Intracellular calcium dynamics and anisotropic reentry in isolated canine pulmonary veins and left atrium

Chung Chuan Chou, Motoki Nihei, Shengmei Zhou, Alex Tan, Ayaka Kawase, Edgar S. Macias, Michael C. Fishbein, Shien Fong Lin, Peng Sheng Chen

Research output: Contribution to journalArticle

100 Citations (Scopus)

Abstract

Background - Rapid activations due to either focal discharge or reentry are often present during atrial fibrillation (AF) in the pulmonary veins (PVs). The mechanisms of these rapid activations are unclear. Methods and Results - We studied 7 isolated, Langendorff-perfused canine left atrial (LA) and PV preparations and used 2 cameras to map membrane potential alone (Vm, n=3) or Vm and intracellular calcium simultaneously (Cai, n=4). Rapid atrial pacing induced 26 episodes of focal discharge from the proximal PVs in 5 dogs. The cycle lengths were 223±52 ms during ryanodine infusion (n=13) and 133±59 ms during ryanodine plus isoproterenol infusion (n=13). The rise of Ca, preceded Vm activation at the sites of focal discharge in 6 episodes of 2 preparations, compatible with voltage-independent spontaneous Ca, release. Phase singularities during pacing-induced reentry clustered specifically at the PV-LA junction. Periodic acid-Schiff (PAS) stain identified large cells with pale cytoplasm along the endocardium of PV muscle sleeves. There were abrupt changes in myocardial fiber orientation and increased interstitial fibrosis in the PV and at the PV-LA junction. Conclusions - PV muscle sleeves may develop voltage-independent Cai release, resulting in focal discharge. Focal discharge may also be facilitated by the presence of PAS-positive cells that are compatible with node-like cells. During reentry, phase singularities clustered preferentially at sites of increased anisotropy such as the PV-LA junction. These findings suggest that focal discharge caused by spontaneous calcium release and anisotropic reentry both contribute to rapid activations in the PVs during AF.

Original languageEnglish (US)
Pages (from-to)2889-2897
Number of pages9
JournalCirculation
Volume111
Issue number22
DOIs
StatePublished - Jun 7 2005

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Pulmonary Veins
Heart Atria
Canidae
Calcium
Ryanodine
Periodic Acid
Atrial Fibrillation
Endocardium
Muscles
Anisotropy
Isoproterenol
Membrane Potentials
Cytoplasm
Fibrosis
Coloring Agents
Dogs

Keywords

  • Anisotropy
  • Calcium
  • Fibrillation
  • Imaging
  • Mapping

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Intracellular calcium dynamics and anisotropic reentry in isolated canine pulmonary veins and left atrium. / Chou, Chung Chuan; Nihei, Motoki; Zhou, Shengmei; Tan, Alex; Kawase, Ayaka; Macias, Edgar S.; Fishbein, Michael C.; Lin, Shien Fong; Chen, Peng Sheng.

In: Circulation, Vol. 111, No. 22, 07.06.2005, p. 2889-2897.

Research output: Contribution to journalArticle

Chou, Chung Chuan ; Nihei, Motoki ; Zhou, Shengmei ; Tan, Alex ; Kawase, Ayaka ; Macias, Edgar S. ; Fishbein, Michael C. ; Lin, Shien Fong ; Chen, Peng Sheng. / Intracellular calcium dynamics and anisotropic reentry in isolated canine pulmonary veins and left atrium. In: Circulation. 2005 ; Vol. 111, No. 22. pp. 2889-2897.
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abstract = "Background - Rapid activations due to either focal discharge or reentry are often present during atrial fibrillation (AF) in the pulmonary veins (PVs). The mechanisms of these rapid activations are unclear. Methods and Results - We studied 7 isolated, Langendorff-perfused canine left atrial (LA) and PV preparations and used 2 cameras to map membrane potential alone (Vm, n=3) or Vm and intracellular calcium simultaneously (Cai, n=4). Rapid atrial pacing induced 26 episodes of focal discharge from the proximal PVs in 5 dogs. The cycle lengths were 223±52 ms during ryanodine infusion (n=13) and 133±59 ms during ryanodine plus isoproterenol infusion (n=13). The rise of Ca, preceded Vm activation at the sites of focal discharge in 6 episodes of 2 preparations, compatible with voltage-independent spontaneous Ca, release. Phase singularities during pacing-induced reentry clustered specifically at the PV-LA junction. Periodic acid-Schiff (PAS) stain identified large cells with pale cytoplasm along the endocardium of PV muscle sleeves. There were abrupt changes in myocardial fiber orientation and increased interstitial fibrosis in the PV and at the PV-LA junction. Conclusions - PV muscle sleeves may develop voltage-independent Cai release, resulting in focal discharge. Focal discharge may also be facilitated by the presence of PAS-positive cells that are compatible with node-like cells. During reentry, phase singularities clustered preferentially at sites of increased anisotropy such as the PV-LA junction. These findings suggest that focal discharge caused by spontaneous calcium release and anisotropic reentry both contribute to rapid activations in the PVs during AF.",
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AU - Nihei, Motoki

AU - Zhou, Shengmei

AU - Tan, Alex

AU - Kawase, Ayaka

AU - Macias, Edgar S.

AU - Fishbein, Michael C.

AU - Lin, Shien Fong

AU - Chen, Peng Sheng

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N2 - Background - Rapid activations due to either focal discharge or reentry are often present during atrial fibrillation (AF) in the pulmonary veins (PVs). The mechanisms of these rapid activations are unclear. Methods and Results - We studied 7 isolated, Langendorff-perfused canine left atrial (LA) and PV preparations and used 2 cameras to map membrane potential alone (Vm, n=3) or Vm and intracellular calcium simultaneously (Cai, n=4). Rapid atrial pacing induced 26 episodes of focal discharge from the proximal PVs in 5 dogs. The cycle lengths were 223±52 ms during ryanodine infusion (n=13) and 133±59 ms during ryanodine plus isoproterenol infusion (n=13). The rise of Ca, preceded Vm activation at the sites of focal discharge in 6 episodes of 2 preparations, compatible with voltage-independent spontaneous Ca, release. Phase singularities during pacing-induced reentry clustered specifically at the PV-LA junction. Periodic acid-Schiff (PAS) stain identified large cells with pale cytoplasm along the endocardium of PV muscle sleeves. There were abrupt changes in myocardial fiber orientation and increased interstitial fibrosis in the PV and at the PV-LA junction. Conclusions - PV muscle sleeves may develop voltage-independent Cai release, resulting in focal discharge. Focal discharge may also be facilitated by the presence of PAS-positive cells that are compatible with node-like cells. During reentry, phase singularities clustered preferentially at sites of increased anisotropy such as the PV-LA junction. These findings suggest that focal discharge caused by spontaneous calcium release and anisotropic reentry both contribute to rapid activations in the PVs during AF.

AB - Background - Rapid activations due to either focal discharge or reentry are often present during atrial fibrillation (AF) in the pulmonary veins (PVs). The mechanisms of these rapid activations are unclear. Methods and Results - We studied 7 isolated, Langendorff-perfused canine left atrial (LA) and PV preparations and used 2 cameras to map membrane potential alone (Vm, n=3) or Vm and intracellular calcium simultaneously (Cai, n=4). Rapid atrial pacing induced 26 episodes of focal discharge from the proximal PVs in 5 dogs. The cycle lengths were 223±52 ms during ryanodine infusion (n=13) and 133±59 ms during ryanodine plus isoproterenol infusion (n=13). The rise of Ca, preceded Vm activation at the sites of focal discharge in 6 episodes of 2 preparations, compatible with voltage-independent spontaneous Ca, release. Phase singularities during pacing-induced reentry clustered specifically at the PV-LA junction. Periodic acid-Schiff (PAS) stain identified large cells with pale cytoplasm along the endocardium of PV muscle sleeves. There were abrupt changes in myocardial fiber orientation and increased interstitial fibrosis in the PV and at the PV-LA junction. Conclusions - PV muscle sleeves may develop voltage-independent Cai release, resulting in focal discharge. Focal discharge may also be facilitated by the presence of PAS-positive cells that are compatible with node-like cells. During reentry, phase singularities clustered preferentially at sites of increased anisotropy such as the PV-LA junction. These findings suggest that focal discharge caused by spontaneous calcium release and anisotropic reentry both contribute to rapid activations in the PVs during AF.

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KW - Fibrillation

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KW - Mapping

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