Transient entrainment of bundle-branch reentry by atrial and ventricular stimulation: elucidation of the tachycardia mechanism through analysis of the surface ECG.
(9/251)
BACKGROUND: Different responses to entrainment have been reported in relation to the pacing site of a variety of tachycardias. However, transient entrainment of bundle-branch reentrant tachycardia (BBRT) has not been investigated systematically. METHODS AND RESULTS: We attempted entrainment of 13 BBRTs in 9 patients by pacing first the right ventricle and then the right atrium. The initial pacing cycle length (CL) was 10 ms faster than the tachycardia CL. Subsequent pacing sequences were performed with 5- to 10-ms CL decrements until tachycardia termination or loss of postatropine 1:1 AV conduction. Both full ventricular-paced and AV-conducted QRS complex references were obtained during sinus rhythm pacing from the same sites and with similar CL as during entrainment. Transient entrainment was achieved by ventricular and atrial stimulation in 11 and 8 tachycardias, respectively. Constant fusion was always present during entrainment by ventricular stimulation. There was no change in the QRS complex (orthodromically concealed fusion) during entrainment by atrial stimulation in 6 of 6 tachycardias with left bundle-branch block morphology and in 1 of 2 tachycardias with right bundle-branch block morphology. CONCLUSIONS: BBRT, especially if it has a left bundle-branch block morphology, can be differentiated from other wide-QRS-complex tachycardia mechanisms through analysis of the ECGs recorded during tachycardia entrainment by atrial and ventricular stimulation. This diagnostic approach may be especially useful when it is difficult to record a stable or sufficiently sized His bundle electrogram or when spontaneous changes in the ventricular CL precede similar changes in the His bundle CL. (+info)
Radiofrequency ablation of a right atriofascicular Mahaim fiber and two contralateral left free-wall accessory pathways.
(10/251)
We report a rare combination of a right atriofascicular Mahaim fiber and two left-sided atrioventricular accessory pathways in a 57-year-old female presenting with an antidromic atrioventricular reciprocating tachycardia. Radiofrequency ablation was first targeted at the left lateral accessory pathway that served as the retrograde limb of the tachycardia. After elimination of the left lateral pathway, a bystander left posterolateral pathway was detected, and it too was successfully ablated. Although no tachycardia was reinducible, the Mahaim pathway was ablated because of its short effective refractory period. A discrete Mahaim potential recorded at the right atrial free-wall successfully guided the ablation. (+info)
Permanent, direct His-bundle pacing: a novel approach to cardiac pacing in patients with normal His-Purkinje activation.
(11/251)
BACKGROUND: Direct His-bundle pacing (DHBP) produces synchronous ventricular depolarization and improved cardiac function relative to apical pacing. Although it has been performed transiently in the electrophysiology laboratory and persistently in open-chested canines, permanent DHBP in humans has not been achieved. METHODS AND RESULTS: A total of 18 patients aged 69+/-10 years who had a history of chronic atrial fibrillation, dilated cardiomyopathy, and normal activation (ie, QRS< or =120 ms) were screened for permanent DHBP using an electrophysiology catheter. In 14 patients, the His bundle could be reliably stimulated. Of these 14, permanent DHBP using a fixed screw-in lead was successful in 12 patients. Radiofrequency atrioventricular node ablation was performed in patients exhibiting a fast ventricular response. All patients received single-chamber rate-responsive pacemakers. Acute pacing thresholds were 2.4+/-1.0 V at a pulse duration of 0.5 ms. Lead complications included exit block requiring reoperative adjustment and gross lead dislodgment. Echocardiographic improvement in heart function was shown by reductions in the left ventricular end-diastolic dimension from 59+/-8 to 52+/-6 mm (P+info)
Baroreceptor control of atrioventricular conduction in man.
(12/251)
Although human baroreflexes are known to exert a powerful physiological control on heart rate, little information exists on the physiological control they exert on the atrioventricular conduction system. In 11 normotensive subjects with normal atrioventricular conduction, we altered baroreceptor activity by injection of pressor and depressor drugs (phenylephrine and trinitroglycerin) and recorded mean arterial pressure (MAP, catheter measurements), R-R interval, and pre-His and post-His intervals (A-H and H-V, His bundle recording). With the subjects in sinus rhythm, increasing MAP by 21+/- 1 mm Hg caused a marked lengthening (250 +/- 28 msec), and decreasing MAP by 17 +/- 2 mm Hg a marked shortening (142 +/- 16 msec) of the R-R interval. There was little change in the A-H interval and no change at all in the H-V interval. However, when the R-R interval was kept constant in these subjects by atrial pacing, a similar increase and decrease in MAP caused, respectively, a marked lengthening (49 +/- 6 msec) and shortening (19 +/- 3 msec) of the A-H interval, although the H-V interval remained unaffected. Thus physiological ranges of baroreceptor activation have a marked influence on the atrioventricular node but apparently not on the ventricular portion of the atrioventricular conduction system. This influence is unmasked when pacing prevents the baroreceptor influence on the sinoatrial node. (+info)
Proximal atrioventricular bundle, atrioventricular node, and distal atrioventricular bundle are distinct anatomic structures with unique histological characteristics and innervation.
(13/251)
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. (+info)
A simple technique for anatomical slow pathway ablation in atrioventricular nodal reentrant tachycardia.
(14/251)
The slow pathway potential or the slow potential serves as a useful marker in catheter ablation of the slow pathway. However, an anatomical approach without recording of these potentials is also an effective way to cure atrioventricular nodal reentrant tachycardia (AVNRT). Moreover, the origin of these potentials is a matter of controversy. We compared 2 approaches to ascertain whether or not recording of these potentials is necessary in eliminating the slow pathway and to estimate the usefulness of the simple anatomical approach. The study population consisted of 24 patients with a conventional approach (Group P) and 19 patients with an anatomical approach (Group A). In group A, the ablation site was determined by fluoroscopy, which was the lowest one-third of the area between the His bundle electrogram recorded position and the coronary sinus orifice at the right anterior oblique view, and just in front of and above the coronary sinus orifice also posterior to the His catheter at the left anterior oblique view where the His catheter was seen tangentially. The slow pathway was successfully ablated in all patients without any complications, including more than first-degree AV block. Although there were no significant differences in total energy or number of applications between the 2 groups, the procedure time was significantly shorter in group A (p < 0.01). In conclusion, recording of the slow pathway potential or the slow potential is not always necessary for slow pathway ablation in the treatment of AVNRT. Because our anatomical approach was performed simply, effectively and safely, it is recommended for the slow pathway ablation of AVNRT. (+info)
Increased sympathetic activity after atrioventricular junction ablation in patients with chronic atrial fibrillation.
(15/251)
OBJECTIVES: The aim of this study was to determine the changes in sympathetic nerve activity (SNA) after atrioventricular junction (AVJ) ablation in patients with chronic atrial fibrillation (AF). BACKGROUND: Polymorphic ventricular tachycardia (PMVT) has been reported after AVJ ablation in patients paced at a rate of < or =70 beats/min. We hypothesized that AVJ ablation results in sympathetic neural changes that favor the occurrence of PMVT and that pacing at 90 beats/min attenuates these changes. METHODS: Sympathetic nerve activity, 90% monophasic cardiac action potential duration (APD90), right ventricular effective refractory period (ERP) and blood pressure measurements were obtained in 10 patients undergoing AVJ ablation. Sympathetic nerve activity was analyzed at baseline and during and after successful AVJ ablation for at least 10 min. Data were also collected after ablation at pacing rates of 60 and 90 beats/min. The APD90 and ERP were measured before and after AV block during pacing at 120 beats/min. RESULTS: Sympathetic nerve activity increased to 134 +/- 16% of the pre-ablation baseline value (p < 0.01) after successful AVJ ablation plus pacing at 60 beats/min and decreased to 74 +/- 8% of baseline (p < 0.05) with subsequent pacing at 90 beats/min. Both APD90 and ERP increased significantly. CONCLUSIONS: 1) Ablation of the AVJ followed by pacing at 60 beats/min is associated with an increase in SNA. 2) Pacing at 90 beats/min decreases SNA to or below the pre-ablation baseline value. 3) Cardiac APD and ERP increase after AVJ ablation. The increase in SNA, along with the prolongation in APD, may play a role in the pathogenesis of ventricular arrhythmias that occur after AVJ ablation. (+info)
High-resolution optical mapping of the right bundle branch in connexin40 knockout mice reveals slow conduction in the specialized conduction system.
(16/251)
Connexin40 (Cx40) is a major gap junction protein that is expressed in the His-Purkinje system and thought to be a critical determinant of cell-to-cell communication and conduction of electrical impulses. Video maps of the ventricular epicardium and the proximal segment of the right bundle branch (RBB) were obtained using a high-speed CCD camera while simultaneously recording volume-conducted ECGs. In Cx40(-/-) mice, the PR interval was prolonged (47.4+/-1.4 in wild-type [WT] [n=6] and 57.5+/-2.8 in Cx40(-/-) [n=6]; P<0.01). WT ventricular epicardial activation was characterized by focused breakthroughs that originated first on the right ventricle (RV) and then the left ventricle (LV). In Cx40(-/-) hearts, the RV breakthrough occurred after the LV breakthrough. Additionally, Cx40(-/-) mice showed RV breakthrough times that were significantly delayed with respect to QRS complex onset (3.7+/-0.7 ms in WT [n=6] and 6.5+/-0.7 ms in Cx40(-/-) [n=6]; P<0.01), whereas LV breakthrough times did not change. Conduction velocity measurements from optical mapping of the RBB revealed slow conduction in Cx40(-/-) mice (74.5+/-3 cm/s in WT [n=7] and 43.7+/-6 cm/s in Cx40(-/-) [n=7]; P<0.01). In addition, simultaneous ECG records demonstrated significant delays in Cx40(-/-) RBB activation time with respect to P time (P-RBB time; 41.6+/-1.9 ms in WT [n=7] and 55.1+/-1.3 ms in [n=7]; P<0.01). These data represent the first direct demonstration of conduction defects in the specialized conduction system of Cx40(-/-) mice and provide new insight into the role of gap junctions in cardiac impulse propagation. (+info)