Ventricular Vulnerable Period Research Articles

Cardiac impact of high-frequency irreversible electroporation using an asymmetrical waveform on liver in vivo

BackgroundHigh-Frequency Irreversible Electroporation (H-FIRE) is a novel technology for non-thermal ablation. Different from Irreversible electroporation (IRE), H-FIRE delivers bipolar electrical pulses without muscle contraction and does not cause electrolysis. Currently, little is known regarding the cardiac safety during the administration of H-FIRE on liver. The aim of this study was to evaluate the changes of electrocardiogram (ECG) and biomarkers of cardiac damage during asymmetrical waveform of H-FIRE therapy in vivo.MethodsThe swines (n = 7) in IRE group, which used 100 pulses (2200 V, 100–100 μs configuration), were administrated with muscle relaxant under anesthesia. In the absence of muscle relaxant, 7 swines in H-FIRE group were performed with 2400 pulses (3000 V, 5–3–3–5 μs configuration). Midazolam (0.5 mg/kg) and xylazine hydrochloride (20 mg/kg) were given to induce sedation, followed by Isoflurane (2.5%, 100% oxygen, 3 L/min) to maintain sedation in all the swines. Limb lead ECG recordings were analyzed by two electrophysiologists to judge the arrhythmia. Cardiac and liver tissue was examined by pathology technique.ResultsThe ablation zones were larger in H-FIRE than IRE. Both IRE and H-FIRE did not affect the autonomous cardiac rhythm. Even when the electrical signal of IRE and H-FIRE fell on ventricular vulnerable period. Moreover, cTnI in IRE group showed an increase in 4 h after ablation, and decreased to baseline 72 h after ablation. However, cTnI showed no significant change during the administration of H-FIRE.ConclusionsThe study suggests an asymmetrical waveform for H-FIRE is a promising measure for liver ablation. The results were based on normal liver and the swines without potential cardiac diseases. With the limitations of these facts, asymmetrical waveform for H-FIRE of liver tissue seems relatively safe without major cardiac complications. The safety of asymmetrical waveform for H-FIRE needs to evaluate in future.

Influence of acute stress on cardiac electrophysiological stability in male goats

Objective Stress plays an important role in the pathogenesis of ventricular arrhythmias. This study was designed to examine the effect of acute stress and metoprolol, a beta adrenergic receptor blocker, on cardiac electrophysiological stability of male goats.Methods Fifteen male goats were randomly divided into three groups: (i) control animals (n = 5), (ii) a compound stimuli group including noise and red flash (n = 5), (iii) and a compound stimuli group with metoprolol treatment (n = 5). Plasma catecholamines were determined by using high performance chromatography with electrochemical detection. Heart rate turbulence (HRT) and heart rate variability (HRV) were analysed with the MGY-H12L analysis system. Also, the ventricular fibrillation threshold (VFT) and the ventricular vulnerable period (VVP) were determined by programmed S1S2 stimulus with bipolar electrodes at the apex of the goat hearts.Results Compound stimuli increased plasma catecholamine levels progressively and decreased the negative value of turbulence onset (TO), turbulence slope (TS), SDNN, PNN50. Moreover, compound stimuli broadened VVP and decreased VFT significantly. Although metoprolol treatment failed to affect plasma catecholamine levels, TS and PNN50 value of the compound stimuli group, it significantly increased the negative value of TO, SDNN, VFT and narrowed VVP.Conclusion Our data demonstrates that compound stimuli can induce acute stressful reactions, and decrease the cardiac electrophysiological stability of male goats, which can be counteracted by metoprolol treatment.

Inhibition of Small‐Conductance Ca2+‐activated K+ Channels Protects Against Ventricular Fibrillation (VF) In Rats With Acute Myocardial Infarction (AMI)

In vitro study has shown that up‐regulation of SK channels in the ventricular epicardial myocytes is responsible for the spontaneous VF in failing ventricle. The present study determined the role of SK channels in regulating VF in AMI rats. AMI was induced by coronary artery ligation and ventricular programmed stimulation was used to evaluate ventricular vulnerable period (VVP), VF threshold (VFT) and ventricular effective refractory period (VERP) in anesthetized rats. In AMI animals, VVP was prolonged and VERP was shortened (p<0.05, n=6). Pre‐treatment in the AMI group with the SK channel blocker UCL1684 significantly shortened VVP and prolonged VERP (p<0.05, n=6). No effects were observed in sham‐operated controls (n=9). Additionally, VT was reduced in the AMI group, and UCL1684 increased VFT in the AMI group (p<0.05, n=6), but, again, was without effect in sham‐operated controls (n=9). Finally, monophasic action potential duration (MAPD90) was examined using an electrode placed on the left ventricular epicardium. The data showed that MAPD90 was shortened in AMI group (p<0.05, n=7), and UCL1684 significantly prolonged the MAPD90 (p<0.05, n=5), but was without effect in sham‐operated controls (n=9). We conclude that activation of SK channels may underlie the mechanisms of VF. Inhibition of SK channels reduced shorting of MAPD90, which may be responsible for the inhibitory effect on VF in AMI rats. Support: NNSF‐30971223 (JHZ); AHA 10SDG2640130 (QHC).

Evolution of our knowledge of sudden death due to commotio cordis

Commotio cordis refers to circulatory arrest due to a nonpenetrating blow to the chest. First discovered in 1932 in a study using large rabbits, it came to the attention of clinicians who encountered children dying suddenly from a chest blow while engaging in sports activities. This review traces the history of commotio cordis, establishes the conditions necessary for sudden death from a nonpenetrating chest blow, and presents the first ECG record showing that a chest blow landing in the ventricular vulnerable period can produce ventricular fibrillation. The conditions necessary for sustaining ventricular fibrillation and numerous examples of sudden death by commotio cordis are presented.

Commotio Cordis in Children, Including a Translation of the First Paper That Describes the Condition

A nonpenetrating blow to the chest may cause sudden death to children engaged in sports, such as baseball, hockey, etc. This condition is known as commotio cordis. The circulatory arrest associated with commotio cordis is due to atrioventricular block or ventricular fibrillation because the projectile struck the chest during the ventricular vulnerable period. Therefore, all medical personnel who encounter a child with circulatory arrest should be aware of commotio cordis as the causative factor and be prepared to apply CPR immediately. The cause for the circulatory arrest can only be confirmed by the ECG demonstrating ventricular fibrillation.

Horatio B. Williams and the first electrocardiographs made in the United States.

Horatio Burt Williams was likely the first American clinical electrophysiologist. He published the first paper on ECG in the western hemisphere, constructed the first string galvanometer in America, plotted the first vectorcardiogram, discovered the ventricular vulnerable period, and first quantitated the amount of 60-Hz current required to produce ventricular fibrillation with body-surface electrodes; he also showed that ventricular defibrillation could be achieved with body-surface electrodes using high-intensity 60-Hz current. Williams died at the age of 78 on November 1, 1955, at the Presbyterian Hospital in New York. He was born on September 17, 1877, in Utica, New York.

Clinical and Electrophysiological Significance of Induction of Morphologically Different Ventricular Fibrillation During Ventricular Vulnerable Period in Humans

Clinical and Electrophysiological Significance of Induction of Morphologically Different Ventricular Fibrillation During Ventricular Vulnerable Period in Humans

Clinical and elactrophysiological significance of induction of morphologically different ventricular fibrillation during ventricular vulnerable period in humans

Clinical and elactrophysiological significance of induction of morphologically different ventricular fibrillation during ventricular vulnerable period in humans

Dramatically prolonged ventricular vulnerable period of abnormal ventricular activations during atrial defibrillation

Dramatically prolonged ventricular vulnerable period of abnormal ventricular activations during atrial defibrillation

Atrioventricular nodal function in the immature canine heart [corrected and republished article orginally printed in Pediatr Res 1987 Nov;22(5):616-20

Previous studies have suggested that the atrioventricular nodal functional refractory period in the neonate is equal to or shorter than that of the ventricle, providing little or no protection to the ventricle against rapid atrial rates and allowing closely coupled atrial beats to fall within the ventricular vulnerable period. We evaluated atrioventricular node function in 21 mongrel neonatal puppies, 3-15 days old, and 15 adult dogs utilizing intracardiac His bundle recording and stimulation techniques. The mean atrioventricular nodal functional refractory period (173.1 +/- 20.0 ms) exceeded both the ventricular effective refractory period (139.5 +/- 14.3) and ventricular functional refractory period (163.3 +/- 14.5) in the neonates. Furthermore, the atrioventricular node was the site of limiting antegrade conduction in all neonates. No ventricular arrhythmias were induced by atrial extrastimulation in any of the neonates. The site of conduction delay during atrial extrastimulation was confined to the atrioventricular node in 15/16 neonates (94%) while 1/16 (6%) had combined nodal and infranodal delay. The neonates developed Wenckebach, at significantly faster heart rates than the adults, but both groups developed Wenckebach at approximately twice the resting heart rate. Retrograde conduction was a consistent finding in the neonates. However, antegrade Wenckebach occurred at a significantly faster heart rate than retrograde Wenckebach suggesting different functional properties. Our data suggest that in the neonatal canine, the atrioventricular node functional refractory period is longer than both the ventricular effective refractory period and ventricular functional refractory period. Furthermore, the degree of protection offered by the neonatal atrioventricular node to the ventricle appears to be comparable to that of the adult.

Atriovenous Nodal Function in the Immature Canine Heart

ABSTRACT. Previous studies have suggested that the atriovenous nodal functional refractory period in the neonate is equal to or shorter than that of the ventricle, providing little or no protection to the ventricle against rapid atrial rates and allowing closely coupled atrial beats to fall within the ventricular vulnerable period. We evaluated atriovenous node function in 21 mongrel neonatal puppies, 3-15 days old, and 15 adult dogs utilizing intracardiac His bundle recording and stimulation techniques. The mean atriovenous nodal functional refractory period (173.1 ± 20.0 ms) exceeded both the ventricular effective refractory period (139.5 ± 14.3) and ventricular functional refractory period (163.3 ± 14.5) in the neonates. Furthermore, the atriovenous node was the site of limiting antegrade conduction in all neonates. No ventricular arrhythmias were induced by atrial extrastimulation in any of the neonates. The site of conduction delay during atrial extrastimulation was confined to the atriovenous node in 15/16 neonates (94%) while 1/16 (6%) had combined nodal and infranodal delay. The neonates developed Wenckebach, at significantly faster heart rates than the adults, but both groups developed Wenckebach at approximately twice the resting heart rate. Retrograde conduction was a consistent finding in the neonates. However, antegrade Wenckebach occurred at a significantly faster heart rate than retrograde Wenckebach suggesting different functional properties. Our data suggest that in the neonatal canine, the atriovenous node functional refractory period is longer than both the ventricular effective refractory period and ventricular functional refractory period. Furthermore, the degree of protection offered by the neonatal atriovenous node to the ventricle appears to be comparable to that of the adult.

Comparison of the effects of atrial and ventricular stimulation on sinus node function in man

Although sinus node function has been evaluated during premature atrial stimulation, no study of retrograde ventriculoatrial sinus node activation following premature ventricular stimuli has been reported. The purpose of this study was to investigate the production of compensatory and noncompensatory pauses by premature ventricular contractions through a comparison of the effects of atrial and ventricular stimulation on sinus node function. Eleven patients in sinus rhythm were studied with programmed introduction of premature atrial and ventricular stimuli outside the ventricular vulnerable period. The onset of sinus node reset, duration of return sinus cycle (A2-A3) during reset, and estimated sinoatrial conduction times were recorded. Sinus node function during premature ventricular stimulation was approximated by utilizing the interval between the last sinus beat and onset of retrograde atrial depolarization (A1-A2 interval). The return cycle length (A2-A3) during sinus reset compared at equal A1-A2 intervals was significantly less with ventriculoatrial conduction (1,145 +/- 52 msec. atrial vs. 1,076 +/- 52 msec ventriculoatrial; P less than 0.01 by paired t test) and the estimated sinoatrial conduction time was significantly less with ventriculoatrial conduction (71 +/- 7 msec. atrial vs. 25 +/- 7 msec. ventriculoatrial; P less than 0.01 by paired t test). Ventriculoatrial sinus reset occurred later in the sinus cycle than atrial reset in three of seven patients with sinus reset produced by both atrial and ventricular prematures. This study shows that the effects of ventriculoatrial conduction on sinus node function are significantly different from those of atrial stimulation alone. The return sinus cycle length during reset and estimated sinoatrial conduction time are significantly reduced with ventriculoatrial conduction. Although the zones of sinus reset with atrial and ventricular stimulation are approximately equal, ventriculoatrial depolarization may produce sinus reset later in the sinus cycle in some cases.

Vulnerability to ventricular fibrillation during acute coronary arterial occlusion and release

The effect of 10 minutes of occlusion, and release of occlusion, of the left anterior descending coronary artery on vulnerability to ventricular fibrillation was studied in 15 dogs. Ventricular fibrillation threshold was determined by inducing a sequence of three closely coupled extrasystoles (sequential R/T pulsing). Within 3 minutes of occlusion the current required to induce fibrillation decreased from a control value of 56 ± 7 ma (mean ± standard error) to 1.6 ± 0.3 ma ( P < 0.001). It remained at this level for about 4 minutes and then rapidly returned to the control level in 8 of 10 dogs. Upon release of occlusion at 10 minutes, the ventricular fibrillation threshold was again greatly reduced; this period of reduction occurred shortly after reperfusion and was of brief duration. After both occlusion and release the duration of the ventricular vulnerable period was prolonged. The time course of change in cardiac vulnerability parallels the altered susceptibility to ventricular fibrillation after coronary arterial occlusion and release. These results recommend sequential R/T pulsing as a useful technique for probing changes in cardiac vulnerability under diverse experimental conditions.

Effect of current pulses delivered during the ventricular vulnerable period upon the ventricular fibrillation threshold

The effect of current delivered to the myocardium as either a pulse or train of pulses upon the recovery of excitability and upon the subsequent threshold for initiating ventricular fibrillation was studied in open chest dogs. Bipolar epicardial electrodes delivered current during the vulnerable period, and a circular array of six electrodes surrounding the central current electrode recorded the time course of recovery of myocardial excitability. Increasing the current intensity of either a pulse or train of pulses at the central site increased the temporal dispersion in recovery of excitability among the six peripheral electrode sites. This increase in temporal dispersion was associated with a decrease in ventricular fibrillation threshold immediately after the application of current. The degree of temporal dispersion in recovery after the train was increased by coronary occlusion but decreased by administration of lidocaine. Increasing the intensity of current delivered during the vulnerable period increases the degree of inhomogeneity in recovery of the myocardium until a level is attained that allows multiple asynchronous reentry and fibrillation. Interventions that increase or decrease the intrinsic amounts of inhomogeneity in the myocardium modify the amount of “extra inhomogeneity” that the current pulses must add during a fibrillation threshold determination to bring the myocardium to a level for fibrillation. In this way current delivered during the vulnerable period assesses vulnerability to fibrillation. These experiments also suggest that the ventricular fibrillation threshold following premature ventricular beats evoked by malfunctioning cardiac pacemakers may be lower than that following spontaneously occurring premature beats at the same coupling interval.

A vulnerable period for ventricular tachycardia following myocardial infarction.

Following ligation of left anterior descending coronary artery in dogs, low energy shocks delivered in the ventricular vulnerable period result in ventricular tachycardia—VT(υp). These disorders degenerate to ventricular fibrillation. VT(υp) can be reverted to sinus rhythm with transthoracic shocks of less than 1 Wsec. Within 7 days after infarction, VT(υp) can no longer be evoked. Similar arrhythmias have been noted in men with acute myocardial infarction.

Cardioversion and digitalis drugs: changed threshold to electric shock in digitalized animals.

The relationships between the action of digitalis drugs and the effects of cardioversion were studied in 44 dogs. Ventricular tachycardia provoked by either acetyl strophanthidin (AS) or ouabain could not be reverted to sinus rhythm by DC shock. When ventricular fibrillation was induced electrically during digitalis toxicity, defibrillation could be accomplished readily but the toxic arrhythmia due to digitalis remained unaltered. When ventricular fibrillation was induced by AS, it was also unaffected by repeated high energy discharges. In control animals the median energy to produce ventricular tachycardia by electrical discharge was 400 watt-seconds. Repeated electrical shocks did not change the level of energy required to produce ventricular tachycardia. However, following recovery from ouabain-induced ventricular tachycardia, the electrical threshold for ventricular tachycardia was 0.2 watt-second. A similar but less consistent response was noted after AS-induced ventricular tachycardia. The sensitization to electrical shock lasted for five to ten minutes after AS and for approximately one hour after recovery from ouabain toxicity. This same phenomenon of sensitization to electrical discharge was observed during digitalization. About 80% of the potentially toxic dose of ouabain had to be administered before the electrical threshold was lowered. The sensitivity to DC shock in the digitalized animal was not related to any specific phase of the cardiac cycle. Digitalization did not change the duration, location or energy limits of the ventricular vulnerable period. These experiments lead to the following conclusions of clinical importance: 1) Cardioversion will not be effective in arrhythmias induced by digitalis toxicity and 2) in the presence of overdigitalization cardioversion discharge may provoke serious disturbance of rhythm.