Search

A case of atypical AV nodal reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation, masquerading as tachycardia using a left-sided accessory pathway, is reported. Initially, it appeared that the tachycardia was a typical slow-fast form of AVNRT. The earliest retrograde activation, however, was registered at a site approximately 3 cm from the coronary sinus orifice (left atrial free wall), indicating atypical AVNRT. Atrial tachycardia and orthodromic AV reciprocating tachycardia using an accessory AV pathway were excluded. Slow pathway ablation at the posteroseptal right atrium eliminated the tachycardia. It was suggested that the anterograde limb of the tachycardia circuit was a slow AV nodal pathway with typical posteroseptal location, whereas the retrograde limb was a long atrionodal pathway connecting the compact AV node and the left atrial free wall near the mid-coronary sinus.

The presence or absence of ventriculoatrial (VA) conduction in the human heart is assessed by investigating whether 1:1 retrograde atrial capture is observed during constant cycle length ventricular pacing. In this study, a new pacing protocol for assessing VA conduction was designed in which the ventricular extrastimulus was delivered during basic ventricular and atrial simultaneous pacing (VE-VASP method). The effect of this pacing protocol on VA conduction was investigated in 12 patients who showed no evidence of VA conduction with the constant cycle length ventricular pacing method. In 5 of 12 patients, intact VA conduction was demonstrated with the VE-VASP method, while VA conduction was not observed in the remaining 7 patients. These results suggest that VE-VASP method sometimes demonstrates the presence of intact VA conduction in patients who show no evidence of VA conduction during constant cycle length ventricular pacing.

Although the recordings of the His potential have been shown to be very useful in the study of cardiac conduction and rhythm disturbances, there remain some problems regarding the clinical His bundle electrogram. Some of the studies were performed to solve in the perfused dog hearts and in situ dog hearts, and consequently the following results were obtained. In some experiments, recording of the His potential could not be achieved even in the perfused hearts in spite of the preserved A-V conduction, suggesting that, as experienced sometimes in the clinical cases, inability to record the His potential might not be due to the technical failure or the anatomical abnormalities of the His bundle. On the other hand, real "splitting of H" occurred in association with the increase in the duration and decrease in the amplitude of the His potential after the ligation of the anterior septal artery. In addition, the true Mobitz II type A-H block, and Wenckebach type intra-Hisian and H-V block could be produced experimentally.

By employing electrographic electrodes, suction electrodes and microelectrodes, 2 conduction pathways were discovered in the anteromedial portion and in the posteromedial portion along the AV ring at the lower margin of the left atrium in the isolated rabbit heart. They were found to conduct the left atrial impulses to the right atrium and separately through the AV node to the ventricle. The one in the posteromedial portion was found to be different from the inferior interatrial pathway reported recently by Scherlag et al. Histological examination after functional studies revealed that each pathway was embedded in the fibrofatty tissues at the site of the attachment of the mitral valve to the left atrium. The anterior pathway encircled the anterior portion of the mitral ring and entered the anterosuperior portion of the AV node. The posterior pathway encircled the posterior portion of the mitral ring and entered the posteroinferior portion of the AV node. They can be regarded as interatrial pathways and in a sense as accessory AV conduction pathways from the left atrium.

Employing the apparatus which we made of analog computers, spatial velocity electrocardiograms were taken from 321 cases composed of 54 normal cases, 71 cases of left ventricular hypertrophy, 12 cases of right ventricular hypertrophy, 14 cases of complete left bundle branch block, 30 cases of complete right bundle branch block, 10 cases of incomplete right bundle branch block, 41 cases of myocardial infarction and 89 cases of ventricular premature beats. The normal sVECG was composed of 8 chief deflections: π1 and π2 as the counterpart of the P wave of the electrocardiogram, ξ, ρ1, ρ2 and σ as that of the QRS, and τ1 and τ2 as that of the T wave. Normally ρ2 and τ2 were larger than ρ1 and τ1, respectively. In ventricular hypertrophy ξ ρ σ tended to show more splitting and τ to be flatter or the ratio τ1/τ2 was smaller than normal. In left bundle branch block splitting of ξ Ρ σ was most marked and in right bundle branch block σ was wide, frequently making a separate σ'. In myocardial infarction ξ was wide occasionally, and σ was usually wide. ρ1 was often larger than ρ2 in anterior myocardial infarction and was smaller than ρ2 in pos-terior myocardial infarction. τ was variously abnormal in most cases. These and other findings were found useful for diagnosis and the sVECG was found to be especially useful when combined with the vectorcardiogram by effectively supplementing its weak points.

Propranolol, diphenylhydantoin and tetrodotoxin showed inhibitory or removal effects on fibrillation induced in isolated rabbit atrial muscle strip. Depending upon methods of induction of fibrillation, effects of these drugs were different. The mode of their action seemed to be due to following electrical natures of each drug in its effective dose.Diphenylhydantoin decreased rate of rise and amplitude of the action potential of dog ventricular fibers and rabbit atrial fibers, which was also a cause of prolongation of conduction time. Duration of action potential was slightly prolonged in an effective low concentration. In contrast propranolol showed a relatively little effect on these items, but depressed ectopic spontaneous activity. Tetrodotoxin had both effects more markedly.

(1) Vectorcardiograms of ventricular premature beats were taken from100 cases of normal and of various cardiac patients by the Frank lead system. In order to include also ventricular premature beats occurring only occasionally, they were first recorded by a tape recorder.(2) Vectorcardiograms of ventricular premature beats were classified into 3 main types according to the loop configuration and its direction. Type A resembled more or less left bundle branch block. Type B resembled also left bundle branch block in configuration of the vector loop, but its direction was different, the QRS loop being oriented to the right posteriorly. Type C resembled right ventricular hypertrophy with a conduction delay. Types A and C were divided into a few subgroups.(3) The T vector loop was usually oriented opposite to the maximum QRS vector in Types A and B and the terminal QRS portion in Type C. In the shape and the direction of inscription of the T loop, no specific tendency was found, except for a tendency that the secondary T vector loop was observed in occasional ventricular premature beats in normal cases to be inscribed most often in the same direction of the QRS loop.(4) Type A1 was more often found in cases of good conditions and Types B and C were found in cases of relatively poor conditions. Type A2 fell between.(5) Among the cases 35 cases had ventricular premature beats occurring only occasionally. No difference could be found from those occurring frequently in their vectorcardiographic configuration and clinical significances.

Adaline was applied to select automatically the characteristics of the vectorcardiographic configuration of various conditions, taking vectorcardiograms from 114 cases by Frank's method. Among the 28 parameters, those showing a larger weight were selected. Some selected parameters were found to be relatively common for differentiation of pairs of various conditions and other parameters rather specific.In addition, an attempt was made to decrease the number of parameters without changing the accuracy significantly. For some differentiations only several parameters were sufficient, but for others it can be decreased to less than half only with difficulty.

Histological determination was made on the preparations from the rabbit heart presumed to be bypass tracts by the previous functional study. As the first bypass tract a muscle strip composed of the apparently ordinary cardiac muscle was found to leave the right atrium and reach the bundle of His at or near the bifurcation, bypassing the A-V node. As the second bypass tract a bundle of apparently ordinary cardiac muscle fibers leaves the lateral wall of the right atrium above the A-V groove, descending and reaching the lateral wall of the right ventricle. A part of the third bypass tract was found below the right atrium close to the interatrial septum and its terminal part was found to enter the left side of the A-V node anterior to the ordinary atrio-nodal connection.Since its middle part could not be differentiated clearly from the ordinary atrial muscle fibers, the histological confirmation is not considered to be complete as yet, as far as the third bypass tract is concerned.These histological findings explain the short P-R interval and the almost normal ventricular complex of the first bypass conduction, the short P-R interval and the abnormal configuration of the ventricular complex of the second bypass conduction, and the long P-R interval and normal ventricular complex of the third bypass conduction. As additional functional findings the short P-R interval of the first bypass was found to show relatively constant values in spite of the change in the stimulus frequency and the longer than normal P-R interval of the third bypass to decrease at first and increase markedly later as the stimulus frequency was increased.

An intracardiac electrophysiologic study was performed in a patient with paroxysmal tachycardia. The patient had two previous episodes of myocardial infarction, but abnormal Q waves were absent in previously obtained electrocardiograms. Electrocardiographic diagnosis of inferior and anterior infarction was made because the electrocardiogram taken on admission temporarily showed abnormal Q waves. Atrioventricular reentry with anterograde conduction over a fasciculoventricular Mahaim fiber and retrograde conduction over a concealed Kent bundle was observed during the tachycardia. It was also demonstrated that electrocardiographic masking of the Q waves was caused by conduction over a fasciculoventricular Mahaim fiber.

By altering the calcium, sodium and potassium content of the Tyrode solution, the relationship between the shape of the action potential and of the contraction curve in regard to the changes induced by l-isoproterenol, dl-norepinephrine and ouabain, and at the same time the mode of action of these drugs were sought for. In the normal Tyrode solution, shortening of the duration of the action potential at 25% and 50% repolarization showed a significant correlation with the increment of the contractile force, and the total duration of the action potential showed a significant correlation with the time to the peak tension and with the total duration of the contraction curve at the maximal effect period of these drugs. This relationship was found to be more or less true qualitatively also when the extracellular ions were altered variously.By analyzing the observed changes, it was concluded that l-isoproterenol increases the contraction, employing chiefly the extracellular calcium ions, whereas dl-norepinephrine and ouabain can increase the contraction by mobilizing in addition the intracellular calcium ions in a calcium-free solution. The increase of contraction by l-isoproterenol is mostly independent of the potassiumion, whereas that by ouabain and dl-norepinephrine occurs in connection with this ion. l-Isoproterenol and dl-norepinephrine increase the contraction directly by driving the calcium ions into the cell rather than by exchanging the sodium ions with the calcium ions. The inotropic action of ouabain does not seem to have any relation with either the sodium ions or the calcium ions entering at this phase.

Unipolar His bundle electrograms were recorded with the muscle preparation isolated from the rabbit or the dog heart at as various sites as possible on and near the A-V conduction system and changes in appearance time and configuration of the so-called His (H) potential were examined. When the exploring electrode was shifted from the coronary sinus orifice down to the transition between the A-V node and the His bundle, the H potential was small but observed distinctly and its appearance time was rather fixed. The earliest excitation of the His bundle is thus assumed to be not much earlier than 1/3 or 1/4 the P-R interval before the Q wave. The nodal (N) potential appeared in addition to the H potential at variable time points while the electrode was shifted on the A-V node and disap-peared when it was reached the His bundle. The appearance did not give the impression that the N potential changed to the H potential accord-ing to the electrode shift. Over the His bundle the H potential changed its appearance time successively. The H potential was also compared with the action potential obtained from the points as close as possible to the ex-ploring electrode or with the other reference electrogram. It took the electrical field generated by the electrical activity of the whole of the His bundle, but it was influenced more by the local electrical activity than in the case of the electrocardiogram of the whole heart in situ.

The pacemaker site of the so-called "nodal" rhythm was examined by the His bundle electrogram with the in situ heart and also by the microelectrode technique with the isolated cardiac muscle preparation of dogs. The His deflection showed a decrease and an alteration in shape in this subsidiary pacemaker beat or rhythm and was found to originate from the area which was not affected by vagal stimulation and acetylcholine administration. In a similar condition the same deformation of the His deflection and slow diastolic depolarization with slow rise of the action potential appeared in the intracellular recording of the His bundle in the isolated muscle preparation. Therefore, more confirmatory evidence was obtained that the pacemaker site was the His bundle, especially when deformed His deflection was found.