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Ann Thorac Surg 1992;54:717-724
© 1992 The Society of Thoracic Surgeons
Second Department of Surgery and First Department of Physiology, Kochi Medical School, Kochi, Japan
Accepted for publication February 19, 1992.
* Address reprint requests to Dr Tamiya, Second Department of Surgery, Kochi Medical School, Nankoku, Kochi, Japan 783.
Experiments were conducted with 159 dogs to investigate the mechanism of persistent dysrhythmias clinically encountered after atrial-level operations. Those found after incisions to the internodal pathways (INPs) of the right atrium were analyzed using cardiac mapping in an anesthetized or extracorporeally perfused state. Longitudinal incisions of the posterior INP often allowed inducible sustained atrial flutter, with circus movement of excitation around the right atrium near the tricuspid orifice. Sustained atrial flutter thus produced was modified in cycle length by coexisting division of the middle INF but inhibited by that of the anterior INP. Its incidence increased at chronic stage, with marked cicatricial changes. The disrupted anterior INP markedly prolonged conduction time to the atrioventricular node and A-H interval compared with the other disruptions. Persistent atrioventricular junctional rhythm developed in about 50% of the animals after disruption of all three INPs or anterior and posterior INPs; division of the anterior INP was the common potent factor, although no single blocked INP produced persistent junctional rhythm. Our results support the "summation theory." The incidence of junctional rhythm and hypoxia of the sinoatrial node (flow rate of less than 10 mL · 100 g–1 · min–1) were markedly enhanced by coexisting blockade of atrial feeding arteries in addition to division of the anterior INP. In conclusion, massive posterior INP disruption is a potent anatomic substrate in producing sustained atrial flutter, middle INP division a modifier, and anterior INP division an inhibitor. Division of the anterior INP is a potent anatomic substrate in producing junctional rhythm, and hypoxia involving the sinoatrial node reacts as its synergic factor.
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