg to 46.6+/-7.7 mmHg, p<0.004). Cumulatively, the administration of EPI followed by EPI/AMIO achieved ROSC after defibrillation in 10 of 11 animals compared to 3 of 10 in the control group (91% versus 30%, n=21, p=0.0075). In this model of severe hypothermia, the use of standard 2000 protocols for VF resulted in a significant increase of CPP, and, a higher ROSC rate compared to placebo controls. This study suggests that AHA normothermic algorithms may be beneficial in severe hypothermia.

Spontaneous onset of ventricular fibrillation in Brugada syndrome with J wave and ST-segment elevation in the inferior leads

We report the case of a 52-year-old man with variant Brugada syndrome who was successfully resuscitated from ventricular fibrillation (VF). Resting ECG showed J wave and ST-segment elevation in the inferior leads but no coved or saddleback ST-segment elevation in the right precordial leads. Pilsicainide infusion provoked coved-type ST-segment elevation in the right precordial leads and mild ST-segment elevation 80 ms after the J point in the inferior leads. During an emergency, 12-lead ECG showed that spontaneous onset of VF was preceded by left bundle branch block and superior axis-type ventricular extrasystoles. The present case provides additional information on the site of origin of VF in patients with Brugada syndrome.

Amiodarone and Bretylium in the Treatment of Hypothermic Ventricular Fibrillation in a Canine Model

AbstractRefractory ventricular fibrillation (VF) is a complication of severe hypothermia. Despite mixed experimental data, some authors view bretylium as the drug of choice in hypothermic VF. Bretylium was removed from Advanced Cardiac Life Support guidelines, and, to date, efficacy of amiodarone in hypothermia is unknown. Objectives: To compare defibrillation rates from hypothermic VF after drug therapy with amiodarone, bretylium, and placebo. Methods: This was a randomized, blinded, and placebo‐controlled laboratory experiment. Thirty anesthetized dogs were mechanically ventilated and instrumented to monitor coronary perfusion pressure (CPP), rectal core temperature, and electrocardiogram (ECG). Animals were cooled to 22°C or the onset of spontaneous VF. Ventricular fibrillation was induced as needed with a transthoracic AC current. Cardiopulmonary resuscitation (CPR) was initiated and animals were randomized (n= 10 each group) to receive amiodarone 10 mg/kg (A), bretylium 5 mg/kg (B), or placebo (P) intravenously. CPR was continued while monitoring for chemical defibrillation. Rewarming was limited to removal from the cold environment. After 10 minutes, up to three escalating defibrillatory shocks were administered. Hemodynamic monitoring continued after resuscitation. Return of spontaneous circulation (ROSC) was defined as a sustainable ECG rhythm generating a corresponding arterial pressure tracing lasting a minimum of 15 minutes. Sample size permitted 80% power to detect a 60% difference in conversion rate between groups. Results: CPR was adequate based on CPP &gt; 15 mm Hg in all animals. Mean (±SD) CPP was 35.3 ± 18.8 mm Hg with an overall lower trend in the amiodarone group (p = 0.06). Baseline variables were similar between groups. No instance of chemical defibrillation was noted. There was no significant difference in ROSC rates between groups. Resuscitation rates were: amiodarone = 1/10, bretylium = 4/10, and placebo = 3/10 (p = 0.45). Conclusions: In this model of severe hypothermic VF, neither amiodarone nor bretylium was significantly better than placebo in improving the resuscitation rate.

Mode of onset of ventricular fibrillation in patients with Brugada syndrome detected by implantable cardioverter defibrillator therapy

OBJECTIVESWe sought to demonstrate the mode of spontaneous onset of ventricular fibrillation (VF) in patients with Brugada syndrome.BACKGROUNDThe electrophysiologic mechanisms of VF in Brugada syndrome have not been fully investigated.METHODSNineteen patients (all male, mean age 47 ± 12 years) with Brugada syndrome were treated with an implantable cardioverter defibrillator (ICD). The implanted devices were capable of storing electrograms during an arrhythmic event. We investigated the mode of spontaneous onset of VF according to the electrocardiographic features during the episode of VF, which were obtained from stored electrograms of ICDs and/or electrocardiographic (ECG) monitoring.RESULTSDuring a follow-up of 34.7 ± 19.4 months (range 14 to 81 months), 46 episodes of spontaneous VF attacks were documented in 7/19 (37%) patients. The event-free period between ICD implantation and the first spontaneous occurrence of VF was 14.6 ± 12.1 months (range 3.7 to 27.4 months). We investigated 33/46 episodes of VF, for which electrocardiographic features (10 to 20 s before and during VF) were obtained from ICDs and/or ECG monitoring in five patients. A total of 22/33 episodes of VF were preceded by premature ventricular contractions (PVCs), which were almost identical to the initiating PVCs of VF. Furthermore, in three patients who had multiple VF episodes, VF attacks were always initiated by the same respective PVC. The coupling interval of the initiating PVCs of VF was 388 ± 28 ms.CONCLUSIONSSpontaneous episodes of VF in patients with Brugada syndrome were triggered by specific PVCs. These findings may provide important insights into the pathophysiological mechanisms causing VF in Brugada syndrome.

Heart rate dynamics before spontaneous onset of ventricular fibrillation in patients with healed myocardial infarcts

The traditional methods of analyzing heart rate (HR) variability have failed to predict imminent ventricular fibrillation (VF). We sought to determine whether new methods of analyzing RR interval variability based on nonlinear dynamics and fractal analysis may help to detect subtle abnormalities in RR interval behavior before the onset of life-threatening arrhythmias. RR interval dynamics were analyzed from 24-hour Holter recordings of 15 patients who experienced VF during electrocardiographic recording. Thirty patients without spontaneous or inducible arrhythmia events served as a control group in this retrospective case control study. Conventional time- and frequency-domain measurements, the short-term fractal scaling exponent (α) obtained by detrended fluctuation analysis, and the slope (β) of the power-law regression line (log power − log frequency, 10 −4 −10 −2 Hz) of RR interval dynamics were determined. The short-term correlation exponent α of RR intervals (0.64 ± 0.19 vs 1.05 ± 0.12; p <0.001) and the power-law slope β (−1.63 ± 0.28 vs −1.31 ± 0.20, p <0.001) were lower in the patients before the onset of VF than in the control patients, but the SD and the low-frequency spectral components of RR intervals did not differ between the groups. The short-term scaling exponent performed better than any other measurement of HR variability in differentiating between the patients with VF and controls. Altered fractal correlation properties of HR behavior precede the spontaneous onset of VF. Dynamic analysis methods of analyzing RR intervals may help to identify abnormalities in HR behavior before VF.

Changes in the surface electrocardiogram during the onset of spontaneous ventricular fibrillation in man

The aim of this study was to quantify electrocardiographic changes during the onset and early stages of ventricular fibrillation. Thirty recordings of ventricular fibrillation (mean duration 57 s, range 24-160 s) were obtained from 23 Coronary Care Unit patients. Each recording was investigated using frequency analysis on 1 s epochs of data. A significant rise in the mean dominant frequency of ventricular fibrillation from 3.9 Hz (SD 0.8 Hz) to 5.9 Hz (SD 1.0 Hz) was observed between 1 s and 30 s (P < 0.0001). At the same time, the width of the dominant peak decreased significantly (P < 0.001) and the height of higher frequency harmonics fell (P < 0.01). There was no significant change in peak height as ventricular fibrillation evolved. This study shows that the electrocardiogram retains periodic characteristics during the first 30 s of ventricular fibrillation and that these periodic characteristics become concentrated in a progressively narrower band of frequencies. These findings would suggest that during the early stages of ventricular fibrillation myocardial activation is both accelerating and coherent, rather than incoherent as has been traditionally believed.