Repolarization characteristics indicate electrical instability in ventricular arrhythmia originating from papillary muscle

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
P Muenkler ◽  
N Klatt ◽  
K Scherschel ◽  
P Kuklik ◽  
C Jungen ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Ventricular Arrhythmia ◽  
Papillary Muscle ◽  
Cycle Length ◽  
Cardiovascular Research ◽  
Density Mapping ◽  
Recovery Interval ◽  
Electrical Instability ◽  
Dispersion Of Repolarization ◽  
Specificity And Sensitivity

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): DZHK (German Center for Cardiovascular Research) Introduction Cardiac arrhythmia originating from the papillary muscle can trigger ventricular fibrillation and cause sudden cardiac death even in the absence of structural heart disease. Yet, no clinical parameters are known to reflect the propensity of arrhythmia to degenerate into ventricular fibrillation. Purpose We aimed at identification of parameters associated with degeneration of ventricular arrhythmia into ventricular fibrillation. Methods Ventricular arrhythmia was induced by aconitine injection into the papillary muscle of healthy sheep (n = 12) in an open-chest model. Endocardial high-density-mapping and epicardial mapping were performed. We determined repolarization time and activation-recovery-interval according to the Wyatt method. Results During focal arrhythmia faster conduction occurred in longitudinal and basal direction than transversal and apical direction. The electrical restitution curve, modelling relation of diastolic interval and activation-recovery-interval, is steeper in aconitine-induced ventricular arrhythmia than in ventricular pacing or sinus rhythm. Steeper restitution curves reflect electrical instability and propensity to degenerate into ventricular fibrillation. The repolarization-related parameters activation-recovery interval and repolarization time exhibit higher heterogeneity per beat in ventricular arrhythmia preceding degeneration into ventricular fibrillation. Repolarization time in relation to cycle length (RT/CL), which can easily be measured during electrophysiological procedures, differentiates self-limiting from degenerating arrhythmia with high specificity and sensitivity. Conclusion In structurally normal ovine hearts, the ratio of repolarization and cycle length (RT/CL) in ventricular arrhythmia and greater dispersion of repolarization are indicators of subsequent degeneration into ventricular fibrillation. While dispersion of repolarization is not easily acquired in clinical routine, a simple index (RT/CL) may be sufficient to differentiate between self-limiting and electrically instable arrhythmia with propensity to degenerate to ventricular fibrillation. Abstract Figure. Repolarization in VA model

Reentrant wavefronts anchoring to the papillary muscle during ventricular fibrillation in open chest swine and dogs

Heart Rhythm ◽  
2005 ◽  
Vol 2 (5) ◽  
pp. S87 ◽  
Author(s):  
Hui-Nam Pak ◽  
Hong Euy Lim ◽  
Chung-Chuang Chou ◽  
Yasushi Miyauchi ◽  
Young Ho Bang ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Papillary Muscle ◽  
Open Chest

scholarly journals Atrial septal defect patients with greater shunts show susceptibility for ventricular arrhythmias

2020 ◽  
Vol 4 (Issue 3) ◽  
Author(s):  
Osman Can Yontar
Keyword(s):  
Ventricular Arrhythmia ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Ventricular Repolarization ◽  
Systolic Pulmonary Artery Pressure ◽  
T Wave ◽  
Dispersion Of Repolarization ◽  
Increased Risk ◽  
Shunt Group ◽  
Ventricular Arrhythmogenesis

Objective: Ventricular arrhythmia episodes are not infrequent in patients with atrial septal defect (ASD). Disturbance in cardiac volume and pressures may lead to enlargement and fibrosis in heart. An interatrial volume displacement through septal defect, briefly interatrial shunt, is the major reason for this complication. Prolongation of the interval between the peak and end of the T wave (Tpeak to Tend, Tp-e) on the 12-lead electrocardiogram (ECG), is utilized as a marker of ventricular arrhythmogenesis during last years. The aim of this study was to assess if there is an impact of shunt ratio on ventricular repolarization in patients with ASD by using Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. Methods: Patient records of Samsun Training and Research Hospital were retrospectively analyzed. Electrocardiograms of 133 patients, who were diagnosed as ASD between January 2016 and December 2019 were obtained and scanned. ECG intervals were measured. Shunt ratios, right ventricle diameters and volumes were also acquired. Patients were grouped into two by their calculated shunt ratio, ratio of ≥2.0 is accepted as a high shunt group and <2.0 as a low shunt group. Results: Both groups’ baseline characteristics were similar. Right ventricular dimensions and systolic pulmonary artery pressure were higher in high shunt group. Furthermore, ASD patients with higher shunt ratio had significantly higher ECG measurements than controls, Tp-e: 103.0 (22.1) vs 76.2 (10.2); Tp-e/QT: 0.25 (0.03) vs 0.21 (0.02); Tp-e/QTc: 0.22 (0.03)  vs, 0.17 (0.02); for all p<0.001). Of all ECG parameters; Tp-e (r=0.631, p<0.001), Tp-e/QT (r=0.531, p<0.001) and Tp-e/QTc (r=0.614, p<0.001) had moderate correlation with shunt ratio. Conclusion: T wave peak-to-end interval is a measure of transmural dispersion of repolarization and accepted as a surrogate for increased ventricular arrhythmogenesis risk. Our findings show that ASD patients whose shunt ratio are ≥2.0 show increased risk for arrhythmias. Key words: atrial septal defect, electrocardiogram, ventricular arrhythmia, risk, ventricular repolarization

scholarly journals Ventricular arrhythmia susceptibility in a new porcine model of heart failure (HF) with reduced ejection fraction

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
J Melka ◽  
A Helbert ◽  
L Lesage ◽  
K Moreau ◽  
K Romariz ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Ejection Fraction ◽  
Ventricular Arrhythmia ◽  
Ventricular Arrhythmias ◽  
Sham Group ◽  
Pig Model ◽  
Vehicle Group ◽  
Electrical Remodeling ◽  
Reduced Ejection Fraction ◽  
Lv Remodeling

Abstract Introduction Sudden death secondary to ventricular arrhythmias is common in HF patients, with no effective treatment available outside of implantable cardiac defibrillators. While animal models are essential for the discovery of anti-arrhythmic drugs, no reliable large animal HF models with associated ventricular arrhythmias have been described so far. Objectives We aimed at evaluating ventricular remodeling and arrhythmia susceptibility in an HF pig model with reduced ejection fraction (EF) following myocardial infarction (MI). Methods MI was induced in 53 male Göttingen minipigs (12–15 months, 20–25 kg) by coronary embolization in mid-left anterior descending and mid-left circumflex coronary arteries using endovascular coils. Seven other pigs underwent sham operation and were used as control. Two weeks after surgery, cardiac function was assessed by echocardiography, and animals were included based on EF<50% (n=15/53), assigned either to 12 weeks of vehicle (n=9) or perindopril (n=6, 1 mg/kg/d, per os) group. At the end of the study, their left ventricular (LV) electrical remodeling was studied by echocardiography/electrocardiography and a programmed-electrical stimulation protocol was performed to evaluate the susceptibility to develop ventricular arrhythmias. Results At the end of the study, animals in the vehicle group had a significant LV remodeling associated with a reduced EF (p<0.05 vs. sham, see table). This remodeling was associated with cardio-pulmonary congestion, significant increases in LV end-diastolic pressure, left atrial volume, and lung mass (all p<0.05 vs. sham, see table), fully prevented by perindopril treatment. They had also an electrical remodeling as evidenced by an increase in PR, QRS, and QTc intervals, as well as LV effective refractory period (+18%, 14%, 33%, and 13%, respectively, p<0.05, compared to sham animals). Electrical changes were mitigated by perindopril treatment (p=NS vs. sham). LV mechanical dispersion measured with speckle-tracking echocardiography was significantly increased in vehicle group (58±5 vs. 22±1 ms in sham group, respectively) as well as in perindopril group. Programmed-electrical stimulations induced in 6/8 vehicle animals either non-sustained (n=3) or sustained (n=2) ventricular tachycardia, or ventricular fibrillation (n=1). In sham group only 1/7 animal had a ventricular fibrillation. No inducible ventricular arrhythmia was observed in animals treated with Perindopril. Conclusion In this new pig model of congestive HF with reduced EF, LV remodeling was associated with electrical remodeling and susceptibility to develop arrhythmias. Chronic angiotensin-converting enzyme inhibitor treatment prevented congestion, mitigated electrical remodeling, and suppressed arrhythmia susceptibility. FUNDunding Acknowledgement Type of funding sources: Private company. Main funding source(s): Servier Research Institute - CardioVascular & Metabolic Diseases Center for Therapeutic Innovation Table 1

scholarly journals Intramural optical mapping of Vm and Cai2+ during long-duration ventricular fibrillation in canine hearts

2012 ◽  
Vol 302 (6) ◽  
pp. H1294-H1305 ◽  
Author(s):  
Wei Kong ◽  
Raymond E. Ideker ◽  
Vladimir G. Fast
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Short Duration ◽  
Action Potential Duration ◽  
Cycle Length ◽  
The Other ◽  
Membrane Voltage ◽  
Long Duration ◽  
Intracellular Ca ◽  
Rapid Pacing

Intramural gradients of intracellular Ca2+ (Cai2+) Cai2+ handling, Cai2+ oscillations, and Cai2+ transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Cai2+ handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Cai2+ handling contribute to LDVF, we measured membrane voltage ( Vm) and Cai2+ during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, Vm and Cai2+ progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed Vm upstrokes during pacing and LDVF. In conclusion, the fact that Vm upstrokes always preceded CaTs indicates that spontaneous Cai2+ oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong Vm-Cai2+ desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Cai2+ handling and may potentially contribute to LDVF maintenance.

High-dose lidocaine does not affect defibrillation efficacy: implications for defibrillation mechanisms

1998 ◽  
Vol 274 (4) ◽  
pp. H1113-H1120 ◽  
Author(s):  
Michael R. Ujhelyi ◽  
J. Jason Sims ◽  
Allison Winecoff Miller
Keyword(s):  
Ventricular Fibrillation ◽  
Cycle Length ◽  
Low Dose ◽  
High Dose ◽  
Channel Blockade ◽  
Group 3 ◽  
Baseline Values ◽  
Group 2 ◽  
Very High ◽  
Group 1

This study assessed the effect of low (10 mg ⋅ kg−1 ⋅ h−1) and very high (18 mg ⋅ kg−1 ⋅ h−1) doses of lidocaine on defibrillation energy requirements (DER) to relate changes in indexes of sodium-channel blockade with changes in DER values using a dose-response study design. In group 1 (control; n = 6 pigs), DER values were determined at baseline and during treatment with 5% dextrose in water (D5W) and with D5W added to D5W. In group 2 ( n = 7), DER values were determined at baseline and during treatment with low-dose lidocaine followed by high-dose lidocaine. In group 3 ( n = 3), DER values were determined at baseline and high-dose lidocaine. Group 3 controlled for the order of lidocaine treatment with the addition of high-dose lidocaine after baseline. DER values in group 1 did not change during D5W. In group 2, low-dose lidocaine increased DER values by 51% ( P = 0.01), whereas high-dose lidocaine added to low-dose lidocaine reduced DER values back to within 6% of baseline values ( P = 0.02, low dose vs. high dose). DER values during high-dose lidocaine in group 3 also remained near baseline values (16.2 ± 2.7 to 12.9 ± 2.7 J), demonstrating that treatment order had no impact on group 2. Progressive sodium-channel blockade was evident as incremental reduction in ventricular conduction velocity as the lidocaine dose increased. Lidocaine also significantly increased ventricular fibrillation cycle length as the lidocaine dose increased. However, the greatest increase in DER occurred when ventricular fibrillation cycle length was minimally affected, demonstrating a negative correlation ( P = 0.04). In summary, lidocaine has an inverted U-shaped DER dose-response curve. At very high lidocaine doses, DER values are similar to baseline and tend to decrease rather than increase. Increased refractoriness during ventricular fibrillation may be the electrophysiological mechanism by which high-dose lidocaine limits the adverse effects that low-dose lidocaine has on DER values. However, there is a possibility that an unidentified action of lidocaine is responsible for these effects.

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