SUMMARY To investigate the mechanism of atrial flutter (AF) in humans, we studied 13 patients during episodes of spontaneous common AF, with simultaneous multiple atrial endocavitary recordings and atrial programmed stimulation. In all patients, low paraseptal atrial activation preceded high right atrial activation, and the latter preceded mid-or low lateral right atrial activation (recorded in five patients). Programmed atrial stimulation resulted in early reset of the AF cycle, with an unchanged poststimulation AF activation pattern. The poststimulation cycle recorded from an even potential to the site of stimulation was always shorter than the basic flutter cycle length. The poststimulation cycle recorded at the site of stimulation was always equal to or longer than the flutter cycle length.These results strongly favor the existence of a reentry circuit to which the extrastimulus has access. We recently documented induction and termination of episodes of common AF in man by programmed atrial stimulation.'6 17 Although this strongly favors reentry, it is not a definitive demonstration of it, because a triggered activity cannot be excluded.'8 We studied the effects of programmed atrial stimulation on the basic AF cycle in man, and observed that the poststimulation cycle, recorded at the stimulation point, was equal to the basic AF cycle in some cases.'6 17In this paper we report the results of studies using simultaneous multiple atrial endocavitary recordings and atrial programmed stimulation. Materials and MethodsThe study population consisted of 13 patients, 11 males and two females, ages 32-72 years (mean 54.3 years).The underlying heart disease was coronary atherosclerotic heart disease in five patients, idiopathic cardiomyopathy in five and mitral valvular disease in two. One patient had no clinical evidence of heart disease except for the arrhythmia ( After diazepam, 10 mg i.m., at least two quadripolar catheters (1 cm between electrodes) were inserted for atrial endocavitary recordings and stimulation. Initially, all patients had one catheter positioned in the low paraseptal atrium (low right septal wall in eight and proximal coronary sinus in five) and another in the high right atrium (lateral wall in 10 and septal wall in three). These two sites were named points 1 and 2, respectively. The different catheter positions were chosen so as to attain a firm position with good atrial potentials and atrial capture during stimulation.Programmed atrial stimulation was first performed at point 2, with a coupling interval progressively decreased by 10 msec until the atrial refractory period was attained. If the interruption or transformation of the arrhythmia was unsuccessful, the coupling interval of this extrastimulus was fixed at a slightly higher value than that of the effective atrial refractory period; a second extrastimulus was then given at progressively decreasing coupling intervals. In case offailure, a third extrastimulus was given in the same way.In five cases, the same pattern of stimulation was repe...

Familial persistent atrial standstill (PAS) has been rarely documented. Five patients, three male and two female (mean age 46 years at first observation), with familial 'complete' PAS, all from a small mountain community (900 residents) have been studied. Diagnostic criteria were: absence of P wave in any lead of the standard electrocardiogram; no electrical activity of the atria with extremely slow junctional escape rhythm on the endocavitary recordings; lack of atrial excitability; absence of atrial wall movement at fluoroscopy; no mitral A wave on the echocardiogram. All patients had marked cardiac enlargement primarily due to atrial enlargement and all had impaired functional class. Some had bradycardia for many years but none had syncope. Permanent cardiac pacing was carried out in all. Two had cerebral embolism. In the same community there were three patients, one male and two female (mean age 34 years at first observation), with 'partial' atrial standstill characterized by absence of P waves in any lead of the standard electrocardiogram and by endocavitary recording of electrical activity limited to a localized region of the atrium. These three patients also had cardiac enlargement primarily due to atrial enlargement but to a lesser degree than the patients with complete PAS. One patient had cerebral embolism. The familial and endemic character of the disease is stressed. Cardiac enlargement due primarily to atrial enlargement seems to be a common feature of both the complete and partial form of the PAS syndrome.

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