Mark A. McGuire

Atrioventricular Junctional Tissue Discrepancy Between Histological and Electrophysiological Characteristics

BACKGROUNDnPrevious work has demonstrated that cells with AV nodal-type action potentials are not confined to Kochs triangle but may extend along the AV orifices. The aim of this study was to examine the histological and electrophysiological characteristics of this tissue.nnnMETHODS AND RESULTSnStudies were performed in isolated, blood-perfused dog and pig hearts. Microelectrode recordings revealed cells with nodal-type action potentials around the tricuspid and mitral valve rings. These cells were found within 1 to 2 mm of the valve annuli. A zone of cells with intermediate action potentials, approximately 1 cm wide, separated cells with nodal-type action potentials from cells with atrial-type action potentials in the body of the atria. In cells with nodal-type action potentials, adenosine caused a reduction in action potential amplitude (49 +/- 2 versus 33 +/- 2 mV, mean +/- SE; P < .001), upstroke velocity (2.5 +/- 0.2 versus 2.0 +/- 0.2 V/s, P < .05), and duration (150 +/- 4 versus 96 +/- 8 ms, P < .001). The light microscopic appearance of AV junctional cells was similar to that of myocytes in the body of the atrium. A polyclonal antibody raised against connexin-43 bound to atrial and ventricular tissue but not to the AV junctional tissue or AV nodal region. The absence of connexin-43 correlated with the sites of cells with nodal-like action potentials. With pacing techniques, the AV junctional tissue in the region of the posterior AV nodal approaches could be electrically dissociated from atrial, AV nodal, and ventricular tissue. AV nodal echoes were induced with ventricular pacing in three dog hearts. In each case, retrograde conduction was through the slow pathway, and anterograde conduction was through the fast pathway. During echoes, activation of AV junctional cells preceded atrial activation during retrograde slow pathway conduction, but these cells were not activated during anterograde fast pathway conduction.nnnCONCLUSIONSnAV junctional cells around both annuli are histologically similar to atrial cells but resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin-43. The light microscopic appearance of AV junctional cells is a poor guide to their action potential characteristics. The AV junctional cells in the posterior AV nodal approaches appear to participate in slow pathway conduction. These cells may be the substrate of the slow AV nodal pathway.

Routine programmed electrical stimulation in survivors of acute myocardial infarction for prediction of spontaneous ventricular tachyarrhythmias during follow-up: Results, optimal stimulation protocol and cost-effective screening

Of 3,286 consecutive patients treated for acute myocardial infarction, electrophysiologic testing was performed in 1,209 survivors (37%) free of significant complications at the time of hospital discharge to determine their risk of spontaneous ventricular tachyarrhythmias during follow-up. Sustained monomorphic ventricular tachycardia was inducible by programmed electrical stimulation in 75 (6.2%). Antiarrhythmic therapy was not routinely prescribed regardless of the test results. During the 1st year of follow-up, 14 infarct survivors (19%) with inducible ventricular tachycardia experienced spontaneous ventricular tachycardia or fibrillation in the absence of new ischemia compared with 34 (2.9%) of those without inducible ventricular tachycardia (p less than 0.0005). During the extended follow-up period (median 28 months) of those with inducible ventricular tachycardia, 19 (25%) had a spontaneous electrical event; 37% of these first events were fatal. These results suggest that the most cost-effective strategy for predicting arrhythmia will be obtained by restricting electrophysiologic testing to infarct survivors whose left ventricular ejection fraction is less than 40% and using a stimulation protocol containing four extrastimuli. Electrophysiologic testing is the single best predictor of spontaneous ventricular tachyarrhythmias during follow-up in infarct survivors. The majority (94%) with a negative test benefit from the more reliable reassurance that all is well, whereas the 25% risk of electrical events in those with inducible ventricular tachycardia justifies a prospective trial of effective prophylactic antiarrhythmic interventions.

High resolution mapping of Koch's triangle using sixty electrodes in humans with atrioventricular junctional (AV nodal) reentrant tachycardia.

BACKGROUNDnRecent evidence suggests that atrioventricular junctional reentrant tachycardia (AVJRT) uses a reentrant circuit that involves the atrioventricular (AV) node, the atrionodal connections, and perinodal atrial tissue. Electrogram morphology has been used to target the delivery of radiofrequency energy to the site of the slow pathway, a component of this reentrant circuit. The aim of this study was to localize precisely the sites of atrionodal connections involved in AVJRT and to examine atrial electrogram morphologies and their spatial distribution over Kochs triangle.nnnMETHODS AND RESULTSnElectrical activation of Kochs triangle and the proximal coronary sinus was examined in 13 patients using a 60-point plaque electrode and computerized mapping system. Recordings were made during sinus rhythm (n = 12), left atrial pacing (n = 8), ventricular pacing (n = 12), and AVJRT (n = 12). During sinus rhythm electrical activation approached Kochs triangle and the AV node from the direction of the anterior limbus, activating the anterior part of the triangle before the posterior part. A zone of slow conduction during sinus rhythm was found within Kochs triangle in 64% of patients. The pattern of atrial activation in Kochs triangle during anterograde fast pathway conduction was similar to that seen during anterograde slow pathway conduction. Retrograde fast pathway conduction during ventricular pacing and during anterior (typical) AVJRT caused earliest atrial activation at the apex of Kochs triangle near the AV node-His bundle junction. In individual patients the site of earliest atrial activation was similar for both anterior AVJRT and retrograde fast pathway conduction during ventricular pacing. Retrograde slow pathway conduction during ventricular pacing and during posterior (uncommon or atypical) AVJRT caused earliest atrial activation posterior to the AV node near the orifice of the coronary sinus. This posterior or slow pathway exit site was 15 +/- 4 mm from the His bundle. In individual patients the site of earliest atrial activation was similar for both posterior AVJRT and retrograde slow pathway conduction during ventricular pacing. In one patient anterograde and retrograde conduction occurred via separate slow pathways during AVJRT: Complex atrial electrograms with two or more components were observed near the coronary sinus orifice and in the posterior part of Kochs triangle in all cases. These were categorized as either low or high frequency potentials according to the rapidity of the second component of the electrogram. Low frequency potentials were present at the site of earliest atrial excitation during retrograde slow pathway conduction in 5 of 5 cases (100%) and high frequency potentials in 4 of 5 cases (80%). However, both slow and high frequency potentials could be found at sites up to 16 mm from the site of earliest atrial excitation.nnnCONCLUSIONSnAt least two distinct groups of atrionodal connections exist. The site of earliest atrial activation during anterior AVJRT is similar to that of fast pathway conduction during ventricular pacing. This site is close to the His bundle-AV node junction. The site of earliest atrial activation during posterior AVJRT is similar to that of slow pathway conduction during ventricular pacing. This site is near the coronary sinus orifice, approximately 15 mm from the His bundle. The anterograde slow pathway appears to be different from the retrograde slow pathway in some patients. Double atrial electrograms are an imprecise guide to the site of earliest atrial excitation during retrograde slow pathway conduction.

Origin and significance of double potentials near the atrioventricular node. Correlation of extracellular potentials, intracellular potentials, and histology.

BACKGROUNDnAtrioventricular junctional (AV nodal) reentrant tachycardia can be cured by catheter ablation of the slow pathway, which is part of the reentrant circuit. Previous work has suggested that extracellular double potentials may help identify the site of the slow pathway, but the origin and significance of these potentials are controversial. The aim of this study was to identify the source of these potentials.nnnMETHODS AND RESULTSnStudies were performed in isolated, blood-perfused porcine (n = 8) and canine (n = 4) hearts. Several methods were used to identify the origin of potentials: microelectrode recording, extracellular mapping, pacing from multiple sites, and light microscopy. Two types of double potentials, similar to those found in humans, were found in all hearts. LH potentials consisted of a low-frequency deflection followed by a high-frequency deflection during sinus rhythm or anterior septal pacing. HL potentials consisted of a high-frequency deflection followed by a low-frequency deflection. LH potentials were found close to the coronary sinus orifice. They were caused by asynchronous activation of the sinus septum and the region between the coronary sinus orifice and tricuspid annulus. HL double potentials were found along the tricuspid annulus. They were caused by asynchronous activation of two cell layers. The high-frequency component was caused by depolarization of atrial-type cells in the deep subendocardial layer. The low-frequency component was caused by depolarization of cells with nodal characteristics close to the endocardium. These cells were present around the entire tricuspid annulus, were not part of the compact AV node, and could be dissociated from the bulk of the atria by rapid atrial pacing.nnnCONCLUSIONSnLH potentials are caused by asynchronous activation of muscle bundles above and below the coronary sinus orifice. Their proximity to the site of the slow pathway is probably serendipity. HL double potentials are caused by asynchronous activation of atrial cells and a band of nodal-type cells close to the tricuspid annulus. The band of nodal-type cells is not part of the compact AV node and may represent the substrate of the slow AV nodal pathway.

Patients with two types of atrioventricular junctional (AV nodal) reentrant tachycardia. Evidence that a common pathway of nodal tissue is not present above the reentrant circuit.

BackgroundThe site of the reentrant circuit in atrioventricular (AV) junctional reentrant tachycardia has not been defined; in particular, the existence of a common pathway ofAV nodal tissue above the reentrant circuit is controversial. Methods and ResultsTwo types of AVjunctional reentrant tachycardia were induced in each of three patients at electrophysiological study. In one type of tachycardia (anterior), the onset of atrial activity occurred from 0 to 12 msec before the onset of ventricular activation, and earliest atrial activity was recorded near the His bundle. In the second type of tachycardia (posterior), the ventriculoatrial intervals were longer (76-168 msec), and earliest atrial activity was recorded near the mouth of the coronary sinus. In individual patients, the two types of tachycardia had different cycle lengths. Posterior AV junctional reentrant tachycardia was not a fast-slow form ofAVjunctional reentry in at least two of the three patients. Surgical cure was attempted in two patients. In one patient, anterior AV junctional reentrant tachycardia was abolished by dissection of the anterior perinodal atrium, but posterior AVjunctional reentrant tachycardia could still be induced. At reoperation 4 months later, dissection of the posterior perinodal atrium abolished posterior AVjunctional reentrant tachycardia while preserving AV conduction. ConclusionsDifferences in ventriculoatrial intervals and cycle lengths and the results of selective surgery suggest that the two types of AV junctional reentrant tachycardia used different reentrant circuits. These observations imply that a common pathway of AV nodal tissue is not present above the reentrant circuit and suggest that perinodal atrium is part of these circuits.

AV nodal reentry: Part II: AV nodal, AV junctional, or atrionodal reentry?

AV Nodal Reentry. The classical model of “atrioventricular (AV) nodal” reentrant tachycardia suggests that the reentrant circuit is entirely within the compact AV node and that AVnodal tissue is present proximal and distal to the circuit. Recent evidence from mapping studiesand from examination of the effects of curative procedures, however, suggests that the upperend of the circuit uses perinodal atrial or transitional tissue. Moreover, the anatomical suhstrate of dual “AV nodal” pathways is likely to be the multiple connections between compactAV node and atrium rather than discrete intranodal pathways. The antegrade slow pathwayappears to he situated at the posteroinferior approaches to the AV node in the region betweenthe coronary sinus orifice and the tricuspid annulus, The retrograde fast pathway appears lobe situated in the anterior atrionodal connections at the apex of Kochs triangle, close tothe His bundle. The lower turnaround point of the circuit is likely to be within the AV node.

Does the induction of ventricular flutter or fibrillation at electrophysiologic testing after myocardial infarction have any prognostic significance

This study examines the significance of inducing sustained ventricular fibrillation (VF) or ventricular flutter by programmed stimulation after infarction. Programmed ventricular stimulation was performed for prognostic reasons from the right ventricular apex at twice diastolic threshold using a protocol containing 4 extrastimuli. Of 502 patients tested 11 +/- 4 days after acute infarction, VF was induced in 164 (33%), ventricular flutter in 134 (27%), ventricular tachycardia (VT) in 44 (9%), and no arrhythmia in 160 (32%). All groups were similar in age, sex distribution, and sites of index infarction. Those with inducible VT had a higher incidence of multiple infarctions and a lower mean left ventricular ejection fraction at the time of testing. Without antiarrhythmic drug therapy, 8 patients (18%) with inducible VT experienced spontaneous VT or died instantaneously during the first year of follow-up. By contrast, only 1 (0.6%) patient with inducible VF, 1 (0.7%) with ventricular flutter, and 1 (0.6%) without any inducible arrhythmias experienced similar events in the same period (p < 0.001). By relating the cycle length of the induced monomorphic arrhythmia to later spontaneous electrical events, induced arrhythmias with cycle length as low as 230 ms still identified patients at high risk for spontaneous arrhythmias. Only the induction of sustained monomorphic VT with a cycle length > 230 ms indicates patients with ventricular electrical instability after infarction. The induction of VF or ventricular flutter is a negative test result with no adverse long-term prognostic significance.

Dimensions of the Triangle of Koch in Humans

Abstract The atrioventricular (AV) node is situated in the lower atrial septum at the apex of a triangle described by Koch.1 The sides of Kochs triangle are formed by the tendon of Todaro and the tricuspid annulus. The base is marked by the coronary sinus orifice (Figure 1). At the apex of the triangle the AV node penetrates the central fibrous body to become the His bundle. Increasing interest is now focused on this region because several techniques have been developed for the cure of supraventricular arrhythmias arising near the AV node.2–4 Both surgical and catheter ablation techniques make use of the anatomic landmarks of Kochs triangle.2–4 The aim of the current study was to define the size and variability of Kochs triangle in the human.

Dimensions of the human posterior septal space and coronary sinus

Accurate anatomic localization of accessory pathways during preoperative electrophysiologic study and during operative mapping depends on a knowledge of the dimensions of the posterior septal space and the left free wall. These dimensions were therefore studied in 48 human cadaver hearts. Mean distance from the coronary sinus orifice to the left margin of the posterior septal space was 2.3 +/- 0.4 cm and mean length of the left free wall was 5.0 +/- 1.0 cm. The posterior septal space at the level of the valve anuli extended a mean of 3.4 +/- 0.5 cm around the epicardium. The width of the posterior septum measured in the coronary sinus was related to heart weight and a combination of body weight and patient age (p less than 0.05). The probability of an accessory pathway being located in the left free wall or the posterior septum during catheter mapping was calculated for various distances from the coronary sinus orifice for adults of different ages and body weights. In adults, accessory pathways located in the proximal 1.5 cm of the coronary sinus are almost always in the posterior septum. Those located between 1.5 and 3 cm from the coronary sinus orifice may be in either the left free wall or the posterior septum, and those located greater than 3 cm from the coronary sinus orifice are almost invariably in the left free wall.

Electrophysiologic and histologic effects of dissection of the connections between the atrium and posterior part of the atrioventricular node

OBJECTIVESnThis study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) node.nnnBACKGROUNDnSurgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia. Some of these destroy the posterior approaches to the AV node.nnnMETHODSnAtrioventricular node function and electrical excitation of Kochs triangle and the proximal coronary sinus were examined in 18 dogs. Dissection of the posterior atrionodal connections was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, repeat electrophysiologic and mapping studies were performed to assess changes in AV node function and the routes of AV and ventriculoatrial (VA) conduction. The AV junction was then examined with light microscopy.nnnRESULTSnThe compact AV node was undamaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atrionodal connections lying between the coronary sinus orifice and the tricuspid annulus were replaced by scar tissue in all cases, but the left-sided posterior connections and the anterior connections remained intact. Atrioventricular and VA conduction intervals and refractory periods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterior (slow pathway) retrograde exists from the AV node were present in seven dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that the site of exit from the AV node was more leftward than it had been preoperatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway potentials were found in all dogs.nnnCONCLUSIONSnThis procedure ablates the posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is not denervated. The mechanism of cure of AV junctional reentrant tachycardia is probably damage to the perinodal atrium. This suggests that part of the slow AV node pathway may lie outside the compact AV node. Dual AV node exits and double atrial electrograms are present in the normal canine heart.