Tokuhiro Kawara

Electrical Conduction in Canine Pulmonary Veins: Electrophysiological and Anatomic Correlation

Background—Paroxysmal atrial fibrillation in patients is often initiated by foci in the pulmonary veins. The mechanism of these initiating arrhythmias is unknown. The aim of this study was to determine electrophysiological characteristics of canine pulmonary veins that may predispose to initiating arrhythmias. Methods and Results—Extracellular recordings were obtained from the luminal side of 9 pulmonary veins in 6 Langendorff-perfused dog hearts after the veins were incised from the severed end to the ostium. Pulmonary veins were paced at the distal end, the ostium, and an intermediate site. During basic and premature stimulation, extracellular electrical activity was recorded with a grid electrode that harbored 247 electrode terminals. In 4 hearts, intracellular electrograms were recorded with microelectrodes. Myocyte arrangement immediately beneath the venous walls was determined by histological analysis in 3 hearts. Extracellular mapping revealed slow and complex conduction in all pulmonary veins. Activation delay after premature stimulation could be as long as 96 ms over a distance of 3 mm. Action potential duration was shorter at the distal end of the veins than at the orifice. No evidence for automaticity or triggered activity was found. Histological investigation revealed complex arrangements of myocardial fibers that often showed abrupt changes in fiber direction and short fibers arranged in mixed direction. Conclusions—Zones of activation delay were observed in canine pulmonary veins and correlated with abrupt changes in fascicle orientation. This architecture of muscular sleeves in the pulmonary veins may facilitate reentry and arrhythmias associated with ectopic activity.

Correlation between electroencephalography and heart rate variability during sleep

Abstract It is known that autonomic nervous activities change in correspondence with sleep stages. However, the characteristics of continuous fluctuations in nocturnal autonomic nerve tone have not been clarified in detail. The study aimed to determine the possible correlation between the electroencephalogram (EEG) and autonomic nervous activities, and to clarify in detail the nocturnal fluctuations in autonomic nerve activities. Overnight EEGs and electrocardiograms of seven healthy males were obtained. These EEGs were analyzed by fast Fourier transformation algorithm to extract delta, sigma and beta power. Heart rate and heart rate variability (HRV) were calculated in consecutive 5‐min epochs. The HRV indices of low frequency (LF), high frequency (HF) and LF/HF ratio were calculated from the spectral analysis of R‐R intervals. The sleep stages were manually scored according to Rechtschaffen and Kales’ criteria. Low frequency and LF/HF were significantly lower during non‐rapid eye movement (NREM) than REM, and were lower in stages 3 and 4 than in stages 1 and 2. Furthermore, delta EEG showed inverse correlations with LF (r = − 0.44, P < 0.001) and LF/HF (r = − 0.41, P < 0.001). In contrast, HF differed neither between REM and NREM nor among NREM sleep stages. Detailed analysis revealed that correlation was evident from the first to third NREM, but not in the fourth and fifth NREM. Delta EEG power showed negative correlations with LF and LF/HF, suggesting that sympathetic nervous activities continuously fluctuate in accordance with sleep deepening and lightening.

Heterogeneity of anterograde fast-pathway and retrograde slow-pathway conduction patterns in patients with the fast–slow form of atrioventricular nodal reentrant tachycardia: electrophysiologic and electrocardiographic considerations

OBJECTIVES This study sought to define the electrophysiologic and electrocardiographic characteristics of fast-slow atrioventricular nodal reentrant tachycardia (AVNRT). BACKGROUND In fast-slow AVNRT the retrograde slow pathway (SP) is located in the posterior septum, whereas the anterograde fast pathway (FP) is located in the anterior septum; however, exceptions may occur. METHODS Twelve patients with fast-slow AVNRT were studied. To determine the location of the retrograde SP, atrial activation during AVNRT was examined while recording the electrograms from the low septal right atrium (LSRA) on the His bundle electrogram and the orifice of the coronary sinus (CS). Further, to investigate the location of the anterograde FP, single extrastimuli were delivered during AVNRT both from the high right atrium and the CS. RESULTS The CS activation during AVNRT preceded the LSRA in six patients (posterior type); LSRA activation preceded the CS in three patients (anterior type), and in the remaining three both sites were activated simultaneously (middle type). In the anterior type, CS stimulation preexcited the His and the ventricle without capturing the LSRA electrogram (atrial dissociation between the CS and the LSRA), suggesting that the anterograde FP was located posterior to the retrograde SP. In the posterior and middle types, high right atrial stimulation demonstrated atrial dissociation, suggesting that the anterograde FP was located anterior to the SP. In the posterior and middle types, retrograde P waves in the inferior leads were deeply negative, whereas they were shallow in the anterior type. CONCLUSIONS Fast-slow AVNRT was able to be categorized into posterior, middle and anterior types according to the site of the retrograde SP. The anterior type AVNRT, where an anteriorly located SP is used in the retrograde direction and a posteriorly located FP in the anterograde direction, appears to represent an anatomical reversal of the posterior type which uses a posterior SP for retrograde and an anterior FP for anterograde conduction. Anterior type AVNRT should be considered in the differential diagnosis of long RP (RP > PR intervals) tachycardias with shallow negative P waves in the inferior leads.

Reentrant Circuits in the Canine Atrioventricular Node During Atrial and Ventricular Echoes: Electrophysiological and Histological Correlation

Background—The anatomic-electrophysiological correlation of AV nodal reentry is unclear. To localize reentrant circuits during atrial and ventricular echoes and to characterize sites of slow conduction and block, we correlated histology with electrophysiology of the AV node. Methods and Results—In 10 isolated dog hearts, extracellular electrical activity was recorded in Koch’s triangle at 208 or 247 sites (interelectrode distance, 0.5 and 0.3 mm) after removal of 0.7 to 1.5 mm of overlying atrial tissue. Resection did not affect refractory periods. Five hearts were subjected to histology. Complete atrial echoes were induced in 1 heart, incomplete atrial echoes in 5 hearts. Unidirectional conduction block occurred at the atrial–transitional cell junction in the superior area. Zones of slow conduction arose at the atrial–transitional or the transitional–compact node junction in the inferior area. Complete reentrant circuits of ventricular echoes were obtained in 5 hearts. Unidirectional conduction block occurred at the compact node–transitional cell junction in the superior area. Localized zones of slow conduction arose at the junctions between the different types of tissue in the inferior area. Conclusions—In the dog heart, tissue architecture and functional dissociation between the inferior and the superior region of the AV node enable dual physiology and reentry. Slow conduction and functional conduction block occur at the junctions between the different types of tissue in the AV nodal area. Atrial echoes were enabled by conduction block at the atrial-transitional cell junction, whereas during ventricular echoes conduction block occurred at the compact node-transitional cell junction.

Pathological Aspects of Radiofrequency Catheter Ablation of the Canine Atrioventricular Node and Bundle of His

Radiofrequency catheter ablation of the atrioventricular (AV) node or bundle of His was performed in 12 adult mongrel dogs. The aim was to create chronic incomplete AV block (first‐ and second‐degree AV block) and to examine the histopathology of the ablated lesions. However, the late electrophysiological results (2 4 weeks follow up) were various: normal in 2 dogs, mild PR prolongation (< 50%) in 2 dogs, first‐degree AV block (PR prolongation a 50%) in 2 dogs, second degree AV block in 2 dogs, complete AV block in 4 dogs. The maximally ablated area (%) of the atrioventricular conduction system in serial histologic sections from dogs with these conditions was 69%, 75%, 89.5%, 95% and 99.5%, respectively. The number of intact conduction cells at the maximally ablated site varied from 6 to 30 in the four cases of incomplete AV block. The mean ablated volume (%) of either the AV node or penetrating His bundle correlated roughly with the degree of AV block. The ablated lesions were well demarcated and almost replaced by dense fibrous tissue at 4 weeks. Interruption (3 dogs) or thinning (1 dog) of the endocardial elastic lamellae was detected, in association with endocardial thickening (mean 913 μm). Endocardial thrombi were found in 3 dogs (2 fresh, 1 organized). We conclude that radiofrequency catheter ablation does not cause severe complicated lesions. Several possible conditions for creating chronic incomplete AV block are discussed. Acta Pathol Jpn 41: 487–498, 1991.

Electrophysiological Demonstration of Anterograde Concealed Conduction in Accessory Atrioventricular Pathways Capable Only of Retrograde Conduction

Anterograde concealed conduction into the concealed accessory atrioventricular (AV) pathway has been postulated to be one of the factors preventing the reciprocating process via the accessory pathway in patients with the concealed Wolff‐Parkinson‐White(WPW) syndrome but its presence has not been documented. To demonstrate the occurrence of anterograde concealment, 12 patients with the concealed WPW syndrome were selected for study. A pacing protocol was designed in which the retrograde conduction of the ventricular extrastimulus over the accessory pathway was assessed during ventricular pacing aione (conventional method) and during the AV simultaneous pacing (simultaneous method); the results were then compared. When the high right atrium was simultaneously paced, the effective refractory period of the concealed accessory pathway shortened as compared with the conventional method in five of 12 patients (from 341.7 ± 110.8 to 312.5 ± 108.2 msec, n = 12), whereas, it decreased in all patients studied when the coronary sinus near the accessory pathway was simultaneously paced (from 375.7 ± 135.0 to 287. ± 116.1 msec, n = 7). These results demonstrate that the AV simultaneous pacing frequently shortens the refractoriness of the concealed accessory AV pathway and such facilitation seems to he well explained by the probable anterograde concealment in it and peeling back of the refractory barrier.

Molecular heterogeneity of urinary albumin in glomerulonephritis: Comparison of cardiovascular disease with albuminuria

BACKGROUND Despite the unstable structure of urinary albumin in kidney diseases, urinary albumin fragments have been identified by denaturing methods such as two-dimensional electrophoresis. This study examined the relationship between the structural heterogeneity of urinary albumin and protease effects. METHODS Urine samples from patients with glomerulonephritis (GN), cardiovascular diseases (CVD), and healthy subjects were analyzed by non-reducing sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS PAGE), Western blot, diagonal 2-dimensional non-reducing/reducing (d2D) SDS PAGE, and albumin zymography. RESULTS The major band was monomer albumin in CVD and healthy subjects; however, 13 urinary albumin bands ranging from 55 to 172 kDa were identified by non-reducing SDS PAGE in GN. The results from d2D SDS PAGE showed urinary albumin polymerization between disulfide bridges, interactions with other proteins, and reduction induced degradation in GN patients. The results from albumin zymography showed that low-molecular mass forms of albumin did not necessarily correspond to high protease activity. Furthermore, concentrated healthy urine showed similar protease digestion as in GN without low-molecular mass of albumin. CONCLUSIONS The molecular alterations observed cannot be explained only by urinary proteases. The specific alteration of urinary albumin molecules in GN can be attributed to different mechanisms to CVD.

Coronary Sinus Pacing Initiates Counterclockwise Atrial Flutter While Pacing From the Low Lateral Right Atrium Initiates Clockwise Atrial Flutter Analysis of Episodes of Direct Initiation of Atrial Flutter

INTRODUCTION Rapid atrial pacing in sinus rhythm may directly induce atrial flutter without provoking intervening atrial fibrillation, or initiate atrial flutter indirectly, by a conversion from an episode of transient atrial fibrillation provoked by rapid atrial pacing. The present study was performed to examine whether or not the direct induction of clockwise or counterclockwise atrial flutter was pacing-site (right or left atrium) dependent. METHODS AND RESULTS We analyzed the mode of direct induction of atrial flutter by rapid atrial pacing. In 46 patients with a history of atrial flutter, rapid atrial pacing with 3 to 20 stimuli (cycle length = 500 - 170 ms) was performed in sinus rhythm to induce atrial flutter from 3 atrial sites, including the high right atrium, the low lateral right atrium, and the proximal coronary sinus, while recording multiple intracardiac electrograms of the atria. Direct induction of atrial flutter by rapid atrial pacing was a rare phenomenon and was documented only 22 times in 15 patients: 3, 11, and 8 times during stimulation, respectively, from the high right atrium, low lateral right atrium, and the proximal coronary sinus. Counterclockwise atrial flutter (12 times) was more frequently induced with stimulation from the proximal coronary sinus than from the low lateral right atrium (8 vs 1, P = .0001); clockwise atrial flutter (10 times) was induced exclusively from the low lateral right atrium (P = .0001 for low lateral right atrium vs proximal coronary sinus, P = .011 for low lateral right atrium vs high right atrium). CONCLUSIONS Direct induction of either counterclockwise or clockwise atrial flutter was definitively pacing-site dependent; low lateral right atrial pacing induced clockwise, while proximal coronary sinus pacing induced counterclockwise atrial flutter. Anatomic correlation between the flutter circuit and the atrial pacing site may play an important role in the inducibility of counterclockwise or clockwise atrial flutter.

Demonstration of Right and Left Atrial Dissociation by Atrial Rapid Pacing or Extrastimulation During Fast‐Slow (Uncommon) Form of Atrioventricular Nodal Reentrant Tachycardia

Some recent works suggest that extranodal atrial fibers may form part of the reenlry circuit in the atrioventricular (AV) nodal reentrant tachycardia (AVNRT). This hypothesis is based on the fact that the perinodal dissection successfully abolished AVNRT while preserving intact AV conduction. Apart from the surgical success, the electrophysiological evidence supporting this hypothesis has not been demonstrated, especially in the uncommon (fast‐slow) form of AVNRT. We present some electrophysiological evidence suggesting atrial participation in eight patients with the fast‐slow form of AVNRT. During the tachycardia, rapid pacing or extrastimulation was done from the orifice of the coronary sinus (CS) and the right atrium (RA), while recording the electrograms of the CS and the low septal RA. In seven patients, right and left atrial dissociation was demonstrated during pacing from the RA, while in the remaining one this was demonstrated from the CS. The interatrial dissociation will be unlikely if the intranodal reentry circuit connects with the atria via a single upper common pathway. This suggests that the upper turnaround of the reentry circuit involves atrial tissue and that the extranodal accessory pathway with long conduction times may form the ascending limb of the circuit (atrionodal reentry). Alternatively, the reentry circuit is entirely intranodal and two or more connecting pathways are present between the atria and the circuit.

Marked anterograde decremental conduction over a rapidly conducting accessory pathway after radiofrequency ablation

We report on a patient with the Wolff-Parkinson-White syndrome who temporarily exhibited a marked anterograde decremental conduction over a rapidly conducting accessory atrioventricular pathway after successful radiofrequency ablation. By recording the intracardiac electrogram via the ablation catheter placed at the successful ablation site, we were able to exclude the possibility of the occurrence of anterograde decremental conduction in the atrial or ventricular myocardium between the accessory pathway and the recording electrodes.