Catheter ablation of cardiac autonomic nerves for prevention of vagal atrial fibrillation.
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BACKGROUND: Vagal stimulation shortens the atrial effective refractory period (AERP) and maintains atrial fibrillation (AF). This study investigated whether the parasympathetic pathways that innervate the atria can be identified and ablated by use of transvenous catheter stimulation and radiofrequency current catheter ablation (RFCA) techniques. METHODS AND RESULTS: In 11 dogs, AERPs were determined at 7 atrial sites during bilateral cervical vagal nerve stimulation (VNS) and electrical stimulation of the third fat pad (20 Hz) in the right pulmonary artery (RPA). VNS shortened the AERP at all sites (from 123+/-4 to 39+/-4 ms, P<0.001) and increased the covariance of AERP (COV-AERP) (from 9+/-3% to 27+/-13%, P<0.001). RPA stimulation shortened the AERP at all sites from 123+/-4 to 66+/-13 ms (P<0.001) and increased the COV-AERP from 9+/-3% to 30+/-12% (P<0.001). In 7 dogs, transvascular RFCA of the parasympathetic pathways along the RPA was performed, and in 3 dogs, additional RFCA of parasympathetic fibers along the inferior (n=2) or superior (n=1) vena cava was performed. RFCA blunted the AERP shortening at all sites during VNS (114+/-4 ms after RFCA), abolished the increase of COV-AERP during VNS (12+/-7% after RFCA), and led to an increase of the baseline AERP (123+/-4 ms before versus 127+/-3 ms after RFCA, P=0.002). Before RFCA, AF could be induced and maintained as long as VNS was continued, whereas after RFCA, AF was no longer inducible during VNS. CONCLUSIONS: -Transvascular atrial parasympathetic nerve system modification by RFCA abolishes vagally mediated AF. This antifibrillatory procedure may provide a foundation for investigating the usefulness of neural ablation in chronic animal models of AF and eventually in patients with AF and high vagal tone. (+info)
Cryothermal ablation of the slow pathway for the elimination of atrioventricular nodal reentrant tachycardia.
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BACKGROUND: We report the first successful slow pathway ablation using a novel catheter-based cryothermal technology for the elimination of atrioventricular nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Eighteen patients with typical AVNRT underwent cryoablation. Reversible loss of slow pathway (SP) conduction during cryothermy (ice mapping) was demonstrated in 11 of 12 patients. Because of time constraints, only 2 sites were ice mapped in 1 patient. Seventeen of 18 patients had successful cryoablation of the SP. One patient had successful ice mapping of the SP, but inability to cool beyond -38 degrees C prevented successful cryoablation. A single radiofrequency lesion at this site eliminated SP conduction. No patient has had recurrent AVNRT over 4.9+/-1.7 months of follow-up. During cryoablation, accelerated junctional tachycardia was not seen and was therefore not available to guide lesion delivery. Adherence of the catheter tip during cryothermy (cryoadherence) allowed atrial pacing to test for SP conduction. Cryoablation in the anterior septum produced inadvertent transient PR prolongation consistent with loss of fast pathway conduction in 1 patient and transient (6.5 seconds) 2:1 AV block in another. On rewarming, the PR interval returned to normal, and the AV nodal effective refractory period was unchanged in both. Accelerated junctional tachycardia was seen on rewarming in both but not during cryothermy. CONCLUSIONS: Cryothermal ablation of the SP was achieved in patients with this novel technique. Successful ice mapping of both the SP and fast pathway was demonstrated. The ability to test the functionality of specific ablation sites before production of a permanent lesion may eliminate inadvertent AV block. (+info)
Premonitory sign of heart block in acute posterior myocardial infarction.
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The appearance of the ARS complex in leads V3R and V4R was analysed in a series of 94 patients with acute posterior myocardial infarction. The cases of posterior myocardial infarction with direct signs of injury (ST segment elevation with a rise of 0.5 mm or more of point F and/or QS pattern) in leads V3R and/or V4R were complicated three times as often by atrioventricular block as those in which such signs were absent (66% and 22%, respectively; P smaller than 0.001). When one of these signs was present in leads V3R and/or V4R, the disorder of conduction was "severe" (complete atrioventricular block or sinotrial block with pauses) in half the cases and "unstable" (bradycardia below 50 beats/min; ventricular pause with or without syncope; widening of QRS complex; ventricular hyperexcitability) in one-third, justifying the introduction of a stimulating catheter. Such disorders were found, respectively, only 1 in 7 (14%), and less than 1 in 10 (8%) when these signs were absent (P smaller than 0.001). The association of ST segment elevation and QS pattern was rarer (15 cases) than the isolated finding of either sign. It was found in the most severe disorders of atrioventricular conduction. The changes observed in leads V3R and/or V4R before the appearance of atrioventricular block enable one to predict which patients with posterior myocardial infarction are the most likely to develop atrioventricular block. These electrocardiographic features seem to indicate septal involvement. (+info)
A partial agonist of the A(1)-adenosine receptor selectively slows AV conduction in guinea pig hearts.
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The use of full agonists of the A(1)-adenosine receptor (A(1)-ADOR) as antiarrhythmic agents is limited by their actions to cause high-grade atrioventricular (AV) block, profound bradycardia, atrial fibrillation, and vasodilation. It may be possible to avoid these undesired actions by use of partial agonists. We determined the effects of CVT-2759, a potential partial agonist of A(1)-ADORs, on guinea pig hearts. CVT-2759 (0.1-100 microM) increased the S-H interval of the isolated heart from 45 +/- 1 to 60 +/- 3 ms (P < 0. 01) with a half-maximal effect at 3.1 microM. CVT-2759 did not cause second-degree AV block. CVT-2759 significantly attenuated the actions of the full agonists N(6)-cyclopentyladenosine and adenosine. CVT-2759 caused a moderate slowing of atrial rate by 10 microM. In contrast, CVT-2759 was a full agonist to decrease cAMP content of rat adipocytes and Fischer rat thyroid line 5 cells. Results of radioligand binding assays indicated that CVT-2759 stabilized a high-affinity, G protein-coupled state of the A(1)-ADOR in membranes prepared from rat adipocytes but not in membranes prepared from the guinea pig brain. The results suggest that a weak A(1)-ADOR agonist, such as CVT-2759, may be useful to slow AV nodal conduction and thereby ventricular rate without causing AV block, bradycardia, atrial arrhythmias, or vasodilation. (+info)
Coronary artery stenosis after radiofrequency catheter ablation of accessory atrioventricular pathways in children with Ebstein's malformation.
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BACKGROUND: Complications concerning the coronary arteries that are directly related to radiofrequency catheter ablation procedures have not been reported in children. Coronary artery lesions, however, have been demonstrated after the endocardial application of radiofrequency current in young animals. METHODS AND RESULTS: Two boys with Ebstein's anomaly of the tricuspid valve developed clinically asymptomatic coronary artery stenosis after radiofrequency catheter ablation of right-sided accessory atrioventricular pathways with standard catheter technology. CONCLUSIONS: The complication of coronary artery stenosis demonstrates a substantial risk after right atrial free wall radiofrequency current application in children. The risk of late coronary alterations should be considered when the use of catheter ablation procedures to young patients is proposed. (+info)
Molecular characterization of the ventricular conduction system in the developing mouse heart: topographical correlation in normal and congenitally malformed hearts.
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OBJECTIVES: Within the adult heart, it is convention to distinguish the conduction system and working (atrial and ventricular) myocardium. The adult conduction system (CS) comprises the sinoatrial (SAN), and atrioventricular (AVN) nodes, the atrioventricular bundle (AVB), the bundle branches and the peripheral Purkinje fibers, each of which display distinct functional properties and distinct profile of gene expression. Characterization of the mouse cardiac conduction system during development is rudimentary at present, even though genetically-modified mice are an increasing source of information regarding cardiac function and embryonic heart development. METHODS: We have performed a detailed study of the pattern of expression of myosin heavy chain (MHC), myosin light chain (MLC), troponin I (TnI) isoforms, connexin 43 (Cx43), desmin and alpha-smooth muscle actin (alpha-SMA), in the ventricular conduction system of normal and congenitally malformed mouse hearts (iv background) from embryonic day 14.5 to 19.5. RESULTS: The AVN is characterized by co-expression of MHC and MLC isoforms and no detectable expression of Cx43, desmin or alpha-SMA. The AVB expresses betaMHC and MLC2v, but no alphaMHC, MLC2a, Cx43, desmin or alpha-SMA. The right and left bundle branches display enhanced expression of desmin and alpha-SMA but no Cx43. The normal expression profile is maintained in congenitally malformed hearts such as double-outlet right ventricle and common atrioventricular canal. Three-dimensional reconstruction of the conduction system shows normal arrangement of the bundle branches in congenitally malformed hearts, but abnormal location and/or extension of the AVN. CONCLUSIONS: Molecular characterization allows to follow the development of the CS in both, normal and malformed mouse hearts. Normal phenotypic expression of the CS is independent of heart situs but shows minor modifications in the presence of heart malformations. It is concluded that the AVN derives from the atrioventricular canal myocardium, the bundle of His from the ventricular myocardium, and the bundle branches from the ventricular trabeculations. Our results do not provide evidence to support an extra-cardiac origin of the ventricular CS. (+info)
Fluorescent imaging of a dual-pathway atrioventricular-nodal conduction system.
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A dual-pathway theory to explain atrioventricular-nodal (AVN) reentry has been proposed previously. However, the exact anatomical and functional correlates of the fast pathway (FP) and slow pathway (SP) have not yet been elucidated. We used optical mapping to reconstruct patterns of activation during retrograde conduction through the AVN and during AVN reentry in the triangles of Koch of 12 rabbits. Reentry was inducible by a premature stimulation of the bundle of His in 6 preparations (50%). A functional FP and SP appear to be anatomically correlated with posterior and posterolateral extensions of the AVN, which were recently described. Retrograde breakthrough points in 6 noninducible preparations were clustered near the apex of the triangle of Koch (FP), whereas 6 inducible preparations had either cycle length-dependent FP and SP exits (n=3) or only SP exits located near the coronary sinus orifice. The shift of breakthrough points from FP to SP during progressive shortening of the coupling interval was accompanied by a discontinuity in the conduction curve. We observed a transmural reentrant circuit involving the AVN, FP, SP, and the superficial endocardial layer of atrial and transitional cells. The presence of a functional SP during retrograde conduction was associated with inducibility of AVN reentry. The full text of this article is available at http://www.circresaha.org. (+info)
Diagnostic significance of the morphological change in the atrial electrogram during Para-Hisian pacing.
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Para-Hisian pacing (PHP), a pacing method to differentiate between conduction occurring over an accessory pathway (AP) from that over the atrioventricular node (AVN), is assessed essentially by comparing the timing in the atrial electrogams. Morphological change in the atrial electrograms is often observed during PHP, but its significance has not been investigated. Prior to the catheter ablation procedure, PHP was performed in 52 patients with an AP and in 36 patients with AV nodal reentrant tachycardia (AVNRT). The morphological change in the atrial electrograms, which was retrospectively assessed between the His bundle and proximal right bundle branch (HB-RB) captured and non-captured beats, was identified in 15 of 52 patients with an AP and in 26 of 36 patients with AVNRT. The atrial electrogram in the 6 of these 15 AP patients changed its morphology without overlapping the ventricular electrogram. All 6 AP patients exhibited a PHP pattern with the presence of 2 retrograde conduction routes, an AP and the AVN. In the patients demonstrating no morphological change in the atrial electrogram, 33 of 37 AP patients and all 10 AVNRT patients had only one retrograde conduction route. Morphological change in the atrial electrogram without overlapping the ventricular electrogram seems to have diagnostic significance indicating the presence of both AP and AVN conduction. (+info)