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Sinus node electrograms were obtained in two patients with unexplained syncope and the cardioinhibitory form of the hypersensitive carotid sinus syndrome. Direct recordings of sinus node potentials were obtained using a transvenous electrode catheter. Sinus node function was normal in both patients during standard electrophysiologic evaluation. Carotid sinus massage was performed in both patients and the sinus node electrogram was continuously recorded. After the onset of carotid sinus massage, prolongation of sinoatrial time, slowing of sinus rate of depolarization, sinoatrial exit block and finally sinus node arrest were recorded. After termination of carotid sinus massage, sinus node potentials did not precede the first atrial impulse; subsequent beats showed markedly prolonged sinoatrial times as well as changes in the P wave on the surface electrocardiogram. Sinus rate and sinoatrial time returned to control values gradually, as did the P wave configuration. Intravenous atropine (1.0 mg) abolished the abnormal response to carotid sinus massage.

This report describes a 23 year old woman with a lifelong history of permanent junctional reciprocating tachycardia refractory to conventional antiarrhythmic medications who was successfully treated with closed chest, transvenous selective ablation of a posteroseptal bypass tract. Two 100 J (stored) direct-current shocks were delivered to the region of the os of the coronary sinus using a quadripolar catheter positioned in the coronary sinus. At a 2 month follow-up interval, the patient is asymptomatic without recurrence of the tachycardia. It is concluded that in patients with permanent junctional reciprocating tachycardia, selective catheter ablation of a posteroseptal accessory pathway is a feasible alternative to a difficult pharmacologic regimen or to ablative surgery.

Ten patients with normal sinus node function were evaluated prospectively, to determine whether the decrease in blood pressure during rapid atrial pacing shortens the corrected sinus node recovery time. All patients had 30 seconds of atrial pacing at cycle lengths from 600 to 300 ms, with continuous arterial pressure monitoring, before and after intravenous administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In the control state, a decrease in corrected sinus node recovery time was recorded with faster atrial pacing rates, which was significantly related to the initial drop in systolic blood pressure at the onset of atrial pacing. Specifically, as the initial pressure drop increased from 15 mm Hg or less to 16 to 45 and 45 to 100 mm Hg, corrected sinus node recovery time decreased from 272 ± 79 to 205 ± 70 ms (p < 0.04) and to 134 ± 120 ms (p < 0.04), respectively. In contrast, after autonomic blockade, the corrected sinus node recovery time was prolonged, in a near linear fashion, as atrial pacing rates increased. The magnitude of blood pressure drop with atrial pacing did not differ significantly from that in the control state at similar pacing rates.

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent suhthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 ± 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 ± 14% of threshold current and the maximal ineffective current was 49 ± 17% of threshold (p < 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 ± 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by suhthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway.