IINTRODUCTION: The lateral (LAB), medial (MAB) and superior (SAB) atrionodal bundles, and proximal AV bundle are part of the Sinoventricular Conduction System by their unique transmembrane (TAPs), ...

INTRODUCTION: The proximal AV bundle (PAVB) has been shown to be the only input to the AV node (AVN) in the canine heart in anatomoelectrical reports over the past 20 years. The anatomic studies utilized photographic correlations of epi- and endocardial aspects of whole hearts through blocking, and serial histologic parallel, perpendicular and transverse plane Goldner Trichrome stained sections of the flattened heart; Karnovsky’s fixative at pH 7.2 and sucrose buffer rinses; direct 3D and stereotaxic analysis. Electrical studies, under direct observation of in-vitro superfused hearts, delineated unique wire, catheter, and micropipet electrode potentials via high K, transections, Lucifer Yellow iontophoresis and photoablations during spontaneous and paced SA node rhythms and with simultaneous SA node, atrionodal bundles, PAVB, AVN and distal AV bundle recordings. HYPOTHESIS: The PAVB exists in the human heart. METHODS AND RESULTS: Explanted normal human hearts, deemed unsuitable for transplantation, processed as above with transverse sections, revealed that the AVN (Figs. A–C ) is joined by the PAVB at a 90-degree angle (Figs. B, C ). These “normal” hearts from older patients (57– 80 yr) had atrophic or absent atrial myocardium. In Figure C , most of the right medial atrial wall myocardium, but not the left atrium (LA), had been replaced by fat. CONCLUSIONS: PAVB is the only AVN input in the human heart. As in the canine heart, PAVB also runs away from the annulus and is apposed to LA. Knowledge of the PAVB should be helpful in decreasing morbidity associated with clinical procedures. Care must be taken in ablating the fast superior atrionodal bundle pathway input to the PAVB. Figures A and B are from the same 60 yr and C is from a 71 yr old heart. AVN (A) is apposed to the left ventricular outflow tract (LVOFT and dotted line) along with the PAVB ( B and C ). But as seen in C , PAVB assumes a position apposed to LA, And, as in the dog heart, thereafter (not shown here) PAVB is completely apposed to LA.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common cause of supraventricular tachycardia seen in clinical practice, yet the “precise” pathways are still unknown. 1 Scheinman M.M. Yang Y. The history of AV nodal reentry. Pacing Clin Electrophysiol. 2005; 28: 1232-1237 Crossref PubMed Scopus (24) Google Scholar Misconceptions regarding the topography of the AV node, its environs, and its transmission pathways may relate to differences in data among anatomic and electrical studies. 2 Goldberger J.J. Unraveling the mysteries of the AV node. Heart Rhythm. 2006; 3: 1001-1002 Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar Topography of the AV nodeHeart RhythmVol. 4Issue 3PreviewWe read with interest the comments of Dr. Racker on our article in the September 2006 issue of Heart Rhythm,1 but we do not concur with her views. First, we believe that Dr. Racker has misunderstood the position of the left–His catheter that was advanced to the left septum through the noncoronary cusp. We did not say that we negotiated the interatrial septum only, simply because one cannot record a His-bundle potential at this site. Second, we disagree with the notion that the His-bundle potential originates from the AV node. Full-Text PDF

We demonstrated in the canine heart that there are heretofore unknown septae separating regions of the right atrium and right ventricle from the aorta at the level of the right (*) and posterior aortic sinus (· PAS) and separating the right atrium from the left ventricle. Here we report the septae in the human heart in a stereotaxic study. Methods and Results Photographs of the epi- and endocardial exposure of whole and flattened hearts and during blocking (8) were compared to photographs of serial orthogonal transverse plane histologic sections stained by Goldner Trichrome (5). Every section was mounted, accessioned and initially evaluated at .5 mm intervals. In human hearts, the same structures and relationships in dog heart differed only in size and pitch. For the septae, the atrioaortic septum extends between the right atrium at the level of an aortic sinus wall; the ventriculoaortic septum (VAS) extends between the right ventricle at level of an aortic sinus wall (Figure, VAS is in the PAS); and the atrioventricular septum-membranous and -muscular components extend between the right atrium and the left ventricle. The membranous ventricular septum extends under the right and posterior aortic sinuses. Conclusions The septae separate low- from high-pressure chambers and can be at risk of breech or puncture with pathology or during cardiac procedures and help to explain rupture of the right sinus of Valsalva into the right ventricular outflow tract imaged via transesophageal echocardiograms (Cullen et al., Circulation, 2002: –e2). Support: NIH HL073261 (DKR).

Our previous studies showed: electrograms traces made with wire (WE) and catheter electrodes (CE) at sites where the atrial and specialized tissues overlap contain waveforms evoked by both tissues. At the atrionodal bundle (AB) site, the so-called low-high amplitude (amp) potentials are seen. The low waveforms reflect AB activation, which persists with high K, the high-amp potentials reflect atrial activation and ceased with high K. Transmembrane potentials (TAPs) made deep to WE at sites where coincident CE and WE traces are found, showed AB TAPs are plateau-shaped and atrial potentials (Ap) are triangular. Using coincident CE, WE, and ME recordings for targeting ABs for Lucifer Yellow (LY) iontophoresis/photoablations, we found some plateau potentials were coincident with the high-amp Ap. Here we report the electrical and anatomic features of myocytes revealed by LY. Methods and Results Standard methods were used for CE and WE recordings in the unipolar mode and for TAPs. Myocytes targeted by their TAPs were LY injected for 10 mins using 20 to 40 nA hyperpolarizing current. Goldner trichrome and unstained serial transverse sections were viewed by light and epifluorescent microscope. LY was confined to (a) sub-endocardial atrial fascicles when coincident high-amp WE, CE and triangular TAPs were targeted; (b) sub-epicardial atrial fascicles when high-amp and plateau TAPs were targeted; and (c) AB fascicles when coincident low-amp and plateau potentials were targeted. The AB potentials displayed a more prominent spike phase 1 and dome than the atrial plateaus. Conclusions Some ordinary atrial myocytes possess plateau potentials. Coincident CE, WE, and ME recordings are essential for delineating the atrial from the AB myocytes for in-vitro studies. Support: NIH HL073261 (DKR).

We hypothesized that myocardial infarction-related alterations in ventricular fibrillation (VF) cycle length (VFCL) would correlate with changes in local cardiac electrophysiological and anatomic properties. An electrophysiological study was performed in normal, subacute, and chronic infarction mongrel dogs. VF was induced by programmed electrical stimulation and mean and minimum early and late VFCL was determined and correlated with local electrophysiological and anatomic properties. Effective refractory period (ERP), activation recovery time (ART), ERP/ART ratio, threshold, and ERP and ART dispersion were determined at 112 sites on the anterior left ventricle. Wave front progression was analyzed over a 2-s period. The extent of local tissue necrosis and of myocardial fiber disarray was also evaluated. The early mean VFCL was significantly longer in the subacute infarction (149 +/- 35 ms) and chronic infarction dogs (129 +/- 18 ms) compared with control dogs (102 +/- 15 ms; P < 0.0001 for both comparisons) as was the early minimum VFCL with similar trends seen during late VF. Complete epicardial reentrant circuits were significantly more common in normal dogs (4.3 +/- 2.4, 22.4% of cycles) than in subacute (0.75 +/- 0.96, 5.3% of cycles, P < 0.05 vs. normal) and chronic infarction dogs (1.3 +/- 1.3, 7.5% of cycles, P < 0.05 vs. normal). There was a poor correlation between the mean and minimum early and late VFCL and local electrophysiological and anatomic properties (R(2) < 0.2 for all comparisons) with a much better correlation between average mean and minimum VFCL (over the entire plaque) and global ERP and ART dispersion during early and late VF. In conclusion, VFCL in normal and infarcted myocardium shows a poor correlation with local ventricular electrophysiological and anatomic properties measured in sinus rhythm. However, there was a much better correlation between the average VFCL with global dispersion of repolarization. The lack of correlation between local VFCL and refractoriness and the infrequent occurrence of epicardial reentry suggests that intramural reentry may be the primary mechanism of VF in this model.

This “Part II morphology and cytoarchitecture” study is based on paraffin-embedded specimens in which the extracellular and intracellular matrix are preserved; single parallel, perpendicular, and transverse serial sections of the entire atrioventricular (AV) junction region (AVJR) and their correlation with photographs of the tissue blocks. As in Part I, the same major new findings are: 1) a coronary sinus fossa is formed by the superoposterior right medial atria wall (MAW), the left atrium, and the coronary sinus roof; 2) the posterior MAW forms two myocardial bridges and is isolated from the sinus venarum by the floor of the inferior vena cava; 3) the tendon of Todaro terminates in the superior lip of the coronary sinus ostium; 4) only ordinary myocardium contacts the annulus fibrosus, and there is little to no collagen separating its myofibers and tissues; 5) the ventricular septum shoulder is humped shaped, completely overlaid by annular myocardium, and joined by struts of papillary muscle; 6) the membranous septum joining the ventricular septum shoulder to the crista supraventricularis forms part of the aortic valve sinus walls; and 7) myocardium of the atrionodal bundles is aggregated into numerous small fascicles encased by collagen and is outside of the MAW as are the other specialized tissues. The proximal AV bundle and medial atrionodal bundle are aligned to the medial leg of Koch's triangle and the tendon of Todaro. These data show, therefore, that the AVJR contains two overlapping atrial circuits. In the MAW, acivation of the posterior region is delayed because of the two myocardial bridges. Puncture of the AVJR can produce communication with an extracardiac space, posteriorly and medially, and with the aorta, anteriorly.

The authors appreciate the important comment made by Kamath and Lip that a hypercoagulable state may be yet another mechanism increasing the risk of thromboembolism in the setting of cardioversion of atrial fibrillation. In our Editorial on the study by Roijer et al., we tried to focus on the mere ‘mechanical’ aspects of thrombus formation in the atria after cardioversion. Yet, as Kamath and Lip point out, there is evidence that patients may be in a hypercoagulable state during atrial fibrillation. In fact, pharmacological cardioversion of recent-onset atrial fibrillation may also lead to some increase in markers of thrombin activity underscoring the importance of a hypercoagulable state in this setting. However, the fact that most thrombi originate in the left atrial appendage indicates that the mechanical dysfunction is the primary insult and that increased coagulability may be a contributing factor, i.e. the reduced contractility during atrial fibrillation or post-cardioversion probably leads to blood stasis which then leads to a hypercoagulable state. As again pointed out by Kamath and Lip, unfractionated heparin is widely used in patients with de novo atrial fibrillation although this is largely based on clinical judgement rather than evidence-based medicine. The advantages of using lowmolecular-weight heparin in these patients seem obvious, although there are again no randomized studies available. In addition to the ACUTE II study mentioned by Kamath and Lip a similar study comparing enoxaparin to a conventional anticoagulation scheme (either with or without guidance by transoesophageal echocardiography) is currently being performed in Germany, the ACE study (Anticoagulation for Cardioversion With Enoxaparin). Hopefully, these two studies will answer many of the still open questions. We also agree that the data of the ACUTE-I study — although not yet published as a full paper — were somewhat disappointing because the study was simply underpowered. Unfortunately, our Editorial was submitted to the European Heart Journal before these data were presented at the meeting of the American College of Cardiology last year. Clearly, more questions were raised than answers provided by the ACUTE data. More studies are needed in order to clarify whether an approach guided by transoesophageal echocardiography is as safe as the conventional approach, whether it is necessary in all patients undergoing cardioversion and what the optimal anticoagulation scheme should be, especially in ‘short-lasting’ atrial fibrillation. Finally, the question, whether aggressive restoration and maintenance of sinus rhythm is beneficial compared to rate control and anticoagulation, is currently being investigated in two trials: the PIAF study (Pharmacological Intervention in Atrial Fibrillation), performed in Germany, and the AFFIRM trial in the U.S.. Both studies, despite many differences in study design and size, principally compare two treatment strategies: restoration and maintenance of sinus rhythm vs rate control during atrial fibrillation. The results of both studies are eagerly awaited.

INTRODUCTION:The existence of an excitable gap during ventricular fibrillation (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. METHODS AND RESULTS:Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction. Experimental infarction was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112-electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 +/- 17 msec and 37 +/- 18 msec, respectively) and chronic infarction dogs (41 +/- 14 msec and 35 +/- 14 msec, respectively) than normal dogs (32 +/- 13 msec and 30 +/- 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. CONCLUSION:During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction. These finding have implications for understanding the pathophysiology of VF and targeting antiarrhythmic therapies.

BACKGROUND Direct 3D analysis (ie, stereotaxic analysis of 3 planes) has shown that the atrioventricular (AV) node (AVN) is continuous with only specialized myocardium of the proximal AV bundle (PAVB) and distal AV bundle (DAVB) or His bundle. The purpose of the present study was to determine whether the PAVB, AVN, and DAVB possess histological features distinct from each other and from the ordinary myocardium. METHODS AND RESULTS A protocol that preserves the cytoplasmic and interstitial integrity of the tissue and permits serial sections of the AV junction region to be made in 3 orthogonal planes showed that the PAVB, AVN, and DAVB are characterized by myocardium aggregated into fascicles containing approximately 8 myofibers. Myofibers within the fascicles are coiled or spiraled about each other; and spiraling is most compact in the PAVB. Collagen encases individual fascicles and segregates primary fascicles into secondary fascicles. Fascicles, and not myofibers, are in parallel array in the PAVB, interwoven in the AVN, and parallel in the DAVB. Narrow junctions of parallel fascicles separate the AVN from the PAVB and DAVB. Myocytes, which are largest in DAVB, possess clear perinuclear regions; thin finger-like end processes, which are most numerous in the AVN; uniform, delicate cross-striations; and intercalated disks, which are broader in the PAVB and form short stacks in the AVN. Sheaves of nerve terminals are found, including boutons as in skeletal muscle [corrected]. CONCLUSIONS The PAVB, AVN, and DAVB have distinct histological features. Collagen septation of primary and secondary fascicles presents natural barriers within the tissues and to surrounding myocardium and structures. These findings confirm that the AV junction region contains a specialized conduction system that is anatomically isolated from ordinary myocardium.

Although the heterogeneity of electrophysiological properties is increased after myocardial infarction, the degree of this heterogeneity has not been well quantitated and its relationship to the histological changes that occur after infarction has not been carefully examined. The purpose of the present study was to test the hypothesis that alterations in electrophysiological properties in healing canine infarction are related to particular histological changes. Experimental infarction was produced by left anterior descending coronary ligation. Six dogs were used as controls, six were studied 5 days following, and six were studied 8 weeks following infarction. Pacing thresholds, effective refractory periods, and activation-recovery times were determined at 112 sites on the anterior left ventricle using a multiple electrode plaque. Conduction velocity, conduction-heterogeneity index--a measure of conduction disturbance--and histology of the epimyocardium underlying the plaque were assessed. The effective refractory periods and activation-recovery times were greater in both infarction groups, most prominently in the subacute group. In subacute infarction, significant postrepolarization refractoriness was present. In healed infarction, conduction velocity was decreased and the conduction-heterogeneity index was increased compared to controls and subacute infarction. Dispersion of excitability and repolarization was associated with more extensive local scarring. Dispersion of myocardial fiber angles was associated with the conduction-heterogeneity index. Some but not all of the electrophysiological changes noted in the animals with infarction were also seen in sham operated animals. Thus, heterogeneity in repolarization and refractoriness is greatest in the subacute phase of myocardial infarction and is associated with the extent of local cell death. In contrast, disturbances in conduction are greatest in healed infarction and associated with disarray of myocardial fibers.

Journal of Cardiovascular ElectrophysiologyVolume 5, Issue 3 p. 309-310 Anatomy of the AV Node Robert H. Anderson M.D., Robert H. Anderson M.D. National Heart and Lung Institute London, United KingdomSearch for more papers by this authorSiew Yen Ho Ph.D., Siew Yen Ho Ph.D. National Heart and Lung Institute London, United KingdomSearch for more papers by this author Robert H. Anderson M.D., Robert H. Anderson M.D. National Heart and Lung Institute London, United KingdomSearch for more papers by this authorSiew Yen Ho Ph.D., Siew Yen Ho Ph.D. National Heart and Lung Institute London, United KingdomSearch for more papers by this author First published: March 1994 https://doi.org/10.1111/j.1540-8167.1994.tb01166.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume5, Issue3March 1994Pages 309-310 RelatedInformation

Journal of Cardiovascular ElectrophysiologyVolume 4, Issue 5 p. 513-525 Transmission and Reentrant Activity in theSinoventricular Conducting System and in theCircumferential Lamina of the Tricuspid Valve DARLENE K. RACKER Ph.D., Corresponding Author DARLENE K. RACKER Ph.D. Physiology Department, Northwestern University Medical School, Chicago, IllinoisDarlene K. Racker, Ph.D., Physiology Department, M211, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, IL 60611. Fax: 312-503-5101.Search for more papers by this author DARLENE K. RACKER Ph.D., Corresponding Author DARLENE K. RACKER Ph.D. Physiology Department, Northwestern University Medical School, Chicago, IllinoisDarlene K. Racker, Ph.D., Physiology Department, M211, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, IL 60611. Fax: 312-503-5101.Search for more papers by this author First published: October 1993 https://doi.org/10.1111/j.1540-8167.1993.tb01240.xCitations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume4, Issue5October 1993Pages 513-525 RelatedInformation