Role of sinoatrial node architecture in maintaining a balanced source-sink relationship and synchronous cardiac pacemaking
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作者:
Unudurthi, Sathya D.
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Ohio State Univ, Coll Engn, Dept Biomed Engn, Columbus, OH 43210 USA
Ohio State Univ, Wexner Med Ctr, Dorothy M Davis Heart & Lung Res Inst, Columbus, OH 43210 USAOhio State Univ, Coll Engn, Dept Biomed Engn, Columbus, OH 43210 USA
Unudurthi, Sathya D.
[1
,2
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Wolf, Roseanne M.
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Univ Dubuque, Dept Math, Dubuque, IA USAOhio State Univ, Coll Engn, Dept Biomed Engn, Columbus, OH 43210 USA
Wolf, Roseanne M.
[3
]
Hund, Thomas J.
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Ohio State Univ, Coll Engn, Dept Biomed Engn, Columbus, OH 43210 USA
Ohio State Univ, Wexner Med Ctr, Dorothy M Davis Heart & Lung Res Inst, Columbus, OH 43210 USA
Ohio State Univ, Wexner Med Ctr, Dept Internal Med, Div Cardiovasc Med, Columbus, OH 43210 USAOhio State Univ, Coll Engn, Dept Biomed Engn, Columbus, OH 43210 USA
Hund, Thomas J.
[1
,2
,4
]
机构:
[1] Ohio State Univ, Coll Engn, Dept Biomed Engn, Columbus, OH 43210 USA
[2] Ohio State Univ, Wexner Med Ctr, Dorothy M Davis Heart & Lung Res Inst, Columbus, OH 43210 USA
[3] Univ Dubuque, Dept Math, Dubuque, IA USA
[4] Ohio State Univ, Wexner Med Ctr, Dept Internal Med, Div Cardiovasc Med, Columbus, OH 43210 USA
Normal heart rhythm (sinus rhythm) depends on regular activity of the sinoatrial node (SAN), a heterogeneous collection of specialized myocytes in the right atrium. SAN cells, in general, possess a unique electrophysiological profile that promotes spontaneous electrical activity (automaticity). However, while automaticity is required for normal pacemaking, it is not necessarily sufficient. Less appreciated is the importance of the elaborate structure of the SAN complex for proper pacemaker function. Here, we review the important structural features of the SAN with a focus on how these elements help manage a precarious balance between electrical charge generated by the SAN ("source") and the charge needed to excite the surrounding atrial tissue ("sink"). We also discuss how compromised "source-sink" balance due, for example to fibrosis, may promote SAN dysfunction, characterized by slow and/or asynchronous pacemaker activity and even failure, in the setting of cardiovascular disease (e.g., heart failure, atrial fibrillation). Finally, we discuss implications of the "source-sink" balance in the SAN complex for cell and gene therapies aimed at creating a biological pacemaker as replacement or bridge to conventional electronic pacemakers.