The infrahisian conduction system and endocavitary cardiac structures: relevance for the invasive electrophysiologist

Syed, Faisal F.; Hai, Jo Jo; Lachman, Nirusha; DeSimone, Christopher V.; Asirvatham, Samuel J.

doi:10.1007/s10840-013-9858-7

Cited by 38 publications

(30 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“… A: Remarkably similar diagrams of the proximal left-sided conduction system as observed in 20 normal human hearts demonstrating the origin of the anterior, posterior and median fascicles from Syed et al from [5]. B: Pig moderator band histology demonstrating conduction tissue (Purkinje fibers) lying within the band from Syed et al [5].…”

Section: Figurementioning

confidence: 63%

“…However today we must consider that Purkinje fiber bundles have been identified morphologically in various compartments of the heart. Figure 1A,B show examples of such where the phenotypes of the major Purkinje bundles of the human proximal LV conduction system are compared to those Purkinje fiber bundles found in the Moderator Band(MB) of the RV 5 . With modern day electromapping and catheter techniques, we now know that premature ventricular depolarizations can originate from the MB often inducing ventricular fibrillation 6 .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cardiac Purkinje fibers and arrhythmias; The GK Moe Award Lecture 2015

2016

View full text Add to dashboard Cite

Purkinje fibers/cells continue to be a focus of arrhythmologists. Here we review several new ideas that have emerged in the literature and fold them into important new points. These points include some proteins in Purkinje cells that are specific to Purkinjes, pacemaker function in Purkinje may be similar to that of the sinus node cell, sink-source concerns about tracts/sheets of Purkinje fibers, role of Ito in arrhythmias and genetic lesions in Purkinjes and their high impact on cardiac rhythm. Although new ideas about the remodeled Purkinje cell are not the focus of this review, one can easily imagine how Purkinjes and their function may be altered in diseased hearts.

show abstract

Section: Figurementioning

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Cardiac Purkinje fibers and arrhythmias; The GK Moe Award Lecture 2015

2016

View full text Add to dashboard Cite

show abstract

“…5 The pathogenesis of PVCs from intracavitary structures overlaps with fascicular PVCs. The papillary muscles have a dense fascicular network, and often both the fascicular tissue and the myocardium, especially the interfaces between the two, are integral to the mechanism of PVCs.…”

Section: Pvcs From Intracavitary Structuresmentioning

confidence: 99%

“…3 PVCs commonly arise from the right ventricular (RV) outflow tract (RVOT) and sometimes the left ventricular (LV) outflow tract (LVOT). 4 Other sites for PVCs include the His-Purkinje system, especially the left posterior fascicle (predominantly in young males); endocavitary structures including the papillary muscles, moderator band, and false tendons 5 ; and the annuli of the aortic, pulmonary, and both atrioventricular (AV) valves. 6,7 In the case of structural heart disease, PVCs can originate from reentry in the presence of unidirectional block and slow conduction through electrically viable tissue within areas of scar.…”

Section: Introductionmentioning

confidence: 99%

Ablating Premature Ventricular Complexes: Justification, Techniques, and Outcomes

Noheria¹,

Deshmukh²,

Asirvatham

2015

Methodist DeBakey Cardiovascular Journal

Self Cite

View full text Add to dashboard Cite

“…Moreover, although pharmacologic approaches and single-cell electrophysiological studies have suggested that abnormal activation of the Purkinje fiber network is a likely arrhythmia trigger in both acquired (e.g., myocardial ischemia) and inherited [long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT)] arrhythmias (11-16), the role of the cardiac conduction system has not been addressed directly in the intact animal so far, mainly due to methodological constraint (17)(18)(19)(20). In fact, the experimental technique most commonly used to Significance Arrhythmias are potentially life-threatening electrical heart diseases that are difficult to predict and are mostly treated by empirical interventions.…”

mentioning

confidence: 99%

Optogenetic determination of the myocardial requirements for extrasystoles by cell type-specific targeting of ChannelRhodopsin-2

Zaglia

Pianca

Borile

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

101

View full text Add to dashboard Cite

Extrasystoles lead to several consequences, ranging from uneventful palpitations to lethal ventricular arrhythmias, in the presence of pathologies, such as myocardial ischemia. The role of working versus conducting cardiomyocytes, as well as the tissue requirements (minimal cell number) for the generation of extrasystoles, and the properties leading ectopies to become arrhythmia triggers (topology), in the normal and diseased heart, have not been determined directly in vivo. Here, we used optogenetics in transgenic mice expressing ChannelRhodopsin-2 selectively in either cardiomyocytes or the conduction system to achieve cell typespecific, noninvasive control of heart activity with high spatial and temporal resolution. By combining measurement of optogenetic tissue activation in vivo and epicardial voltage mapping in Langendorffperfused hearts, we demonstrated that focal ectopies require, in the normal mouse heart, the simultaneous depolarization of at least 1,300-1,800 working cardiomyocytes or 90-160 Purkinje fibers. The optogenetic assay identified specific areas in the heart that were highly susceptible to forming extrasystolic foci, and such properties were correlated to the local organization of the Purkinje fiber network, which was imaged in three dimensions using optical projection tomography. Interestingly, during the acute phase of myocardial ischemia, focal ectopies arising from this location, and including both Purkinje fibers and the surrounding working cardiomyocytes, have the highest propensity to trigger sustained arrhythmias. In conclusion, we used cell-specific optogenetics to determine with high spatial resolution and cell type specificity the requirements for the generation of extrasystoles and the factors causing ectopies to be arrhythmia triggers during myocardial ischemia.optogenetics | heart | Purkinje fiber | arrhythmia | cardiac ectopies A berrant heartbeats, caused by the ectopic depolarization of a group of cardiomyocytes, are associated with a wide range of consequences, from the commonly experienced feeling of "palpitation" to the triggering of potentially lethal ventricular arrhythmias in diseased hearts. Physiological conduction of normal heartbeats is orchestrated by the interaction of at least two functionally and anatomically distinct populations of cardiomyocytes: the working cardiomyocytes and the conduction system (i.e., Purkinje fibers at the ventricular level) (1). The electrotonic coupling of myocardial cells protects the heart from abnormal excitation and allows the effect of spontaneous activity in sparse cardiomyocytes to be "sunk" by the surrounding myocardium. As a result, a minimal "critical" number of cardiomyocytes needs to simultaneously depolarize to prevail over such a protective mechanism and generate conducted beats (2-5). When this occurs, the source-sink mismatch (abnormal depolarization current/ myocardial electrotonic sink) is focally overcome, resulting in a premature ventricular contraction (PVC) that, in the presence of arrhythmogenic substrates, may e...

show abstract

The infrahisian conduction system and endocavitary cardiac structures: relevance for the invasive electrophysiologist

Cited by 38 publications

References 84 publications

Cardiac Purkinje fibers and arrhythmias; The GK Moe Award Lecture 2015

Cardiac Purkinje fibers and arrhythmias; The GK Moe Award Lecture 2015

Ablating Premature Ventricular Complexes: Justification, Techniques, and Outcomes

Optogenetic determination of the myocardial requirements for extrasystoles by cell type-specific targeting of ChannelRhodopsin-2

Contact Info

Product

Resources

About