Intra-atrial Conduction Research Articles

Plasma Levels and Electrophysiological Effects of Acebutolol (M & B 17.803) in the Dog Heart in Situ

The effect of acebutolol a beta-adrenergic receptor blocking agent was tested on the dog heart in situ. The drug decreased heart rate, and caused a reduction in the conduction velocity and a significant increase in the functional refractory period of the atrioventricular node. The functional and the effective refractory period of the right atrium was increased by acebutolol. During sinus rhythm, the drug did not affect conduction velocity in the rest of the conduction pathway. During atrial pacing, however, the intra-atrial and His-Purkinje conduction times were slightly increased. The plasma concentrations of acebutolol were in the range between 0.09 and 0.5 mug/ml, which is far below those values expected to cause a membrane-stabilizing or quinidine-like effect. The clinical applications of the results are discussed.

Simultaneous intermittent intraatrial and intraventricular conduction defects mimicking trifascicular conduction delay

Both intermittent rate related left bundle branch block and intermittent rate related trifascicular conduction delay (left bundle branch block with marked H-V interval prolongation) have been previously described. However intermittent rate related intraatrial block with left bundle branch block has not. No only does the case presented herein reveal intermittent rate related intraatrial block with left bundle branch block, but also PR prolongation secondary to the intraatrial block. This combination mimicked intermittent trifascicular conduction delay. Electrophysiological testing allowed differentiation of this pseudotrifascicular defect from true trifascicular conduction delay.

A vectorcardiographic study of spatial P, QRS and T-loops in diabetic patients without clinically apparent heart disease

Summary Eighty-nine ambulatory normotensive diabetic patients, free of cardiorespiratory symptoms at any time or any clinical or x-ray evidence of cardiac involvement except for electrocardiographic abnormalities (50.5%), have been studied vectorcardiographically. The abnormalities of the spatial QRS, T and P-loops have been analyzed with regard to the presence of bites, T-loop length/width (L/W) ratio and intra-atrial conduction disturbances. Forty-one percent of patients had QRS bites with a duration more than 10 msec and an amplitude more than 0.1 mV. Thirty-eight percent had an abnormal spatial T-loop L/W ratio of less than 2.6. Twenty-five percent had intra-atrial conduction disturbances. The vectorcardiograms (VCGs) showed 75% of diabetic patients presenting abnormalities of the QRS, T or P-loop (single or combined). These abnormalities may be caused by small and large coronary vessels and myocardial involvement, or they may be due to biochemical changes at the level of the cellular between the duration of the disease, diet or hypoglycemic medication and the vectorcardiographic abnormalities. We concluded that vectorcardiography is a reliable and important non-invasive method for detecting subclinical cardiac abnormalities in patients with diabetes mellitus.

The vulnerability of the human atrium. I. Correlations between vulnerability, sinus node recovery time and intraatrial conduction time (author's transl)

Using the extrastimulus method in 100 patients, premature impulses were applied during the relative refractory period of the right atrium. Depending on the atrial response to these impulses we divided our patients in the following 3 groups: Group A: no repetitive firing (61 patients); group B: 1 to 5 additional atrial extrasystoles with a total duration of maximum 1.5 s (27 patients); group C: runs of atrial flutter or fibrilation for at least 8 s (12 patients). The statistical analysis of the following parameters: age, PA interval, absolute and corrected sinus node recovery time did not show any significant difference between the 3 groups. These results suggest that the investigated parameters are of no great importance in the genesis of the atrial vulnerability.

Intraatrial conduction disturbances: Vectorcardiographic patterns

Frank P loop vectorcardiograms were recorded in 30 normal subjects and in 40 patients who had intraatrial conduction disturbances alone or in association with cardiac disease. High magnification of the P loop (0.1 mv = 3 cm) permitted accurate measurement of the P loop duration, magnitude and direction. High-frequency recordings allowed optimal evaluation of the notches, bites and conduction delays in the PsÊ loop. Four vectorcardiographic patterns have been selected as counterparts of the four types of enlarged P waves seen in electrocardiograms of patients with atrial conduction disturbances. When intraatrial conduction disturbances coexisted with left atrial enlargement, the PsÊ loop was larger and smoother. The role of partial or complete block in the specific internodal or interatrial pathways is discussed. High magnification, high-frequency vectorcardiography of the P loop seems to be the best available method for determining a specific pattern of intraatrial conduction disturbance.

Demonstration of the cardiotoxicity of the thermostable direct hemolysin (lethal toxin) produced by Vibrio parahaemolyticus.

Intravenous injection of the thermostable direct hemolysin (lethal toxin) produced by Vibrio parahaemolyticus caused rapid death of rats. Studies by electroencephalography and electrocardiography showed that after intravenous injection of the toxin the electroencephalogram remained normal for quite a long time after the heart of the animals had stopped beating. Depression of intraatrial and intraventricular conduction of electrical activation, including atrioventricular block, was observed in electrocardiograms of animals injected with the toxin. The toxin was also found to be toxic to cultured mouse heart cells. When it was added to the medium, the beating rhythm of the cultured heart cells increased temporarily and then soon stopped abruptly. The effect of the toxin on cultured mouse heart cells was blocked by preincubation of the toxin with a ganglioside mixture. From these results it is concluded that the thermostable direct hemolysin (lethal toxin) had cardiotoxic activity, and thus administration of the toxin causes rapid death of animals.

Clinical studies on the sick sinus syndrome.

1) Overdrive suppression is clinically useful to evaluate depressed cardiac automaticity in the sick sinus syndrome. 2) His bundle electrograms revealed frequent association of atrioventricular conduction defects with the depressed automaticity in this syndrome. 3) Especially in BTS, marked intra-atrial conduction defect was observed, and this conduction defect may play a role for development of re-entrant tachycardia. 4) Pathologic changes in the sick sinus syndrome are supposed to involve the whole atrial tissues including not only the S-A nodal region but the A-V node and its approaches.

Electrophysiologic properties of perhexiline

Perhexiline maleate (Pexid), a promising clinical antiarrhythmic and antianginal drug, was evaluated for its electrophysiologic effects on the entire conduction system of the intact canine heart throughout a wide range of therapeutic and potentially toxic doses. Intracardiac conduction times were measured by bipolar intramyocardial and transvenous endocardial electrodes before and following the intravenous administration of each dose of perhexiline maleate, 3 mg/kg every 30 min for a total of 4 doses in 7 open-chest anesthetized dogs. Eight animals served as controls in which similar operative technique and electrophysiologic variables were recorded after infusion of the maleate diluent. In addition, the effects of perhexiline on atrial and ventricular thresholds to electrical stimulation were recorded, as well as the QRS and QT intervals, sinus rate, and rhythm disorders. It was observed that perhexiline did not significantly (p greater than .05) alter sinus rate, QT interval, QRS duration, PR interval, intra-atrial conduction time, atrioventricular nodal conduction time, and His-Purkinje conduction velocity. The drug did not affect the cardiac threshold to electrical stimulation of less than 0.1 ma. No ectopic atrial or ventricular activity emerged during the accumulated influence of the agent. From this study, it is concluded that perhexiline does not exert deleterious actions on the conduction system of the intact canine heart. In view of the negligible toxic effects and its efficacy in treating ventricular tachyarrhythmias in patients, the drug deserves further clinical evaluation.

The electrophysiological effects of ouabain on sinus node and atrium in man.

Electrophysiological studies were performed in 16 patients before and 30 min after intravenous administration of ouabain (0.1 mg/kg). P-A interval (mean+/-SEM) was 40+/-2.1 ms before and 44+/- 1.5 ms after ouabain (P less than 0.001). Atrial effective and functional refractory periods (ERP and FRP) were measured in all patients during sinus rhythm and during driving at equivalent paced rates in 12 patients. The mean atrial ERP and FRP during sinus rhythm were, respectively, 244+/-10.5 and 307+/-11.0 ms before and 253+/-9.7 and 318+/-11.4 ms after infusion of ouabain (NS). Mean atrial ERP and FRP during driving were, respectively, 231+/-15.3 and 264+/-14.9 ms before and 266+/-18.6 and 296+/-19.7 ms after ouabain (P less than 0.01 and P less than 0.01). Mean sinus cycle length and sinus recovery times were, respectively, 887+/-31.2 and 1,113+/-38.7 ms before and 905+/-38.2 and 1,008+/-30.7 ms after infusion of ouabain (NS and P less than 0.005). Calculated sinoatrial conduction times before and after ouabain were 90+/-6.8 and 110+/-8.5 ms, respectively (P less than 0.005). In summary, ouabain produced depression of intraatrial conduction as manifested by increase in P-A interval and atrial effective and functional refractory periods. Ouabain significantly increased calculated sinoatrial conduction time without significant effect on spontaneous sinus cycle length.

Atrioventricular and intraventricular conduction in hyperkalemia

Twelve patients exhibited electrocardiographic evidence of fascicular block during hyperkalemia. Isolated left posterior hemiblock occurred in four, isolated left anterior hemiblock in two, right bundle branch block with left anterior hemiblock in two, right bundle branch block with left posterior hemiblock in one, left bundle branch block with abnormal left axis deviation in two and advanced atrioventricular block in one. In all seven patients with sinus rhythm the P-R interval shortened after correction of hyperkalemia. Electrophysiologic studies using His bundle recording and atrial pacing in one patient revealed intraatrial conduction delay and marked prolongation of conduction time in the His-Purkinje system. It is concluded that conduction defects in the specialized intraventricular conduction system are common in hyperkalemia and result in electrocardiographic patterns of fascicular block.

Wenckebach phenomenon within the atria

A patient with a history of fainting and a bifacicular block (CRBBB plus LPH) was analyzed by His Bundle electrograms. During atrial pacing at a rate of 138/min, a Wenckebach type of block occurred within the atrium or at the electode-atrium junction, or both. The sinus intra-atrial conduction time (P-A inverval) was normal. During atrial pacing (pacing rate of 138 to 148/min), St-A interval progressively lengthened and ultimately a second degree Wenckebach type of block was obtained. The surface electrocardiogram (ECG) was normal and only electrical pacing brought on the intra-atrial conduction defect. Simultaneous with this atrial block, a second degree (Mobitz II) block developed.

HIS bundle electrogram in rheumatic mitral valve disease with special reference to Bachmann's bundle block in P mitrale.

HBEs were recorded from either the right or left ventricle or simultaneously from both in 26 patients with chronic rheumatic mitral stenosis alone or in association with other mild valvular lesions during the diagnostic cardiac catheterization. Eleven of the patients had auricular fibrillation. Of the remaining 15 patients with sinus mechanism and P mitrale in the surface electrocardiogram, 12 were noted to have H potential preceded the termination of P wave and gave P2H interval of negative value- so-called "Bachmann's bundle block". Among these, double atrial activities (A and A' waves) could be identified on the HBE recorded from the left ventricular endocardial surface with catheter electrodes positioned at the subarotic region in 7 patients studied. Interatrial conduction time (P1A' interval) measured in these patients was prolonged in all and ranged from 47 to 82 with an average of 66 msec. Prolongation of intraatrial (or internodal) conduction time was noted in only one patient who also had first degree A-V block and prolonged A-H interval. There was no correlation of either P1P2 or P2H interval to the degree of left atrial enlargement. The P1P2 or P2H interval also had no correlation with hemodynamic parameters. In patients with auricular fibrillation, all impulses unable to conduct to the ventricle were blocked proximal to the His bundle and concealed conduction was not observed distal to it.

Sinus node re-entry: a mechanism for supraventricular tachycardia.

Data in 20 patients with normal sinus rhythm who, following induced premature atrial beats (PABs), manifested re-entry in the region of the sinus node are presented. PABs at coupling intervals ranging between 230-535 msec were followed by sinus node re-entry (SNR). Several criteria were applied to diagnose SNR: the temporal sequence of atrial excitation, the intra-atrial conduction time, the shape and polarity of the P waves, and manifestation of re-entry independent of atrioventricular (A-V) nodal delays. In 18 patients SNR lasting for one to several beats was observed. In the remaining two patients sustained SNR was manifested as supraventricular tachycardia (SVT), with cycle lengths ranging between 320-500 msec, which persisted for several minutes prior to its termination by properly timed atrial stimuli. In one of the latter two patients sustained SNR and SVT were produced only after atropine administration. Sinus node re-entry could be elicited at will in a specific echo zone with a duration ranging between 10-170 msec. In some cases SNR was also observed during and on cessation of regular atrial pacing. The latter observation provides a possible explanation for the unexpected sinus node acceleration seen sometimes on termination of atrial pacing. It is demonstrated that SNR for a single beat may fallaciously simulate sinus node entrance block. Simultaneous occurrence of re-entry at multiple sites, i.e., the sinus node and the A-V node, with resultant fusion P waves is also demonstrated. This study provides another mechanism for the genesis of regular and irregular SVT. The analysis and localization of the re-entry circuit may prove to be of clinical and therapeutic significance in selected patients.

Effects of propranolol and alprenolol on intra-atrial conduction in the dog

Intra-atrial conduction and its modification by two β-adrenoceptor blocking agents have been investigated in the dog. Premature atrial stimuli (St 2) were applied at variable intervals following regular stimuli (St 1) ensuring atrial pacing. A significant intra-atrial supernormal conduction was spontaneously observed at coupling intervals of 280−180 msec in 9 out of 10 animals. This phenomenon was still observed after propranolol or alprenolol administration but it occurred significantly earlier. With intervals shorter than 180 msec, atrioventricular conduction was decreased and both drugs further decreased it while simultaneously increasing nodoventricular effective and atrial functional refractory periods. In 1 dog, alprenolol induced a typical gap phenomenon in atrio-nodal conduction: as the St 1−St 2 interval became shorter, a point was reached where A 2 (atrial premature depolarization) was no longer conducted through the A-V node. If the St 1−St 2 interval was further decreased, the intra-atrial conduction delay increased sufficiently to allow A 2 to be conducted through the A-V node once again.

Avoiding Postoperative Dysrhythmias and Venous Obstruction Following Mustard's Operation: Technical Considerations

Five infants with uncomplicated transposition of the great arteries underwent correction during which special care was taken to avoid unfavorable hemodynamic and rhythm abnormalities. The late rhythm was sinus in all but 1 patient, who developed atrial flutter three years after operation; the flutter was converted to sinus bradyarrhythmia with dc countershock. Intracardiac electrograms showed normal sinus node function and normal intraatrial conduction despite division of the posterior internodal tracts. Cardiac catheterization done in 3 patients one to three years after operation showed widely patent channels into the systemic venous atria, and contractility studies demonstrated that the right ventricle functioned well as a systemic pump.

Electrophysiologic antagonism of quinidine and bretylium tosylate

Interactions of quinidlne (5 mg/liter) and bretylium tosylate (20 mg/ liter) were studied in isolated perfused rabbit hearts by recording transmembrane potentials from the atrial fibers, the atrioventricular (A-V) junction and the ventricular fibers. The following observations were made on ventricular fibers. As expected, administration of quinidine prolonged action potential duration and reduced the maximal rate of depolarization. Subsequent addition of bretylium to quinidine shortened action potential duration and tended to restore the maximal rate of depolarization. The membrane resting potential, the action potential amplitude and overshoot showed no significant changes. With respect to A-V conduction, bretylium alone shortened intraatrial and His-Purkinje conduction times but prolonged intranodal conduction time. With quinidine, intraatrial and His-Purkinje conduction times were markedly prolonged and intranodal conduction time was only slightly increased. Addition of bretylium to quinidine shortened intraatrial and His-Purkinje conduction times but significantly prolonged intranodal conduction time, resulting in a further prolongation of the total A-V interval. The possible clinical implications of these findings are stressed.

Effect of glucagon on cardiac conduction in man

His bundle electrograms were obtained in 26 patients before and after intravenous administration of glucagon (50 μg/kg). The group consisted of 4 patients with normal conduction and 22 patients with conduction disease. The P-A interval, measured in all patients, was 35 ± 1.4 msec (mean ± standard error of the mean) before and 30 ± 1.5 msec after infusion of glucagon ( P < 0.001). The mean A-H interval during sinus rhythm in all patients and during pacing at 100/min in 21 patients was, respectively, 97 ± 6.0 msec and 114 ± 6.4 msec before, and 96 ± 6.0 msec and 114 ± 6.6 msec after infusion of glucagon (not significant). The mean H-V interval in 25 patients was 48 ± 2.6 msec before and 49 ± 2.0 msec after infusion of glucagon (not significant). The mean sinus rate and sinus recovery times were, respectively, 73 ± 3.0 beats/min and 1,025 ± 42.0 msec before and 81 ± 3.0 beats/min and 919 ± 27.0 msec after infusion of glucagon ( P < 0.001 and < 0.01). Functional and effective refractory periods were measured (In milliseconds) with use of the atrial extrastimulus technique. The mean atrial functional and effective refractory periods (21 patients) were, respectively, 273 ± 11.6 and 252 ± 12.0 before and 256 ± 10.0 and 238 ± 9.6 after infusion of glucagon ( P < 0.001 and < 0.01). Mean atrloventricular (A-V) nodal functional refractory period (22 patients) and effective refractory period (15 patients) were 465 ± 22.0 and 404 ± 33.0 before and 457 ± 23.0 and 395 ± 32.0 after the infusion (not significant). The mean effective refractory period of the His-Purkinje system (2 patients) was 440 ± 45.0 before and 425 ± 55.0 after infusion of glucagon (not significant). In summary, glucagon increased sinus nodal automaticity, as manifested by an increase in sinus rate and decrease of sinus nodal recovery time, and improved intraatrial conduction as manifested by a reduction of the P-A interval and atrial functional and effective refractory periods. Glucagon had no effect on A-V nodal or intraventricular conduction.

Atrioventricular conduction in patients with incomplete endocardial cushion defect.

The cause of left axis deviation noted on the electrocardiogram (ECG) in patients with ostium primum atrial septal defect has been attributed to two differing mechanisms: left ventricular overload secondary to mitral insufficiency and a congenitally anomalous atrioventricular conduction system. In order to define the conduction characteristics of the atrioventricular conduction system in patients free from the hemodynamic abnormalities of ostium primum atrial septal defect, seven patients with an ostium primum atrial septal defect were studied in the late postoperative period. Each ECG showed persisting left axis deviation with no new conduction abnormalities. Hemodynamic evaluation, including left ventriculography, showed no intra-atrial shunting and only minimal mitral insufficiency in three patients. His bundle recording techniques were utilized to study the atrioventricular conduction system. The P-A interval was normal in four patients (25-45 msec) and prolonged in three (50, 60 and 60 msec), while the A-H interval was normal in all seven patients (60-130 msec). This is compatible with abnormal intra-atrial conduction and normal conduction through the atrioventricular node. The H-V interval was normal in four patients (35-55 msec) and short in three (20, 25, and 25 msec). Atrial pacing produced the normally expected A-H prolongation, P-A and H-V remaining constant. These results and the persisting left axis deviation can be explained on the basis of the known anatomy of the atrioventricular conduction system in patients with ostium primum atrial septal defect. The left axis deviation is most probably related to early activation of the postero-basal left ventricular wall (patients with short H-V) and/or late activation of the antero-lateral left ventricular wall (patients with normal H-V). Hemodynamics are not important in producing these findings.

Atrial Ultrastructure in Patients with Fixed Intra-atrial Block

This study describes ultrastructural changes seen in the right atria of ten patients with fixed intra-atrial block (FIAB) (P wave duration of 120 msec or more during sinus rhythm). The tissue, which was obtained by biopsy at the time of open heart surgery, is compared to that of three patients with normal right atrial morphology. One sample of left atrial tissue from a rheumatic subject is also described. The ultrastructural changes observed in the right atria of patients with P wave durations of 140 msec or more were much more extensive than in the patients with FIAB and P wave durations of 120–130 msec. These longer delays in intra-atrial conduction may be due to extensive disturbances at the level of the ordinary working atrial myocardium, while the lesser degrees of block may simply be due to sluggish conduction through the anterior internodal tract, as is suggested by the data on intermittent intra-atrial block.

Studies of intra-atrial conduction with bipolar atrial and His electrograms.

Studies of intra-atrial conduction with bipolar atrial and His electrograms.