1988 Fiscal Year Final Research Report Summary
A study on entrainment; with special reference to the continuation mechanism of tachycardia
| Project/Area Number |
62480219
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Saitama Medical School |
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Principal Investigator |
MATSUO Hiroshi Saitama Medical School, Professor, 医学部, 教授 (60010378)
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| Co-Investigator(Kenkyū-buntansha) |
SEGAWA Kazuhiko Saitama Medical School, Assistant, 医学部, 助手 (00179318)
TANAKA Shugo Saitama Medical School, Assistant Professor, 医学部, 講師 (90179755)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Entrainment / Reentry / Concealed WPW syndrome / Atrial flutter / Slow conduction area / 興奮旋回 |
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| Research Abstract |
As one of the criteria of entrainment, Wellens has proposed that after cessation of pacing, the first tachycardia complex occurs at the pacing rate. This is not always so, depending upon the pacing site on the macro reentrant circuit. The first tachycardia cycle length prolongs before returning to the original tachycardia cycle length. In order to see why and how this occurs, we have studied the change of cycle length at each electrogram-recording site during and immediately after pacing in A-V reentrant tachycardia of concealed WPW syndrome and experimental atrial flutter of dog.
In A-V reentrant tachycardia, prolongation of the first tachycardia cycle length necessitates the presence of slow conduction area (SCA),e.g. AV node, in the reentrant circuit. The degree of prolongation equals to the difference of conduction times through SCA during pacing and tachycardia. On pacing from proximal site to SCA (high right atrium), low right atrium, seated proximal to SCA but downstream to pacing site, shows the prolongation. On pacing from distal site to SCA (right vantricle), all recording sites show the prolongation, because these sites lie downstream to the pacing site.
In experimental atrial flutter, however, atrial excitation sequence, constructed by 7 local atrial electrograms, differs slightly during atrial premature stimulation and tachycardia. The failure of precise stimulation of reentry circuit (mother ring) or contrnuously changing of the route of the circuit could be the underlying mechanism. The presence of SCA could not be identified in experimental atrial flutter.
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