His Bundle Activates Faster than Ventricular Myocardium during Prolonged Ventricular Fibrillation

Background

The Purkinje fiber system has recently been implicated as an important driver of the rapid activation rate during long duration ventricular fibrillation (VF>2 minutes). The goal of this study is to determine whether this activity propagates to or occurs in the proximal specialized conduction system during VF as well.

Methods and Results

An 8×8 array with 300 µm spaced electrodes was placed over the His bundles of isolated, perfused rabbit hearts (n = 12). Ventricular myocardial (VM) and His activations were differentiated by calculating Laplacian recordings from unipolar signals. Activation rates of the VM and His bundle were compared and the His bundle conduction velocity was measured during perfused VF followed by 8 minutes of unperfused VF. During perfused VF the average VM activation rate of 11.04 activations/sec was significantly higher than the His bundle activation rate of 6.88 activations/sec (p<0.05). However from 3–8 minutes of unperfused VF the His system activation rate (6.16, 5.53, 5.14, 5.22, 6.00, and 4.62 activations/sec significantly faster than the rate of the VM (4.67, 3.63, 2.94, 2.24, 3.45, and 2.31 activations/sec) (p<0.05). The conduction velocity of the His system immediately decreased to 94% of the sinus rate during perfused VF then gradually decreased to 67% of sinus rhythm conduction at 8 minutes of unperfused VF.

Conclusion

During prolonged VF the activation rate of the His bundle is faster than that of the VM. This suggests that the proximal conduction system, like the distal Purkinje system, may be an important driver during long duration VF and may be a target for interventional therapy.     

Ablation of Premature Ventricular Complexes Triggering Ventricular Fibrillation in a Patient with Long QT Syndrome

We describe the case of a patient with long QT syndrome and recurrent ventricular fibrillation, triggered by premature ventricular complexes (PVCs) with a left bundle branch block pattern and inferior axis of the QRS. Activation mapping demonstrated the origin of the PVCs to be in the right ventricular outflow tract. Ventricular fibrillation (VF) was successfully treated by catheter ablation of the triggering PVCs and there has been no recurrence of VF during a follow-up period of 14 months.     

Long-term Prognosis following Ventricular Fibrillation in Acute Ischaemic Heart Disease

Of 160 patients who survived ventricular fibrillation complicating acute ischaemic heart disease, 80 had had a clinically mild coronary attack. Most of the long-term survivors had ventricular fibrillation within 24 hours of the onset of symptoms. The longterm prognosis of the survivors was similar to that of patients whose myocardial infarction was not complicated by ventricular fibrillation. Those patients who survived ventricular fibrillation which occurred within four hours of the onset of symptoms were younger, usually had had a mild coronary attack, and had the most favourable longterm prognosis. The number of episodes of ventricular fibrillation did not affect adversely the long-term prognosis. Of those who at the time of review were eligible to work, 86% were fit to work and 68% were actually at work.     

A Single-Cell Model of Phase-Driven Control of Ventricular Fibrillation Frequency

The mechanisms controlling the rotation frequency of functional reentry in ventricular fibrillation (VF) are poorly understood. It has been previously shown that Ba²⁺ at concentrations up to 50 μmol/L slows the rotation frequency in the intact guinea pig (GP) heart, suggesting a role of the inward rectifier current (I_K1) in the mechanism governing the VF response to Ba²⁺. Given that other biological (e.g., sinoatrial node) and artificial systems display phase-locking behavior, we hypothesized that the mechanism for controlling the rotation frequency of a rotor by I_K1 blockade is phase-driven, i.e., the phase shift between transmembrane current and voltage remains constant at varying levels of I_K1 blockade. We measured whole-cell admittance in isolated GP myocytes and in transfected human embryonic kidney (HEK) cells stably expressing Kir 2.1 and 2.3 channels. The admittance phase, i.e., the phase difference between current and voltage, was plotted versus the frequency in control conditions and at 10 or 50 μmol/L Ba²⁺ (in GP heart cells) or 1 mM Ba²⁺ (in HEK cells). The horizontal distance between plots was called the “frequency shift in a single cell” and analyzed. The frequency shift in a single cell was −14.14 ± 5.71 Hz (n = 14) at 10 μM Ba²⁺ and −18.51 ± 4.00 Hz (n = 10) at 50 μM Ba²⁺, p < 0.05. The values perfectly matched the Ba²⁺-induced reduction of VF frequency observed previously in GP heart. A similar relationship was found in the computer simulations. The phase of Ba²⁺-sensitive admittance in GP cells was −2.65 ± 0.32 rad at 10 Hz and −2.79 ± 0.26 rad at 30 Hz. In HEK cells, the phase of Ba²⁺-sensitive admittance was 3.09 ± 0.03 rad at 10 Hz and 3.00 ± 0.17 rad at 30 Hz. We have developed a biological single-cell model of rotation-frequency control. The results show that although rotation frequency changes as a result of I_K1 blockade, the phase difference between transmembrane current and transmembrane voltage remains constant, enabling us to quantitatively predict the change of VF frequency resulting from I_K1 blockade, based on single-cell measurement.     

基于支持向量机的室颤信号检测算法

目的:实现室颤信号与非室颤信号的分类,进而实现室颤信号的检测。方法:本文引入了一种基于支持向量机(Support Vec-tor Machine,SVM)和改进的越限区间算法(TCI)的新算法,其中支持向量机在处理分类和模式识别等问题中具有很大的优势。该算法采用4s的滑动窗技术,并利用改进后的越限区间算法(Threshold Crossing Interval,TCI)方法提取心电信号的特征。新算法的实现如下:在每一滑动窗内采用改进的后的绝对值阈值,计算中间2s内的平均越限间隔值。并以此TCI值作为特征参数,输入一个预先设计好的二分类支持向量机中,从而实现分类。结果:成功实现了室颤信号的检测,通过计算该方法的灵敏度、精确度、预测性和准确度且与其他方法相比较,可知此新算法总体可靠性优于其他方法。结论:该算法能够实现室颤信号的实时监测,且简单易行,易于实现,较适合实时的心电监测以及除颤仪器。     

The Role of Photon Scattering in Voltage-Calcium Fluorescent Recordings of Ventricular Fibrillation

Recent optical mapping studies of cardiac tissue suggest that membrane voltage (V_m) and intracellular calcium concentrations (Ca) become dissociated during ventricular fibrillation (VF), generating a proarrhythmic substrate. However, experimental methods used in these studies may accentuate measured dissociation due to differences in fluorescent emission wavelengths of optical voltage/calcium (V_opt/Ca_opt) signals. Here, we simulate dual voltage-calcium optical mapping experiments using a monodomain-Luo-Rudy ventricular-tissue model coupled to a photon-diffusion model. Dissociation of both electrical, V_m/Ca, and optical, V_opt/Ca_opt, signals is quantified by calculating mutual information (MI) for VF and rapid pacing protocols. We find that photon scattering decreases MI of V_opt/Ca_opt signals by 23% compared to unscattered V_m/Ca signals during VF. Scattering effects are amplified by increasing wavelength separation between fluorescent voltage/calcium signals and respective measurement-location misalignment. In contrast, photon scattering does not affect MI during rapid pacing, but high calcium dye affinity can decrease MI by attenuating alternans in Ca_opt but not in V_opt. We conclude that some dissociation exists between voltage and calcium at the cellular level during VF, but MI differences are amplified by current optical mapping methods.     

Effects of Mechano-Electric Feedback on Scroll Wave Stability in Human Ventricular Fibrillation

Recruitment of stretch-activated channels, one of the mechanisms of mechano-electric feedback, has been shown to influence the stability of scroll waves, the waves that underlie reentrant arrhythmias. However, a comprehensive study to examine the effects of recruitment of stretch-activated channels with different reversal potentials and conductances on scroll wave stability has not been undertaken; the mechanisms by which stretch-activated channel opening alters scroll wave stability are also not well understood. The goals of this study were to test the hypothesis that recruitment of stretch-activated channels affects scroll wave stability differently depending on stretch-activated channel reversal potential and channel conductance, and to uncover the relevant mechanisms underlying the observed behaviors. We developed a strongly-coupled model of human ventricular electromechanics that incorporated human ventricular geometry and fiber and sheet orientation reconstructed from MR and diffusion tensor MR images. Since a wide variety of reversal potentials and channel conductances have been reported for stretch-activated channels, two reversal potentials, −60 mV and −10 mV, and a range of channel conductances (0 to 0.07 mS/µF) were implemented. Opening of stretch-activated channels with a reversal potential of −60 mV diminished scroll wave breakup for all values of conductances by flattening heterogeneously the action potential duration restitution curve. Opening of stretch-activated channels with a reversal potential of −10 mV inhibited partially scroll wave breakup at low conductance values (from 0.02 to 0.04 mS/µF) by flattening heterogeneously the conduction velocity restitution relation. For large conductance values (>0.05 mS/µF), recruitment of stretch-activated channels with a reversal potential of −10 mV did not reduce the likelihood of scroll wave breakup because Na channel inactivation in regions of large stretch led to conduction block, which counteracted the increased scroll wave stability due to an overall flatter conduction velocity restitution.