scholarly journals Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts

2010 ◽  
Vol 298 (6) ◽  
pp. H2046-H2053 ◽  
Author(s):  
Li Li ◽  
Qi Jin ◽  
Derek J. Dosdall ◽  
Jian Huang ◽  
Steven M. Pogwizd ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Conduction Block ◽  
Three Dimensional ◽  
Left Ventricular ◽  
The Body ◽  
Long Duration ◽  
Surface Ecg ◽  
Electrode Matrix ◽  
Different Levels

Little is known about the three-dimensional (3-D) intramural activation sequences during long-duration ventricular fibrillation (VF), including the role of the subendocardium and its Purkinje fibers (PFs) in long-duration VF maintenance. Our aim was to explore the mechanism of long-duration VF maintenance with 3-D electrical mapping. We recorded 10 min of electrically induced VF in the left ventricular anterior free wall of six 10-kg, open-chest dogs using a 3-D transmural unipolar electrode matrix (9 × 9 × 6, 2-mm spacing) that allowed us to map intramural activation sequences. At 2.5 ± 1.8 min of VF, although the body surface ECG continued to exhibit a disorganized VF pattern, intramurally a more organized, synchronous activation pattern was first observed [locally synchronized VF (LSVF)]. This pattern occurred one or more times in all dogs and was present 33.4 ± 31.4% of the time during 5–10 min of VF. As opposed to the preceding changing complex activation sequences of VF, during LSVF, wavefronts were large and highly repeatable near the endocardium, first exciting the endocardium almost simultaneously and then rapidly spreading toward the epicardium with different levels of conduction block en route. During LSVF, PF activations always preceded working myocardium activations near the endocardium. In conclusion, long-duration VF in dogs frequently becomes highly organized in the subendocardium, with activation fronts arising in this region and passing intramurally toward the epicardium, even though the surface ECG continues to exhibit a disorganized pattern. PFs appear to play an important role during this stage of VF.

scholarly journals Verapamil reduces incidence of reentry during ventricular fibrillation in pigs

2014 ◽  
Vol 307 (9) ◽  
pp. H1361-H1369 ◽  
Author(s):  
Qi Jin ◽  
Derek J. Dosdall ◽  
Li Li ◽  
Jack M. Rogers ◽  
Raymond E. Ideker ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Conduction Velocity ◽  
Cycle Length ◽  
Conduction Block ◽  
Antiarrhythmic Effect ◽  
Delayed Rectifier ◽  
Activation Patterns ◽  
Long Duration ◽  
Activation Rate

The characteristics of reentrant circuits during short duration ventricular fibrillation (SDVF; 20 s in duration) and the role of Ca++ and rapid-activating delayed rectifier potassium currents during long duration ventricular fibrillation (LDVF; up to 10 min in duration) were investigated using verapamil and sotalol. Activation mapping of the LV epicardium with a 21 × 24 electrode plaque was performed in 12 open-chest pigs. Pigs were given either verapamil (0.136 mg/kg) or sotalol (1.5 mg/kg) and verapamil. Reentry patterns were quantified for SDVF, and, for LDVF, activation patterns were compared with our previously reported control LDVF data. Verapamil significantly increased conduction velocity around the reentrant core by 10% and reduced the reentrant cycle length by 15%, with a net reduction in reentry incidence of 70%. Sotolol had an opposite effect of decreasing the conduction velocity around the core by 6% but increasing the reentrant cycle length by 13%, with a net reduction of reentry incidence of 50%. After 200 s of VF, verapamil significantly slowed wavefront conduction velocity and activation rate compared with control data. Verapamil decreased the incidence of reentry in SDVF by accelerating conduction velocity to increase the likelihood of conduction block, possibly through increased sympathetic tone. The drug slowed activation rate and conduction velocity after 200 s of VF, suggesting that L-type Ca++ channels remain active and may be important in the maintenance of LDVF. Sotalol in addition to verapamil caused no additional antiarrhythmic effect.

scholarly journals Endocardial activation during ventricular fibrillation in normal and failing canine hearts

2000 ◽  
Vol 279 (4) ◽  
pp. H1737-H1747 ◽  
Author(s):  
Gordon L. Pierpont ◽  
Sumeet S. Chugh ◽  
John A. Hauck ◽  
Charles C. Gornick
Keyword(s):  
Ventricular Fibrillation ◽  
Balloon Catheter ◽  
Three Dimensional ◽  
Left Ventricular ◽  
Multielectrode Array ◽  
Three Dimensional Model ◽  
Centroid Frequency ◽  
Rapid Ventricular Pacing ◽  
Fft Analysis ◽  
Endocardial Activation

Because congestive heart failure (CHF) promotes ventricular fibrillation (VF), we compared VF in seven dogs with CHF induced by combined myocardial infarction and rapid ventricular pacing to VF in six normal dogs. A noncontact, multielectrode array balloon catheter provided full-surface real-time left ventricular (LV) endocardial electrograms and a dynamic color-coded display of endocardial activation projected onto a three-dimensional model of the LV. Fast Fourier transform (FFT) analysis of virtual electrograms showed no difference in peak or centroid frequency in CHF dogs compared with normals. The average number of simultaneous noncontiguous wavefronts present during VF was higher in normals (2.4 ± 1.0 at 10 s of VF) than in CHF dogs (1.3 ± 1.0, P < 0.005) and decreased in both over time. The wavefront “turnover” rate, estimated using FFT of the noncontiguous wavefront data, did not differ between normals and CHF and did not change over 5 min of VF. Thus the fundamental frequency characteristics of VF are unaltered by CHF, but dilated abnormal ventricles sustain fewer active wavefronts than do normal ventricles.

Ventricular fibrillation in myopathic human hearts: mechanistic insights from in vivo global endocardial and epicardial mapping

2007 ◽  
Vol 292 (6) ◽  
pp. H2589-H2597 ◽  
Author(s):  
Stéphane Massé ◽  
Eugene Downar ◽  
Vijay Chauhan ◽  
Elias Sevaptsidis ◽  
Kumaraswamy Nanthakumar
Keyword(s):  
Ventricular Fibrillation ◽  
Electrical Activity ◽  
Conduction Block ◽  
Left Ventricular ◽  
Ventricular Cardiomyopathy ◽  
Epicardial Mapping ◽  
Border Regions ◽  
Number Of Cycles ◽  
The Hilbert Transform

Ventricular fibrillation (VF) is an important cause of sudden cardiac death and cardiovascular mortality in patients with cardiomyopathy. Although it was generally believed that chaotic reentrant wavefronts underlie VF in humans, there is emerging evidence of spatiotemporal organization during early VF. The mechanism of this organization of electrical activity in early VF is unknown in myopathic hearts. We studied early VF in vivo, intraoperatively in five cardiomyopathic patients. Simultaneous electrograms were obtained from the epicardium and endocardium in left ventricular cardiomyopathy and from the endocardium in right ventricular myopathy. The Hilbert transform was used to derive the phase of the electrograms. Rotors were identified by isolating phase singularity points. Rotors were present in all of the myopathic hearts studied during VF and cumulatively lasted a mean of 3.2 ± 2.0 s of the 7.0 ± 4.0 s of the VF segments analyzed. For each surface mapped, 3.6 ± 2.9 rotors were identified for the duration mapped. The average number of cycles completed by these rotors was 4.9 ± 4.9. The longest rotor lasted 10.2 ± 6.2 rotations and lasted 2.0 ± 1.2 s. The rotors on the endocardium had a cycle length of 192 ± 33 ms compared with 220 ± 15 ms on the epicardium ( P = 0.08). There is centrifugal activation of electrical activity from these rotors, and they give rise to domains that activate at faster rates with evidence of conduction block at the border with slower domains. These rotors frequently localized to border regions of myocardium with bipolar electrogram amplitude of <0.5 mV. The organization of electrical activity during early VF in myopathic human hearts is characterized by wavefronts emanating from a few rotors.

Discordant S-T alternans contributes to formation of reentry: a possible mechanism of reperfusion arrhythmia

1998 ◽  
Vol 275 (1) ◽  
pp. H116-H121 ◽  
Author(s):  
Hidetada Tachibana ◽  
Isao Kubota ◽  
Michiyasu Yamaki ◽  
Tetsu Watanabe ◽  
Hitonobu Tomoike
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Conduction Block ◽  
Activation Time ◽  
Reperfusion Arrhythmia ◽  
Open Chest ◽  
Life Threatening ◽  
Control State ◽  
Reentrant Circuit

Although a relationship between S-T alternans and life-threatening arrhythmia has been recognized, the mechanism is poorly understood. We examine the role of S-T alternans in the occurrence of ventricular fibrillation (VF) after reperfusion. The left anterior descending coronary artery was occluded for 20 min and then abruptly reperfused in 12 intravenously anesthetized open-chest dogs. Sixty unipolar epicardial electrograms were recorded during the control state, at the end of occlusion, and after reperfusion. The largest magnitude of S-T alternans among 60 leads was defined as the maximum S-T alternans. Isochronal maps of activation time in paced beat and spontaneous ventricular premature contractions (VPC) were analyzed. After reperfusion, VF ensued in six dogs. The maximum S-T alternans augmented progressively with time after reperfusion until VF occurred. In three dogs with VF, when activation of VPC resulted in conduction block and formed reentry, VF ensued. The conduction block was located between sites of discordant S-T alternans (S-T alternans at adjacent leads was out of phase). These data indicate that discordant S-T alternans relates to VF by facilitating the formation of a reentrant circuit.

Canine gallbladder cyclic motor activity

1988 ◽  
Vol 255 (4) ◽  
pp. G409-G416 ◽  
Author(s):  
T. Matsumoto ◽  
S. K. Sarna ◽  
R. E. Condon ◽  
W. J. Dodds ◽  
N. Mochinaga
Keyword(s):  
Motor Activity ◽  
Short Duration ◽  
Sphincter Of Oddi ◽  
The Body ◽  
Phase Iii ◽  
Fasted State ◽  
Long Duration ◽  
The Mean ◽  
Esophageal Sphincter

We investigated whether the gallbladder has cyclic motor activity similar to that of the stomach, lower esophageal sphincter, and sphincter of Oddi in the fasted state. We found that the canine gallbladder infundibulum exhibited a cyclic burst of short duration (69 +/- 3 s) contractions that were closely associated with phase III activity of the antrum. The cyclic motor activity was sometimes less prominent or absent in the body and the fundus of the gallbladder. The mean period of gallbladder cyclic motor activity was not significantly different from the mean period of phase III activity in the stomach and the duodenum. The cyclic bursts of gallbladder contractions lasted for 21 +/- 2 min. The gallbladder cyclic motor activity started at about the same time as the antral phase III activity, and both of these activities started approximately 12 min earlier than the duodenal phase III activity. In addition to the aforementioned cyclic bursts of contractions, the gallbladder sometimes exhibited long duration (6.4 +/- 0.6 min) contractions that occurred irregularly and unpredictably during the duodenal migrating motor complex cycle. We conclude that during fasting the canine gallbladder has a cyclic motor activity that is temporally related to phase III activity of the stomach and the duodenum. The role of short duration phasic contractions during cyclic motor activity may be to periodically stir gallbladder contents, whereas the long duration contractions may partially empty the gallbladder in the fasted state.

scholarly journals Ventricular fibrillation waveform characteristics of the surface ECG: Impact of the left ventricular diameter and mass

Resuscitation ◽  
2017 ◽  
Vol 115 ◽  
pp. 82-89 ◽  
Author(s):  
Judith L. Bonnes ◽  
Jos Thannhauser ◽  
Joris Nas ◽  
Sjoerd W. Westra ◽  
Rutger M.G. Jansen ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Left Ventricular ◽  
Left Ventricular Diameter ◽  
Surface Ecg

Role of left ventricular untwisting in diastolic dysfunction after long duration exercise

2011 ◽  
Vol 112 (2) ◽  
pp. 525-533 ◽  
Author(s):  
Stéphane Nottin ◽  
Arnaud Ménétrier ◽  
Thomas Rupp ◽  
Alain Boussuges ◽  
Nicolas Tordi
Keyword(s):  
Diastolic Dysfunction ◽  
Left Ventricular ◽  
Long Duration

Abstract 149: Role of Pre and Intra-Arrest Hemodynamics in Evolution of the Ventricular Fibrillation Electrocardiogram Waveform

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Caelie E Kern ◽  
David D Salcido
Keyword(s):  
Ventricular Fibrillation ◽  
Trajectory Analysis ◽  
Venous Pressure ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Pressure Transducers ◽  
Surface Ecg ◽  
Electrical Induction

Purpose: Quantitative waveform measures (QWM) of the ventricular fibrillation (VF) waveform have been shown in laboratory and clinical studies to be predictive of return of spontaneous circulation (ROSC) and survival to hospital discharge. During resuscitation, QWM are responsive to hemodynamic changes resulting from CPR. It is not known whether the trajectory of QWM are affected by pre-arrest hemodynamics or intra-arrest arterio-venous pressure equilibration. We sought to investigate the role of hemodynamics on the evolution of VF before and during prolonged VF. Methods: We pooled data from six previous porcine experiments. Each modeled prolonged VF and included electrical induction of VF which was left untreated for up to 10 minutes, followed by attempted resuscitation. All animals were instrumented with pressure transducers (Millar, MikroTip) placed via femoral cutdown in the aorta and right atrium, as well as Lead II surface ECG. Signals were recorded continuously at 1000Hz with a data acquisition unit (PowerLab, ADInstruments). Mean baseline central arterial (CAP) and central venous pressure (CVP) were calculated from 1- minute of immediate pre-VF pressure traces. Coronary perfusion pressure (CPP) during untreated VF was calculated as the continuous difference between the CAP and CVP channels. Median slope (MS), a QWM, was calculated in 1-second windows and interpolated to the full length of the intra-arrest ECG. For trajectory analysis, CPP and MS traces were normalized on a 0-1 scale and grouped by morphological similarity. Pearson’s Correlation coefficient was calculated between corresponding CPP and MS traces. Results: A total of 141 experiments were included in the analysis. Overall mean (SD) correlation between CPP and MS was 0.56 (0.29). CPP-MS correlation strength did not correlate with baseline pressures. However, trajectory analysis revealed multiple patterns of hemodynamic and QWM evolution through untreated VF, with the most well-defined (mean coeff. = 0.58) indicating a shared bimodality temporally offset between CPP and MS. Conclusions: Hemodynamics during untreated VF show some correlation with the trajectory of QWM of the VF signal. More work is needed to understand the mechanism of this relationship.

scholarly journals Numerical Evaluation of Myofiber Orientation and Transmural Contractile Strength on Left Ventricular Function

2015 ◽  
Vol 137 (4) ◽  
Author(s):  
Xiaoyan Zhang ◽  
Premi Haynes ◽  
Kenneth S. Campbell ◽  
Jonathan F. Wenk
Keyword(s):  
Numerical Evaluation ◽  
Critical Role ◽  
Left Ventricular ◽  
The Body ◽  
Fe Model ◽  
Complex Organization ◽  
Physiologic Parameters ◽  
Myocardial Contractile ◽  
Cardiac Muscle Fibers

The left ventricle (LV) of the heart is composed of a complex organization of cardiac muscle fibers, which contract to generate force and pump blood into the body. It has been shown that both the orientation and contractile strength of these myofibers vary across the ventricular wall. The hypothesis of the current study is that the transmural distributions of myofiber orientation and contractile strength interdependently impact LV pump function. In order to quantify these interactions a finite element (FE) model of the LV was generated, which incorporated transmural variations. The influences of myofiber orientation and contractile strength on the Starling relationship and the end-systolic (ES) apex twist of the LV were assessed. The results suggest that reductions in contractile strength within a specific transmural layer amplified the effects of altered myofiber orientation in the same layer, causing greater changes in stroke volume (SV). Furthermore, when the epicardial myofibers contracted the strongest, the twist of the LV apex was greatest, regardless of myofiber orientation. These results demonstrate the important role of transmural distribution of myocardial contractile strength and its interplay with myofiber orientation. The coupling between these two physiologic parameters could play a critical role in the progression of heart failure.

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