Editorials |
From the Institute of Biosciences and Technology, Texas A&M System Health Science Center, Houston.
Correspondence to James F. Martin, Institute of Biosciences and Technology, Texas A&M System Health Science Center, 2121 Holcombe Blvd, Houston, TX 77030.
See related article, pages 902–909
Key Words: atrial fibrillation pulmonary vein left right asymmetry
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Atrial Fibrillation: General Considerations |
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Electrical impulses, critical for a coordinated and physiologic heartbeat, are normally initiated in the sinoatrial (SA) node. However, in AF the disorganized atrial activity overrides normal SA node function resulting in irregular conduction of impulses to the ventricles. In the majority of cases, ectopic electrical activity originates in the pulmonary veins.1
In this issue of Circulation Research, Mommersteeg and colleagues2 make a significant advance in our understanding of pulmonary vein development by making a strong connection between AF and embryonic axis determination. Moreover, their work fits nicely with exciting new data from human genetic studies implicating the same genetic pathways in familial AF.3
Mommersteeg and colleagues make a number of fundamental observations regarding pulmonary vein development. Previous work suggested that pulmonary myocardium derives from atrial myocardium.4 Using lineage tracing, the authors convincingly rule out this possibility. Moreover, they show other data revealing that pulmonary myocardium is derived from Isl1-positive second heart field and has a distinct origin from the systemic venous circulation.5 Together, these findings suggest that the pulmonary vein myocardium forms
Related Article:
Circ. Res. 2007 101: 902-909.
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