Coronary Sinus Region Research Articles

Left-sided accessory pathways successfully ablated from the aortomitral continuity region: distinctive atrial activation patterns and anatomic concerns.

Accessory pathways (APs) successfully ablated at the aortomitral continuity (AMC) were sporadically reported but relevant data are very limited. We aimed to describe the electrophysiological characteristics of AMC-AP and the related anatomy. This study involved eight (male/female = 3/5, mean age 42.6 ± 10.5 years) patients with left-sided AP successfully ablated in the AMC region. The retrograde atrial activation sequence was analysed and compared via recordings at the His-bundle (HB), coronary sinus (CS), and roving catheter during tachycardia, and the peak of QRS from the same cardiac circle used as time reference. Of the eight patients, two received prior ablations. During tachycardia, the activation time at the proximal CS (CSp), lateral CS (CSl), and HB region averaged 120 ± 26 ms, 124 ± 29 ms, and 117 ± 21 ms following the reference, respectively (P = 0.86). The latest atrial activation was recorded in the posterior CS which averaged 135 ± 25 ms following the reference. Placing the ablation catheter to AMC via retrograde approach was attempted in all cases but stable positioning achieved in none. Via transseptal approach, the ablation catheter could be easily placed at the AMC and recorded the earliest retrograde atrial activations with 60 ± 27 ms earlier than the relatively 'earliest' CS/HB recordings, and ablation at this site successfully eliminated AP conduction. No patients had recovered AP conduction after at least 12-month follow-up. AMC-AP is featured by recording comparable retrograde atrial activation times at CSp, CSl, and HB with the latest recordings at the posterior CS. Stable placement and successful ablation in the AMC via retrograde aortic approach was difficult but can be achieved via transseptal approach.

Differentiation of Slow-Slow Form of AVNRT from AVRT through a Posteroseptal Accessory Pathway by Retrograde P-Wave Amplitude.

This study aimed to clarify whether retrograde P-wave amplitude during tachycardia can be used to differentiate slow-slow form of atrioventricular nodal reentrant tachycardia (S/S-AVNRT) from atrioventricular reentrant tachycardia through a posteroseptal accessory pathway (PS-AVRT). Sixteen patients with S/S-AVNRT and 14 patients with PS-AVRT constituted the study group. Electrocardiographic and electrophysiological parameters were compared between both the groups. HA(CS-His), which indicates the location of the earliest atrial activation site during tachycardia, was calculated as the difference of the shortest HA interval in the His bundle region and the coronary sinus region. Negative deflection of the retrograde P wave during tachycardia was significantly greater in S/S-AVNRT than in PS-AVRT in the inferior leads (lead aVF, -0.22 ± 0.04 mV vs -0.10 ± 0.07 mV; P < 0.001). Among the electrocardiographic parameters, retrograde P-wave amplitude in lead aVF had the highest diagnostic accuracy (area under the curve 0.975, sensitivity 93%, and specificity 88% for a cutoff value of -0.16 mV). HA(CS-His) was negatively greater in S/S-AVNRT than in PS-AVRT (-24 ± 13 ms vs -3 ± 18 ms; P = 0.001), and was significantly correlated with the retrograde P-wave amplitude in lead aVF (P = 0.004). Deeper negative deflection of the retrograde P wave in the inferior lead can help differentiate S/S-AVNRT from PS-AVRT.

Atrioventricular nodal block with atrioventricular nodal reentrant tachycardia ablation.

The initial model of atrioventricular nodal tachycardia (AVNRT) as a small circuit of reentry within the AV node precluded a catheter-based cure for this arrhythmia without the occurrence of AV conduction block. Landmark observations that the atria were part of the circuit of AVNRT1 and that the arrhythmia could be reset with paced beats placed at sites anatomically distant from the compact AV node2 set the stage for the present expectation of curative ablation without AV block. Despite this understanding of the AVNRT mechanism and the large accrued operator experience during the past 3 decades when ablating this arrhythmia, AV block still occurs in ≈1% to 2.3% as a complication of ablation.3 See Article p 739 In this installment of teaching rounds, Chen et al4 share with us what we can learn from a series of patients with permanent or transient AV block noted during and soon after radiofrequency energy delivery. The authors provide an honest, transparent, and instructive view of their 5 cases. The fact that we are successful ≈99% of the time without complication suggests that the present methods for maintaining safety, including monitoring junctional rhythm during ablation and relating catheter position to the fluoroscopic anatomic approximation of the AV node location are mostly successful. The student of electrophysiology must, however, be aware of how these precautions can fail us. Even closely spaced bipolar electrodes placed over the compact AV node are not able to record electrograms from the node itself. Because we cannot map the structure we need to avoid, we must estimate anatomically its location and correlate this information with our standard fluoroscopic views. ### Utility The compact AV node is located within Koch’s triangle, approximately in its mid and central position. Using the His bundle as a surrogate for the superior vertex and …

Radiofrequency catheter ablation of pulmonary vein roots results in axonal degeneration of distal epicardial nerves

BackgroundIn treatment of atrial fibrillations (AF), radiofrequency ablation (RFA) at the pulmonary vein (PV) roots isolates AF triggers in the myocardial sleeves, but also can destroy PV ganglia and branches of the intrinsic cardiac nerve plexus. AimTo determine the long-term impact of RFA at the PV roots on the structure of epicardial nerves located distally from the RFA site. MethodsFive black-faced sheep underwent epicardial RFA of the left and middle PV roots. Two to 3months after RFA, we obtained samples of epicardial nerves from remote locations of the left dorsal (LD) neural subplexus that extends along the roots of the superior PVs toward the coronary sinus (CS) and dorsal left ventricle (LV). Right atrial epicardial nerves from the right ventral (RV) neural subplexus of the ablated animals and epicardial nerves from LD neural subplexus of five additional intact sheep were used as control. Nerve morphology was examined using histochemical, immunohistochemical and transmission electron microscopy. ResultsHistochemical acetylcholinesterase staining did not reveal any epicardial nerve alterations. However, tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT) staining showed clearly the reduced numbers of TH and ChAT immunoreactive (IR) nerve fibers within epicardial nerves derived from the remote LD subplexus; control samples from all examined animals were full of evenly distributed TH-IR and ChAT-IR nerve fibers. In sharp contrast to control nerves, numerous swollen or disintegrated axons and Schwann cells with pyknotic nuclei inside unmyelinated and myelinated nerve fibers were identified by electron microscopy of ultrathin sections of epicardial nerves from the CS and LV regions in all ablated animals. ConclusionsDegeneration of remote atrial and ventricular epicardial nerves is evident 2–3months after epicardial RFA at the PV roots. Such nerves are likely to be non-functional. Therefore, long-term autonomic dysfunction is a potential risk of PV isolation by RFA.

Distinct Phases of Repetitive Activity During Atrial Fibrillation in Sheep Atria: High Density Mapping Study

Introduction: Mapping and temporal evolution of atrial fibrillation (AF) remains poorly understood. We aimed to characterise wavefront propagation during AF in an ovine hypertensive model. Methods: Electrical activity during induced AF on the epicardial surface of the left (LA) and right (RA) atria was recorded in vivo using rectangular meshes of electrodes in 11 sheep with an established model of hypertension (1K1C). Trajectory of the wave propagation was reconstructed and used to classify each distinct propagation event. Periods of activity with repetitive wave trajectory were defined as phases of arrhythmia. Results: 9241 distinct activation events in total were analysed. LA had greater than RA ratio of centrifugal activations (41% vs. 0.005%) and wave collisions (7.6% vs. 0.01%). RA had greater ratio of passing waves (88% vs. 51%), rotating waves (0.01% vs. 0%), total conduction blocks (0.001% vs. 0%) and waves circumventing conduction block (0.08% vs. 0%). With relation to anatomical characteristics, 15 distinct phase types were identified in each atria. The most frequent transition in RA was a transition between reentrant phase and phase of waves coming from coronary sinus region (CS) (21%). In LA, the most frequent transitions were between phase of waves train coming from Bachman-Bundle (BB) and phase of interaction between waves coming from BB and CS direction (12%). Conclusion: High density mapping of wavefront trajectory during AF provides new insights into arrhythmia dynamics. The most frequent transition between phases of AF in ovine sheep model is transition in RA between reentrant activity and wave train coming from CS. It points to an important interaction between CS and reentrant activity which may have important implications in AF mapping and treatment.

Abstract 5286: Human AV Junctional Pacemaker Shift Due to Cholinergic and Adrenergic Stimulations: Optical Imaging with a Novel Long Wavelength Voltage-Sensitive Dye

It is well known that under different physiological and pathologic conditions, the atrioventricular junction (AVJ) may become the pacemaker of the heart. However, unlike the well-characterized AVJ pacemaker in animal models, autonomic control of the human AVJ pacemaker has not been studied. Explanted human hearts with different types of cardiomyopathy (n=7) were obtained at the time of cardiac transplantation and perfused with cardioplegic solution. The AVJ was cannulated, isolated from the rest of the heart, immobilized with the excitation-contraction uncoupler blebbistatin (10 μmol/L) and optically mapped using the infrared voltage sensitive dye di-ANBDQBS. Imaging was conducted with 100x100 CMOS camera from endocardial field of view ranging 24x24 to 36x36mm 2 , which allowed to simultaneously map right side of intratrial and intraventricular septa, coronary sinus (CS) and His bundle regions. In control, we found AVJ rhythm of 31+/−15 bpm (2409+/−1264 ms) in all human preparations which originated in compact AV node (N-region, n=4) and/or region between AV node and His bundle (NH-region, n=3). Isoproternol (Iso, 1 μM) induced AVJ rhythm acceleration up to 68+/−12 bpm (913+/−192 ms), temporary pacemaker shift to CS region (n=2) and improved conduction in both slow and fast pathways, which induced reentrant arrhythmias in 3/5 preparations. Acetylcholine (ACh, 1–3 μM) slowed rhythm to 21+/−6 bpm (3130+/−1146 ms) and conduction in both pathways up to complete block, and induced temporary pacemaker shift to CS region in 3/4 preparations. Moreover, we found bifocal activation in 3/4 preparation when two main pacemakers (CS and compact AV node) worked asynchronously with different frequencies, accompanied by the exit block from AV node. We showed by high-resolution optical mapping for the first time that unlike in animal models (rabbit and rat) in isolated coronary perfused human AVJ leading pacemaker localized mostly in the N- or NH-regions. Beta-adrenergic (Iso) and cholinergic (ACh) stimulations of AVJ can significantly accelerate or slow rhythm and conduction, as well as induced pacemaker shift to CS, and result in reentrant arrhythmias. This research has received full or partial funding support from the American Heart Association, AHA Midwest Affiliate (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, South Dakota &amp; Wisconsin).

Impact of Catheter Ablation of the Coronary Sinus on Paroxysmal or Persistent Atrial Fibrillation

This study evaluated the impact of catheter ablation of the coronary sinus (CS) region during paroxysmal and persistent atrial fibrillation (AF). The CS musculature and connections have been implicated in the genesis of atrial arrhythmias. Forty-five patients undergoing catheter ablation of AF were studied. The CS was targeted if AF persisted after ablation of pulmonary veins and selected left atrial tissue. CS ablation was commenced endocardially by dragging along the inferior paramitral left atrium. Ablation was continued from within the vessel (epicardial) if CS electrograms had cycle lengths shorter than that of the left atrial appendage. RF energy was limited to 35 W endocardially and 25 W epicardially. The impact of ablation was evaluated on CS electrogram cycle length (CSCL) and activation sequence, atrial fibrillatory cycle length measured in the left atrial appendage (AFCL) and on perpetuation of AF. Endocardial ablation significantly prolonged CSCL by 17 +/- 5 msec and organized the CS activation sequence (from 13% of patients before to 51% after ablation); subsequent epicardial ablation further increased local CSCL by 32 +/- 27 msec (P < 0.001). AFCL prolonged significantly both during endocardial and epicardial ablation (median: 152 to 167 msec P = 0.03) and was associated with AF termination in 16 (35%) patients (46% of paroxysmal and 30% of persistent AF). AFCL prolongation > or =5 msec and/or AF termination was associated with more rapid activity in the CS region originally: P < or = 0.04. Catheter ablation targeting both the endocardial and epicardial aspects of the CS region significantly prolongs fibrillatory cycle length and terminates AF persisting after PV isolation in 35% of patients.

Coronary Sinus and Fossa Ovalis Ablation: Effect on Interatrial Conduction and Atrial Fibrillation

Interatrial conduction occurs via discrete pathways along the coronary sinus musculature, fossa ovalis region, and Bachman's bundle. We assessed the feasibility of altering interatrial conduction by selectively ablating two of these conduction pathways using a novel mesh electrode ablation catheter. Circular radiofrequency energy catheter ablation lesions were created in the proximal coronary sinus in four dogs and in both the fossa ovalis and the proximal coronary sinus regions in seven pigs. Interatrial conduction was assessed by analyzing intracardiac electrogram and noncontact isopotential mapping data. Inducibility of atrial fibrillation was assessed before and after ablation (in six pigs). Ablation lesions in the proximal coronary sinus eliminated interatrial conduction along the coronary sinus musculature in four dogs and five of seven pigs. Ablation lesions in the fossa ovalis region eliminated interatrial conduction via midseptal pathways in six of seven pigs. Atrial fibrillation, inducible in five of seven pigs at baseline, was rendered noninducible in all five. There was no adverse effect on AV nodal conduction. (1) Using a novel mesh electrode ablation catheter, we were able to ablate interatrial conduction pathways along the proximal coronary sinus and fossa ovalis regions. (2) This altered interatrial conduction and altered atrial fibrillation inducibility and maintenance. (3) Catheter ablation of interatrial conduction pathways may be useful in the therapy of atrial fibrillation.

Localized Sources Maintaining Atrial Fibrillation Organized by Prior Ablation

Endocardial mapping of localized sources driving atrial fibrillation (AF) in humans has not been reported. Fifty patients with AF organized by prior pulmonary vein and linear ablation were studied. AF was considered organized if mapping during AF showed irregular but discrete atrial complexes exhibiting consistent activation sequences for >75% of the time using a 20-pole catheter with 5 radiating spines covering 3.5-cm diameter or sequential conventional mapping. A site or region centrifugally activating the remaining atrial tissue defined a source. During AF with a cycle length of 211+/-32 ms, activation mapping identified 1 to 3 sources at the origin of atrial wavefronts in 38 patients (76%) predominantly in the left atrium, including the coronary sinus region. Electrograms at the earliest area varied from discrete centrifugal activation to an activity spanning 75% to 100% of the cycle length in 42% of cases, the latter indicating complex local conduction or a reentrant circuit. A gradient of cycle length (>20 ms) to the surrounding atrium was observed in 28%. Local radiofrequency ablation prolonged AF cycle length by 28+/-22 ms and either terminated AF or changed activation sequence to another organized rhythm. In 4 patients, the driving source was isolated, surrounded by the atrium in sinus rhythm, and still firing at high frequency (228+/-31 ms) either permanently or in bursts. AF associated with consistent atrial activation sequences after prior ablation emanates mostly from localized sources that can be mapped and ablated. Some sources harbor electrograms suggesting the presence of localized reentry.

Region-specific, pacing-induced changes in repolarization in rabbit atrium: An example of sensitivity to the rare

In subsets of patients paroxysmal firing of ectopic foci in pulmonary veins or coronary sinus is an important cause of atrial fibrillation. This appears to represent a rare event overriding a dominant sinus mechanism to alter the rhythmic firing of the atrium. Hence, we tested the hypothesis that a rare stimulation pattern might alter the myocardial substrate, making it more susceptible to the initiation of arrhythmias. In isolated right and left rabbit atria, a "rare" burst pacing protocol (BPP) was applied as follows: over 3 h, preparations were driven for 4.5 min from sinus node (SN) or Bachmann's bundle (BB) regions at cycle length (CL)=400 ms followed by 30 s of stimulation from coronary sinus (CS) or pulmonary vein (PV) at CL=200 ms. Microelectrodes were used to record action potentials at the end of 4.5 min of pacing at CL=400 ms. We then intervened with 5-min bigeminal pacing to probe atrial vulnerability to arrhythmias: S1 was delivered from SN or BB and S2 from CS or PV, respectively. S1-S2 interval was the shortest eliciting a propagated response. BPP shortened repolarization in CS and PV regions but not in SN or BB, resulting in increased dispersion of repolarization in right and decreased in left atria. Propranolol, atropine and losartan failed to alter the decrease in repolarization induced by BPP whereas apamin, nifedipine and ryanodine prevented BPP effects. Before BPP, bigeminy did not induce arrhythmias in either atrium, but after BPP, bigeminy significantly increased the incidence of arrhythmias in the right atrium. BPP from foci outside the regions of dominant activation alters dispersion of atrial repolarization. Modulation of apamin-sensitive channels may contribute to the shortening of repolarization in CS and PV regions. Alterations of atrial repolarization gradient create an arrhythmogenic substrate and may be an early step in atrial electrophysiologic remodeling.

Coronary Sinus Recordings of Double Potentials Associated with Retrograde Conduction Through Left Atrioventricular Accessory Pathways

In some patients with left AV accessory pathway (AP), double potentials are recorded along the coronary sinus (CS) during retrograde AP conduction only. This electrophysiologic study was performed to clarify the origin and clinical significance of double potentials in 11 patients. The direction of activation of the first, relatively blunt component (DP1) was lateral to septal in 5 patients with anterior or anterolateral AP, centrifugal in 2 patients with posterior or posterolateral AP, and septal to lateral in 4 patients with posteroseptal AP, suggesting the earliest activation of DP1 was near the AP. The direction of activation of the second, sharper potentials (DP2) were septal to lateral in all patients. The double potentials were fused in the paraseptal CS region. Pacing from the lateral CS musculature or lateral left atrium reproduced the double potentials. The effective refractory period of the double potentials was reached by ventricular extrastimulation, and the left atrial deflection preceded the double potentials, excluding a ventricular or AP origin. In patients with connections between the paraseptal CS musculature and left atrium but no connections more laterally, retrograde left AP conduction is associated with double potentials in the CS recordings. The double potentials represent activation of the left atrial insertion of the AP (DP1) and later activation of the CS musculature (DP2) via connections between the paraseptal CS musculature and left atrium, respectively. The activation pattern of DP1 depends on AP location, thus providing important information for AP localization during CS mapping.

Localization of the Initial Fibrillatory Cycle in Patients with Paroxysmal Atrial Fibrillation

Background - Recent reports suggest the presence of conduction delay in the posterior septal region during sinus rhythm in patients with lone paroxysmal atrial fibrillation (AF). Objective - To explore the location of intra-atrial conduction delay associated with initiation of AF. Design - In 8 lone AF patients (51 - 10 years), 20 AF paroxysms were induced during electrophysiological examination. Bipolar electrograms were acquired from a 10-polar catheter in the coronary sinus (CS), a 4-polar His bundle catheter, and a 20-polar Halo catheter in the right atrium. Results - Induced AF paroxysms showed earliest registered atrial activity in interatrial septum (IAS) or proximal CS in 17 cases (85%). Conduction delay at the posterior IAS or proximal CS accompanied induction of 18 AF paroxysms (6 patients). Atrial activation sequence at the beginning of the AF paroxysms was stable and reproducible in six repeatedly induced AF episodes (3 patients). Conclusion - In lone AF patients, induction of AF is associated with conduction disturbances in the IAS and proximal CS regions.

Progressive anterior ablation in the coronary sinus region: evidence to support the presence of a 'slow pathway' input in normal patients?

AV node modification is an emerging approach to rate control in patients with medically refractory atrial fibrillation. The mechanism of benefit of this procedure is not completely understood. Twenty-two patients (age, 65+/-11 years; 16 women) with medically refractory paroxysmal atrial fibrillation referred for complete AV node ablation underwent serial ablations beginning at the level of the coronary sinus os progressing in a superior and anterior direction toward the His bundle. Serial atrial extrastimulus testing was performed to determine the effect of the progressive posteroseptal ablation in the region of the coronary sinus on the AV node antegrade refractory curve. Two of 22 patients had antegrade dual AV node pathways before ablation. Three patterns of response to serial ablation were noted. In 10 patients (45%), loss of the terminal portion of the AV node antegrade refractory curve occurred without evidence of fast pathway injury. In 7 patients (32%) the curve was shifted upward and to the left, consistent with nonspecific AV node damage. In 5 patients (23%), no effect could be attained before induction of complete AV block at superior and anterior ablation sites. Clinical variables and site of ablation did not predict response to serial ablations. These data suggest that the mechanism of benefit of AV node modification in this population may be through elimination of "slow pathway" tissue in half of patients and nonspecific injury in the remainder. Modification without complete AV block may not be possible in a minority of patients, as the response to progressive ablation appears to be "all or none" conduction.

Arterial Supply of the Region of the Coronary Sinus in Man

Patterns of arterial supply to the atria were studied with respect to the coronary sinus region in 60 human hearts obtained from patients with a negative cardiac history and in 2 hearts with ECG-demonstrated coronary sinus rhythm. The atria, including the interatrial septum, were supplied by the right (40%) or left (30%) or both (30%) sinuatrial arteries which, however, did not reach as far as the posterior margin of the oval fossa and the coronary sinus. The region of the coronary sinus with the Eustachian ridge received direct branches from the trunk of the right (41%) or left (11%) coronary artery or both (48%) in the adjacent part of the coronary sulcus. Possible development of the 'coronary sinus rhythm' on the basis of multifocal damage of the sinuatrial arteries is discussed.

Does A-H interval accurately represent intranodal conduction time during ectopic rhythms?

In order to determine whether the A-H interval of the His bundle electrogram accurately represents the AV nodal conduction time under various conditions, His bundle and coronary sinus electrograms were recorded in isolated perfused rabbit hearts, with atrial stimulation from eight different sites. The S-A (stimulus to the A wave) interval was significantly longer, whereas the A-H interval was shorter on stimulations from the coronary sinus and the left atrium than on sinus nodal stimulation. Stimulations from the fossa ovalis and right atrial appendage did not significantly alter the A-H interval. The effective and functional refractory periods of the AV node were almost identical with stimulations from the sinus node, low right atrial appendage, low left atrial appendage or the ostium of coronary sinus. Mapping of the excitation process with microelectrodes revealed that the activation times in low interatrial septal fibers bordering the His bundle [abbreviated as AP(III)] was closest to the A wave as compared with the activation in the ostium of the coronary sinus [AP(I)] or near the AN region [AP(II)] on stimulation from both sinus nodal and coronary sinus regions. On sinus nodal stimulation, AP(III) preceded AP(I) and AP(II) but lagged behind the A wave by 6 msec, whereas AP(III) preceded the A wave by 5 msec on coronary sinus stimulation. Thus, the A-H interval may not always accurately represent the intranodal conduction time, as relative timing of atrial activation responsible for the A wave and that of invasion of the AV node by the atrial wavefront can be grossly altered by different atrial excitation patterns.

Function of atrial preferential conduction routes under normal and abnormal conditions

The function of the atrial preferential conduction routes was examined by the microelectrode technique under normal and abnormal conditions in excised rabbit hearts. The sinus impulse during normal conditions traveled faster along the left and the right branch of the crista terminalis (anterior and posterior preferential routes, respectively) in the atrium toward the A-V node. Cutting of either route caused a delay of the impulse arrival in the zone beyond the lesion. The internodal conduction time was delayed 12 msec upon cutting of the posterior route, but there was no conduction delay after cutting the anterior route. This indicates that the posterior path is the dominant conduction route under normal conditions. When both routes were cut, the internodal conduction time was delayed 33 msec from the control value. During abnormal conditions, an ectopic pacemaker was found to occur mainly in the regions of two routes, as well as in the coronary sinus region. The cutting of either route, combined with the application of acetylcholine or high external K+, resulted in easier provocation of re-entrant arrhythmias in response to premature-stimuli than before the cutting.

Coronary sinus rhythm in sinus venosus defect and persistent left superior vena cava

The frontal P wave axis was +15 ° or less (inverted P wave in lead III) in 8 of 10 patients with secundum atrial septal defect of the sinus venosus type or with left superior vena cava. A similar leftward P wave axis was present in 14 of 20 patients with left superior vena cava associated with other congenital heart lesions but was present in only 3 of 62 patients with uncomplicated atrial septal defect and in only 20 of 150 unselected children. The leftward P waves are thought to arise from an accessory pacemaker in the coronary sinus region of the A-V node, persisting from embryonic life when the left superior vena cava persists, or assuming pacemaker function when the S-A node is deficient in association with sinus venosus defect or is damaged by surgery. The association of sinus venosus defect with left superior vena cava is pointed out.