Physical lineage tracing of cells contributing to the chicken cardiac conduction system

The cardiac pacemaking and conduction system sets and maintains the rhythmic pumping action of the heart. Previously, we have shown that peripheral cells of the conduction network in chick (periarterial Purkinje fibers) are selected within a cardiomyogenic lineage and that this recruitment occurs as a result of paracrine cues from coronary arteries. At present, the cellular derivation of other elements of this specialized system (e.g. the nodes and bundles of the central conduction system) are controversial, with some proposing that the evidence supports a neurogenic and others a myogenic origin for these tissues. While such ontological questions remain, it is unlikely that progress can be made on the molecular mechanisms governing patterning and induction of the central conduction system. Here, we have undertaken lineage-tracing strategies based on the distinct properties of replication-incompetent adenoviral and retroviral lacZ-expressing constructs. Using these complementary approaches, it is shown that cells constituting both peripheral and central conduction tissues originate from cardiomyogenic progenitors present in the looped, tubular heart with no detectable contribution by migratory neuroectoderm-derived populations. Moreover, clonal analyses of retrovirally infected cells incorporated within any part of the conduction system suggest that such cells share closer lineage relationships with nearby contractive myocytes than with other, more distal elements of the conduction system. Differentiation birthdating by label dilution using [(3)H]thymidine also demonstrates the occurrence of ongoing myocyte conscription to conductive specialization and provides a time course for this active and localized selection process in different parts of the system. Together, these data suggest that the cardiac conduction system does not develop by outgrowth from a prespecified pool of ‘primary’ myogenic progenitors. Rather, its assembly and elaboration occur via processes that include progressive and localized recruitment of multipotent cardiomyogenic cells to the developing network of specialized cardiac tissues.

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Dobutamine on the Cardiac Conduction System

Case Medical Research ◽

10.31525/ct1-nct04249258 ◽

2020 ◽

Author(s):

Keyword(s):

Conduction System ◽

Cardiac Conduction ◽

Cardiac Conduction System

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Faculty Opinions recommendation of TBX5 drives Scn5a expression to regulate cardiac conduction system function.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717952867.793458352 ◽

2012 ◽

Author(s):

Céline Fiset ◽

Nabil El Khoury

Keyword(s):

Conduction System ◽

Cardiac Conduction ◽

Cardiac Conduction System ◽

System Function

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Molecular Profiling of the Cardiac Conduction System: the Dawn of a New Era

Current Cardiology Reports ◽

10.1007/s11886-021-01536-w ◽

2021 ◽

Vol 23 (8) ◽

Author(s):

Sruthi Mantri ◽

Sean M. Wu ◽

William R. Goodyer

Keyword(s):

Molecular Profiling ◽

Conduction System ◽

Cardiac Conduction ◽

Cardiac Conduction System ◽

New Era

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Sudden Unexpected Death Associated with Arrhythmogenic Cardiomyopathy: Study of the Cardiac Conduction System

Diagnostics ◽

10.3390/diagnostics11081323 ◽

2021 ◽

Vol 11 (8) ◽

pp. 1323

Author(s):

Giulia Ottaviani ◽

Graziella Alfonsi ◽

Simone G. Ramos ◽

L. Maximilian Buja

Keyword(s):

Fibromuscular Dysplasia ◽

Ventricular Myocardium ◽

Conduction System ◽

Cardiac Conduction ◽

Future Research ◽

Cardiac Conduction System ◽

Arrhythmogenic Cardiomyopathy ◽

Unexpected Death ◽

The Past ◽

The Right

A retrospective study was conducted on pathologically diagnosed arrhythmogenic cardiomyopathy (ACM) from consecutive cases over the past 34 years (n = 1109). The anatomo-pathological analyses were performed on 23 hearts diagnosed as ACM (2.07%) from a series of 1109 suspected cases, while histopathological data of cardiac conduction system (CCS) were available for 15 out of 23 cases. The CCS was removed in two blocks, containing the following structures: Sino-atrial node (SAN), atrio-ventricular junction (AVJ) including the atrio-ventricular node (AVN), the His bundle (HB), the bifurcation (BIF), the left bundle branch (LBB) and the right bundle branch (RBB). The ACM cases consisted of 20 (86.96%) sudden unexpected cardiac death (SUCD) and 3 (13.04%) native explanted hearts; 16 (69.56%) were males and 7 (30.44%) were females, ranging in age from 5 to 65 (mean age ± SD, 36.13 ± 16.06) years. The following anomalies of the CCS, displayed as percentages of the 15 ACM SUCD cases in which the CCS has been fully analyzed, have been detected: Hypoplasia of SAN (80%) and/or AVJ (86.67%) due to fatty-fibrous involvement, AVJ dispersion and/or septation (46.67%), central fibrous body (CFB) hypoplasia (33.33%), fibromuscular dysplasia of SAN (20%) and/or AVN (26.67%) arteries, hemorrhage and infarct-like lesions of CCS (13.33%), islands of conduction tissue in CFB (13.33%), Mahaim fibers (13.33%), LBB block by fibrosis (13.33%), AVN tongue (13.33%), HB duplicity (6.67%%), CFB cartilaginous meta-hyperplasia (6.67%), and right sided HB (6.67%). Arrhythmias are the hallmark of ACM, not only from the fatty-fibrous disruption of the ventricular myocardium that accounts for reentrant ventricular tachycardia, but also from the fatty-fibrous involvement of CCS itself. Future research should focus on application of these knowledge on CCS anomalies to be added to diagnostic criteria or at least to be useful to detect the patients with higher sudden death risks.

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