Hirokazu Hayakawa

Evaluation of Sino-atrial Node Function in Man by Overdrive Suppression

Sino-atrial node (SAN) function was evaluated in 46 patients, three of whom had the sick sinus syndrome. Patients were paced from the right atrium for 15 to 180 sec at rates of 90, 110, 130, and 150 beats/min. The rapid cessation of pacing was associated with suppression of the SAN at all paced rates and at all durations of pacing. The observed pause was terminated by a sinus beat in all instances. The duration of pacing had little influence on the duration of the observed pause. The pause increased as the pacing rate was increased until, at a rate of 150 beats/min, a marked decrease in the pause was noted. Atropine (1.5-3.0 mg iv) diminished but did not eliminate the SAN suppression. Subthreshold pacing did not suppress SAN function. Three patients with sick sinus syndrome had a greater degree of SAN suppression than normal patients (4732 ± 415 msec [SSS] M ± SEM; 1041 ± 56 msec for normal patients).The determination of the duration of the pause following cessation of atrial pacing provides a technique for recognition of abnormalities of SAN function.

Assessment of Sinus Node Function in Patients with the Sick Sinus Syndrome

Thirty-one patients with symptomatic sinus node dysfunction were evaluated with electrocardiograms, Holter monitor recordings, exercise, isoproterenol infusions, atropine administration, Valsalva maneuvers, carotid sinus massage, and overdrive pacing. Four basic clinical subsets were recognized: (1) carotid sinus hypersensitivity (2) bradycardia-tachycardia syndrome, (3) episodic sinus arrest, and (4) persistent symptomatic sinus bradycardia. The study group demonstrated a normal heart rate response to exercise and isoproterenol infusion (%&Dgr; = +95 exercise, +144 isoproterenol) in the face of diminished responsiveness to atropine administration (%&Dgr; = +23). Marked carotid sinus hypersensitivity was demonstrated in eight patients, and four patients demonstrated slight abnormalities during performance of Valsalva maneuvers. Significant suppression of sinus node dysfunction was observed following atrial overdrive in the study group (postpacing pause = 3087 ± 464 msec) as compared to patients without significant sinus node function (postpacing pause = 1073 ± 63 msec) (P < 0.001). In patients with intact V-A conduction, ventricular overdrive also resulted in sinus node suppression (postpacing pause = 1901 ± 357 msec). There was a marked decrease in the degree of sinus node depression following atropine administration. Ten of 31 patients demonstrated various degrees of A-V block following atrial pacing at rates less than 100 beats/min.It is concluded that the present methods of evaluation of sinus function, especially sinus node recovery time following overdrive pacing, may prove of value in the investigation of patients with syncope of unknown etiology.

The Wolff-Parkinson-White syndrome: Pharmacologic effects of procaine amide☆

The effect of procaine amide, 10 mg. per kilogram via intravenous infusion, was studied in 13 patients with the WPW syndrome. The delta wave was eliminated by procaine amide in 10 and modified in three patients. This effect lasted between 30 minutes and 8 1/2 hours and was unrelated to the total dose administered. Anterograde A-V conduction was assessed by atrial pacing with increasing rates. More rapid atrial pacing rates with 1:1 A-V conduction were observed in patients who maintained rather than lost their delta wave during pacing. Ventriculoatrial conduction was assessed with ventricular pacing at increasing rates; ventricular conduction time was fixed regardless on the pacing rate. Procaine amide significantly prolonged V-A conduction time in six and blocked V-A conduction in one patient. In addition, A-V and V-A refractory periods were measured by the extrastimulus technique. Two types of responses were observed: (1) Type I or (2) line of identity. A-V nodal refractoriness was observed to be within the normal range. Procaine amide converted anterograde line of identity responses to Type I responses in all patients who had their delta waves eliminated. In this patient group, bypass refractoriness was shorter than A-V nodal refractoriness. Procaine amide was not observed to alter significantly normal A-V conduction as assessed by atrial pacing or A-V refractory period measurements. Furthermore, a significant disparity between the effects of procaine amide on anterograde and retrograde bypass refractoriness was observed. Tachycardias could be induced in nine of the 13 patients with a mean rate of 167.2 +/- 7.9 beats per minute; delta waves were abent during all episodes of tachycardia. Procaine amide prevented tachycardia induction in six of the none patients. Procaine amide therefore demonstrates electrophysiologic effects which would be beneficial for prevention or treatment of reciprocating tachycardias in the WPW syndrome. Moreover, procaine amide would be an ideal agent for the prevention of rapid ventricular rates in patients with the WPW syndrome and atrial fibrillation.

Lown-Ganong-Levine Syndrome A Study Using His Bundle Electrograms

His bundle recordings were obtained in three patients with histories of recurrent supraventricular tachycardias and electrocardiograms demonstrating a short P-R interval with a normal QRS (the Lown-Ganong-Levine syndrome). The His bundle electrograms obtained during sinus rhythm demonstrated a normal A-H (atrium-to-His bundle) time in one patient and a low normal A-H time in two patients. The H-V (His bundle-to-ventricle) time was short in all three patients. Atrial pacing in two patients produced an attenuated degree of prolongation of the A-H time without a change in conduction distal to the proximal His bundle. The probable mechanisms of accelerated conduction in these three patients include: (1) partial A-V nodal bypass via (a) the posterior intenodal tract or (b) functional bypass fibers within the A-V node; and (2) accelerated conduction within the A-V conduction system distal to the A-V node.

Critical prolongation of AV conduction time as the inciting mechanism in reentrant tachycardia.

Summary Paroxysmal supraventricular tachycardiawas studied by means of His bundle electrogram recordings in a patient with a 15-year history of palpitations. These recordings were obtained: 1) in sinus rhythm; 2) during episodes of supraventricular tachycardia; 3) at the initiation and termination of the arrhythmia. While in sinus rhythm, a prolonged PR interval was found with a long AH time (218 msec) and a normal HV time (49 msec). The tachycardia was initiated in all instances by spontaneous gradual prolongation of PR interval until a critical conduction delay was reached at which time an atrial echo occurred. This resulted in sustained supraventricular tachycardia in all instances. Spontaneous premature depolarizations did not initiate the tachycardia in any instance. The tachycardia could be terminated with atrial pacing which rendered the tissue in the path of the echo beat refractory. The study serves to further elucidate the role of AV conduction delay in the genesis of supraventricular tachycardia.

Effect of lidocaine on the scalar orthogonal electrocardiogram

Abstract In summary, our data indicate that therapeutic serum levels of lidocaine demonstrate no electrocardiographic changes, and especially no shortening of the Q-T interval. This suggests that the therapeutic in vitro lidocaine level may be less than previously assumed.

Diphenidol: a new agent for the treatment of digitalis-induced arrhythmias electrophysiologic and hemodynamic studies

Abstract Diphenidol, a new antiemetic, has been shown to be effective in treating arrhythmias secondary to digitalis intoxication. In a control series of 20 dogs given toxic doses of digoxin, 14 dogs (67 percent) died in 24 hours. In a second group of dogs, given a similar dose of digoxin followed by 0.5 to 4 mg/kg of diphenidol, there was only 1 death ( P 40 μ g/kg), diphenidol (0.5 to 4 mg/kg) shortened the prolonged A-H time in these animals (−22.8 ± 5 percent). In contrast, diphenidol diluent alone exerted no significant effect. No change in sinus rate of isolated right atrial preparations was seen until exposure to diphenidol (≥1 × 10 −4 M), when a marked negative chronotropic effect was seen. Diphenidol was also observed to suppress the enhanced ventricular automaticity induced by digitalis. Hemodynamic studies in the intact animal, after administration of 4 mg/kg of diphenidol, demonstrated no significant effect on cardiac index, total peripheral vascular resistance, arterial pressure, stroke volume or coronary flow. In isolated cat papillary muscle diphenidol, in contrast to equimolar doses of propranolol, demonstrated no significant negative inotropic effect until exposure to a level of ≥1 × 10 −5 M. In conclusion, the experimental data demonstrate that diphenidol possesses desirable antiarrhythmic properties especially for the treatment of digitalis-induced arrhythmias.

Coexisting intra- and subnodal block: an unusual abnormality of atrioventricular conduction.

Abstract The presence of A-V block occurring at two levels of the conducting system was demonstrated in an asymptomatic patient by means of the His bundle recordings. During sinus rhythm, first degree A-V block with complete left bundle branch block was noted, suggesting the presence of bilateral bundle branch block. His bundle recordings demonstrated the coexistence of intranodal (Wenckebach periods, Mobitz Type I) and subnodal (Mobitz Type II) block. The evidence of block below the proximal His bundle offered confirmatory evidence of bilateral bundle branch block. In spite of the abnormal antegrade conduction, there was 1:1 V-A conduction during right ventricular pacing at 110 per minute. With more rapid (130 per minute) ventricular pacing, retrograde Wenckebach periods were observed, suggesting that there was, in addition, possible impairment in retrograde conduction. This report serves to demonstrate (1) the limitations of the body surface ECG in the assessment of A-V conduction and (2) that His bundle electrograms make it possible to detect the presence of coincidental lesions at two levels of the A-V conducting system.