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Purkinje action potentials (A and C) and Ca 2+ transients (B and D) recorded from cell 40 in control and HF at 1 Hz (A and B) and 3 Hz (C and D) stimulation.
Source publication
This study used one-dimensional computer simulation to investigate the influence of heart failure on action potential conduction through the left Purkinje fibres to the left ventricle. The study was based on a rabbit model of left ventricular heart failure caused by volume and pressure overload. To simulate the effect of heart failure, we began wit...
Contexts in source publication
Context 1
... 1D multicellular model (150 cells: 75 PF cells and 75 ventricular cells) was used to investigate the influence of HF on the conduction of the action potential through the PF to the ventricular muscle. The stimulus was applied to the first 3 PF cells (cells 1~3). Fig. 3 shows the PF action potential and Ca 2+ transient recorded from the middle Purkinje cell (cell 40) in the ID model in control and HF at 1 Hz and 3 Hz stimulation. The PF action potential was computed using the 85% qPCR HF model and the ventricular action potential was computed using the 85% qPCR HF, Ruijter HF and Pogwizd HF models. ...
Context 2
... control and HF at 1 Hz and 3 Hz stimulation. The PF action potential was computed using the 85% qPCR HF model and the ventricular action potential was computed using the 85% qPCR HF, Ruijter HF and Pogwizd HF models. After coupling to ventricular muscle, HF caused PF action potential prolongation (without EADs) at 1 Hz stimulation with all models (Fig. 3A). However, with the Ruijter and Powizd HF models, the PF action potential could not follow 3 Hz stimulation because the PF action potential was more prolonged than with the 85% qPCR HF model. Fig. 6 shows APD90 (action potential duration at 90% repolarization) and APD50 (action potential duration at 50% repolarization) of all cells in ...
Citations
... Electrical impulses progress from the branches of the HB towards the Purkinje fibers to finally allow ventricular contraction, and these fibers also have a determining role in generating ventricular arrhythmias, which can be observed at the electrocardiographic level (Li et al. 2015;Aouadi et al. 2019). This underlines the importance of histological study of HB, as enhanced understanding of the cellular and tissue structure associated with cardiac physiology, can enable us to delineate the sites of arrhythmia production in different species. ...
The His bundle is a part of the specialized electrical conduction system that provides a connection between the atrial and ventricular myocardial compartments in both normal and abnormal hearts. The aim of this study was to perform a morphometric analysis of His bundle characteristics of in humans, dogs, horses and pigs and compare them in these studied species. Histological sections of 5 μm thickness were obtained and stained with hematoxylin–eosin and Masson's trichrome; the desmin and periodic acid–Schiff methods were also used for precise identification of cells. The His bundle was found to be longer in horses (2.85 ± 1.02 mm) and pigs (1.77 ± 0.9 mm) than in dogs (1.53 ± 0.8 mm) or humans, in which it was shortest (1.06 ± 0.6 mm). The area and diameters in His bundle cells, were significantly larger in pigs and horses than in humans (p < 0.001) or dogs (p < 0.001). We found two organizational patterns of His bundle components: group I, with large cells and a high amount of collagen fibers in ungulates (pigs and horses); and group II, with smaller cells and lower abundance of collagen fibers in humans and dogs. Documenting cell size variations in the His bundle allows us not only to identify this bundle by histological or anatomical location but also to differentiate these cells from others such as nodal or Purkinje cells. Our analysis revealed that His bundle cells have discrete identities based on their morphometric and histological characteristics.
... Such reentry will also be dependent on slow conduction in the reentry loop; it will be facilitated by the well-known conduction delay of 5 to 20 ms at the Purkinje-ventricle junction. 46,47 This type of reentry may be more likely in the failing heart, because the changes in APD (and, therefore, refractoriness) are more marked and there is a slowing of PF conduction. In HF, because of the prolonged APD in LPFs, but not in LV, at the LPF-LV junction there was a marked APD gradient over a short distance. ...
Background
Purkinje fibers (PFs) control timing of ventricular conduction and play a key role in arrhythmogenesis in heart failure (HF) patients. We investigated the effects of HF on PFs.
Methods
Echocardiography, electrocardiography, micro-computed tomography, quantitative polymerase chain reaction, immunohistochemistry, volume electron microscopy, and sharp microelectrode electrophysiology were used.
Results
Congestive HF was induced in rabbits by left ventricular volume- and pressure-overload producing left ventricular hypertrophy, diminished fractional shortening and ejection fraction, and increased left ventricular dimensions. HF baseline QRS and corrected QT interval were prolonged by 17% and 21% (mean±SEMs: 303±6 ms HF, 249±11 ms control; n=8/7; P =0.0002), suggesting PF dysfunction and impaired ventricular repolarization. Micro-computed tomography imaging showed increased free-running left PF network volume and length in HF. mRNA levels for 40 ion channels, Ca ²⁺ -handling proteins, connexins, and proinflammatory and fibrosis markers were assessed: 50% and 35% were dysregulated in left and right PFs respectively, whereas only 12.5% and 7.5% changed in left and right ventricular muscle. Funny channels, Ca ²⁺ -channels, and K ⁺ -channels were significantly reduced in left PFs. Microelectrode recordings from left PFs revealed more negative resting membrane potential, reduced action potential upstroke velocity, prolonged duration (action potential duration at 90% repolarization: 378±24 ms HF, 249±5 ms control; n=23/38; P <0.0001), and arrhythmic events in HF. Similar electrical remodeling was seen at the left PF-ventricular junction. In the failing left ventricle, upstroke velocity and amplitude were increased, but action potential duration at 90% repolarization was unaffected.
Conclusions
Severe volume- followed by pressure-overload causes rapidly progressing HF with extensive remodeling of PFs. The PF network is central to both arrhythmogenesis and contractile dysfunction and the pathological remodeling may increase the risk of fatal arrhythmias in HF patients.
... Electrical impulses progress from the branches of HB towards PF to nally allow ventricular contraction, but these bers also have a determining role in generating ventricular arrhythmias, which can be observed at the electrocardiographic level (Li et al. 2015;Aouadi et al. 2019). For this reason, we reiterate the importance of the histological study of HB, as with a working knowledge of the cellular and tissue structure associated with cardiac physiology, it is possible to delineate the sites of arrhythmia production in different species. ...
His bundle is a part of the specialized electrical conduction system that, in the normal or anormal hearts, provides connection between the atrial and ventricular myocardial compartments. The aim of this study was to perform a morphometric analysis of the characteristics of His bundle and its association with predetermined electrophysiological variables in humans, dogs, horses, and pigs. We used five hearts of the species studied. Histological sections of 5 µm thickness were obtained and stained with hematoxylin-eosin and Masson's trichrome. We also used the desmin and PAS method for precise identification of cells. His bundle was longer in horses (2.85 x 0.82 mm) and pigs (1.77 x 0.44 mm) than in dogs (1.53 x 0.26 mm) and humans, which was the shortest (1.06 x 0.23 mm). In His bundle cells, the area and diameters were significantly larger in pigs and horses than in humans (p < 0.001) and dogs (p < 0.001). We have found two patterns of organization of the components of His bundle: Group I, with large cells and a high amount of collagen fibers in ungulates (pigs and horses); group II, with smaller cells and less amount of collagen fibers in humans and dogs. Documenting differences in cell size in His bundle allows us to obtain an additional, alternative identification criterion to commonly used ones such as anatomical location. Morphological characteristics of His bundle and its cells in the different species studied coincide with rapid or slow transmission of the electrical impulse when compared with the predetermined electrophysiological variables.
Purkinje fibers (PFs) permit the heart's conduction system to produce synchronized contractions of its ventricles, critical for continuing a reliable heart rhythm. Hardware realization of different parts of heart is done to simulate or dealing with some of diseases and deficiencies. PF performance can be described by models including a set of differential equations. In this paper the Noble model is modified for implementing a hardware to mimic the PF performance. The original model includes non-linear terms which are low speed and high cost regarding the hardware resources because of need to use the units such as multipliers. In modified model, the non-linear terms are converted to 2x terms to be implemented by low cost and high speed digital hardware such as logical SHIFTs, ADDs, and SUBs. The dynamic behavior of proposed model is close to the original model. A digital platform, Spartan 3xc3s50 tq144 Field Programmable Gate Arrays (FPGA) is used to certify the precision and feasibility of proposed model. The results show that the proposed model is easily implemented on this board and is able to produce different PF patterns at the maximum frequency of 162.273MHz meanwhile the original model is not implementable because of its non-linear elements.
Heart failure is associated with electrical remodeling of the electrical properties and kinetics of the ion channels and transporters that are responsible for cardiac action potentials. However, it is still unclear whether heart failure-induced ionic remodeling can affect the conduction of excitation waves at the Purkinje fiber-ventricle junction contributing to pro-arrhythmic effects of heart failure, as the complexity of the heart impedes a detailed experimental analysis. The aim of this study was to employ computational models to investigate the pro-arrhythmic effects of heart failure-induced ionic remodeling on the cardiac action potentials and excitation wave conduction at the Purkinje fiber-ventricle junction. Single cell models of canine Purkinje fiber and ventricular myocytes were developed for control and heart failure. These single cell models were then incorporated into one-dimensional strand and three-dimensional wedge models to investigate the effects of heart failure-induced remodeling on propagation of action potentials in Purkinje fiber and ventricular tissue and at the Purkinje fiber-ventricle junction. This revealed that heart failure-induced ionic remodeling of Purkinje fiber and ventricular tissue reduced conduction safety and increased tissue vulnerability to the genesis of the unidirectional conduction block. This was marked at the Purkinje fiber-ventricle junction, forming a potential substrate for the genesis of conduction failure that led to re-entry. This study provides new insights into proarrhythmic consequences of heart failure-induced ionic remodeling.
Histologically, the cardiac conduction network is formed of electrically isolated subendocardial fibers that comprise specialized cells with fewer myofibrils and mitochondria than cardiomyocytes. Our aim is to uncover regional variations of cardiac conduction fibers through histological and morphometric study in a porcine and human model. We analyzed five male adult human hearts and five male pig hearts. The left ventricles were dissected and sectioned in the axial plane into three parts: basal, middle third and apex regions. Cardiac conduction fibers study was carried out using hematoxylin-eosin and Masson's trichrome staining, and cardiac conduction cells and their junctions were identified using desmin, connexin 40 and a PAS method. Cardiac conduction fibers were difficult to pinpoint in humans, mostly showing a darker color or equal to cardiomyocytes. Cardiac conduction fibers in humans were in the subendocardium and in pigs in the myocardium and subendocardium. Cardiac conduction fibers were located mainly in the septal region in both humans and pigs. In our morphometric analysis, we were able to determine that cardiac conduction cells in humans (18.52 +/− 5.41 μm) and pigs (21.32 +/− 6.45 μm) were large, compared to cardiomyocytes. Conduction fiber-myocardial junctions were present in 10% in humans and 24.2% in pigs. The performance of immunohistochemical methods made it possible to improve the identification of cardiac conduction cells in the species studied. Study of cardiac conduction fibers and cells and their myocardial junctions is vital to gain insight into their normal distribution in the species analyzed, and thus advance the use of pigs in experimental models of the cardiac conduction system in humans.
The principal function of the ventricular conduction system is rapid electrical activation of the ventricles. The aim of this study is to conduct a morphometric study to pinpoint the morphological parameters that define cardiac conduction cells, allowing us to distinguish them from other cells.
Five male horse hearts and five male dog hearts were used in the study. The hearts were fixed in a 5% formaldehyde solution. Histological sections of 5 μm thickness were acquired and stained with hematoxylin-eosin and Masson's trichrome and cardiac conduction cells and their junctions were identified by desmin, connexin 40 and a PAS method.
We found statistically significant differences in cardiac conduction fibers density and thickness, which was much higher in horses than in dogs (p = 0.000 for both values). By comparing the measured parameters of the cells in both species, we determined that cardiac conduction cells area and diameters were greater in horses than in dogs (p = 0.000 for all values). In dogs there are more junctions (30.8%) than in horses (26.1%), a statistically significant difference (p = 0.041). Our findings regarding the cardiac conduction fibers distribution in the animal species studied becomes new knowledge that contributes to the morphological study of this component of the cardiac conduction system and also makes it possible to locate exactly the site with the highest density of cardiac conduction fibers as a contribution to the cardiological study of these structures that lead to the prevention of ventricular arrhythmias and the identification of their treatment site.
