PubMed · 14362260
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J B HOFFMAN, M POMERANCE. 1955. Chronic auricular flutter.. https://doi.org/10.7326/0003-4819-42-4-885
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At 38 weeks of gestation, a woman with a previously unremarkable pregnancy was noted to have fetal tachycardia without obvious cause. Fetal echocardiography resulted in a presumptive diagnosis of fetal atrial flutter with a 2:1 block. The newborn resumed the same rhythm. The neonate underwent transesophageal incremental overdrive pacing. A normal sinus rhythm was restored. The infant had no recurrence to age 6 months.
An association between atrial flutter and atrioventricular nodal reentrant tachycardia (AVNRT) has been observed, but the underlying mechanisms are poorly defined. This issue was therefore investigated by comparing the electrophysiological properties of AVNRT patients with and without inducible atrial flutter and those of patients with a history of flutter. Twenty-nine patients with clinically documented atrial flutter and 104 with AVNRT were studied. Atrial flutter was induced in 38 (37%) AVNRT patients during standardized electrophysiological testing before radiofrequency ablation. The atrial relative refractory periods in AVNRT patients with inducible flutter (260 +/- 30 ms) were significantly shorter than those of either patients with a history of flutter (282 +/- 30 ms; P = 0.02) or AVNRT patients without inducible flutter (284 +/- 38 ms; P = 0.006). The atrial effective refractory periods in AVNRT patients with inducible flutter (205 +/- 31 ms) were shorter than in AVNRT patients without inducible flutter (227 +/- 40 ms; P = 0.01). The maximum AH interval during premature atrial stimulation in patients with clinical flutter (239 +/- 94 ms) was shorter than in AVNRT patients either with (290 +/- 91 ms; P = 0.04) or without inducible flutter (313 +/- 101 ms; P = 0.002). However, no significant differences were found in the maximum AH interval achieved during incremental atrial pacing among different groups. Our data show that a non-clinical flutter could more often be induced in those who had short atrial refractoriness. Despite their anatomical proximity, the slow pathway conduction of AVNRT and the isthmus slow conduction of flutter may be related to different mechanisms.
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