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At least 19 recordsLinked to original sources

Sinus node-atrioventricular node isolation: long-term results with the "corridor" operation for atrial fibrillation.

The "corridor" operation is designed to restore sinus rhythm to patients with atrial fibrillation by electrically isolating the sinus node, a band of atrial tissue and the atrioventricular (AV) node from the remaining atrial tissue. Nine patients with drug-refractory atrial fibrillation underwent this operation; four patients had chronic atrial fibrillation and five had paroxysmal atrial fibrillation; the mean duration of symptoms was 12 +/- 8 years. Patient ages ranged from 25 to 68 years (mean 48 +/- 12). At preoperative electrophysiologic study, no patient had evidence of an accessory AV pathway or AV node reentry. Sinus node recovery time could not be determined in five patients because of recurrent atrial fibrillation during or before programmed stimulation. At operation the corridor of atrial tissue connecting the sinus and AV nodes was successfully isolated from the remaining left and right atrial tissue in all patients. One patient required early reoperation for recurrent atrial fibrillation before hospital discharge. At the predischarge electrophysiologic study, the corridor remained isolated in all patients except for one patient who had intermittent conduction between the corridor and excluded right atrium. One patient had nonsustained atrial fibrillation and one had atrial tachycardia evident in the corridor. Atypical AV node reentry of uncertain significance was induced in one other patient. Over a total follow-up of 191 patient months (mean 21 +/- 20), seven patients remained free of atrial fibrillation. Two patients had recurrent atrial fibrillation, which in one patient was effectively controlled by a single antiarrhythmic agent. A permanent pacemaker was implanted in four patients for sinus node dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmia, Sinus↗

De subitaneis mortibus. XXVII. Histological abnormalities in the sinus node, atrioventricular node and His bundle associated with coarctation of the aorta.

A twenty-year-old carpenter died suddenly and unexpectedly nine years after surgical treatment of coarctation of the aorta. Both before and after surgery he had paroxysmal atrial fibrillation, T wave inversions in the ECG and persisting cardiac hypertrophy. At postmortem examination there was focal fibromuscular dysplasia narrowing the sinus node artery, but other small coronary arteries were normal and there was no focal fibrosis of the ventricular myocardium. Within the sinus node there were several small glomera surrounding branches of the sinus node artery. Pericardial fibrosis was present over much of the heart, including margins of the sinus node. The central fibrous body was thickened, particularly on the left, and the His bundle was smaller than normal in cross section. The His bundle appeared displaced toward the right. The artioventricular (A-V) node was split into an upper and lower half tenuously connected through the central fibrous body which divided it. In its lower half the A-V node was directly continuous with ordinary myocardial cells of the interventricular septum. Possible developmental relationships between these unusual anatomical findings in the conduction system and coarctation of the aorta are discussed. How these findings might relate to the known electrophysiological disturbances and some causes for his sudden death are considered.

Adult↗

Differential sensitivity of sinus node, atrioventricular node, atrium, and ventricle to propranolol.

The purpose of this study was to test the hypothesis that less propranolol was required to block stellate-induced shortening of atrial and ventricular effective refractory periods (ERPs) than was required to prevent stellate-induced shortening of the spontaneous sinus nodal cycle length and atrioventricular (AV) nodal conduction time. Studies were performed in open-chest, neurally decentralized dogs anesthetized with secobarbital. We determined the dose of propranolol (propranolol dose-response curves) required to block the effects of 1 Hz, 2 Hz, and 4 Hz bilateral ansae subclaviae stimulation on sinus nodal automaticity, AV nodal conduction, and atrial and ventricular ERPs. We found that propranolol at a dose of 0.5 mg/kg eliminated ansae subclaviae-induced shortening of atrial and ventricular ERPs, whereas sinus nodal cycle length and AV nodal conduction time still shortened. These data indicate a differential sensitivity of the sinus and AV nodes compared with atrial and ventricular myocardium to the beta-adrenergic receptor-blocking effects of propranolol in response to efferent sympathetic neural stimulation. Clinical implications are that it might be possible to treat sympathetically mediated ventricular arrhythmias with doses of propranolol that still preserve sinus and AV nodal responses.

Animals↗

The electrophysiological effects of intravenous magnesium on human sinus node, atrioventricular node, atrium, and ventricle.

The effects of intravenously (IV) administered magnesium chloride (MgCl) on electrophysiologic and electrocardiographic variables were studied in 13 patients undergoing a routine electrophysiologic assessment for clinical indications. An infusion of 12 mmol of MgCl was given during a 10-min period and relevant electrophysiologic variables were determined before and after the infusion. Serum Mg levels increased from 0.78 +/- 0.03 (mean +/- SEM) before to 1.52 +/- 0.08 ms after the infusion (p less than 0.0001). Magnesium treatment caused a significant prolongation in PR interval (from 151 +/- 8 to 174 +/- 8 ms, p less than 0.001) as well as in QRS duration (from 90 +/- 4 to 101 +/- 6 ms, p less than 0.05). Likewise, intra-atrial (PA) as well as atrioventricular (AV) nodal (AH) conduction times were significantly prolonged (from 33 +/- 3 to 46 +/- 3 ms, p less than 0.01, and from 85 +/- 6 to 94 +/- 6 ms, p less than 0.05, respectively). Mean effective and functional atrial refractory periods increased (from 228 +/- 8 to 256 +/- 10 ms, p less than 0.01 and from 292 +/- 9 to 320 +/- 11 ms, p less than 0.01, respectively), as did mean AV node functional refractory period (from 399 +/- 29 to 422 +/- 27 ms, p less than 0.02). No significant change occurred with regard to sinus node function (as estimated from heart rate, sinus node recovery time, and calculated sinoatrial conduction time) or ventricular refractoriness. It is concluded that IV Mg has several electrophysiologic effects that may be beneficial in the treatment/prevention of supraventricular tachyarrhythmias.

Adolescent↗

Time couse of the blockade effect of propranolol on sinus node and atrioventricular node.

The time course of the blockade effect of propranolol on the sinus node (SN) and the atrioventricular node (AVN) was studied in six normal volunteers. Serial isoproterenol infusions were done before and after oral propranolol administration, 160 mg daily for two days. The inhibition by propranolol of the heart rate increases due to isoproterenol was used to assess the blockade of the sinus node, and the diminution by propranolol of the shortening in the PR interval due to isoproterenol was used to assess the blockade of the atrioventricular node. The blockade effects on the sinus node and the atrioventricular node were identical and persisted more than 24 hours. There was no good relationship between plasma propranolol and blockade effect on sinus node and/or atrioventricular node as propranolol was no longer detectable in the plasma 24 hours after the last dose. A transient hypersensitivity to isoproterenol was present 36 to 48 hours after propranolol withdrawal. The explanation of these phenomena most likely lies in the peculiar nature of beta-adrenergic receptors.

Adult↗

Spatial distribution of nerve processes and beta-adrenoreceptors in the rat atrioventricular node.

Atrioventricular (AV) nodal conduction time is known to be modulated by the autonomic nervous system. The presence of numerous parasympathetic and sympathetic nerve fibres in association with conduction tissue in the heart is well authenticated. In this study, confocal microscopy was used to image the distribution of antibodies directed against the general neuronal marker PGP 9.5, tyrosine hydroxylase (TH), vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP) and beta1 and beta2-adrenoreceptors. Serial 12 microm sections of fresh frozen tissue taken from the frontal plane of the rat atrioventricular node, His bundle and bundle branches were processed for histology, acetylcholinesterase (AChE) activity and immunohistochemistry. It was found that the AV and ventricular conduction systems were more densely innervated than the atrial and ventricular myocardium as revealed by PGP 9.5 immunoreactivity. Furthermore, the transitional cell region was more densely innervated than the midnodal cell region, while spatial distribution of total innervation was uniform throughout all AV nodal regions. AChE-reactive nerve processes were found throughout the AV and ventricular conduction systems, the spatial distribution of which was nonuniform exhibiting a paucity of AChE-reactive nerve processes in the central midnodal cell region and a preponderance in the circumferential transitional cell region. TH-immunoreactivity was uniformly distributed throughout the AV and ventricular conduction systems including the central midnodal and circumferential transitional cell regions. Beta1-adrenoreceptors were found throughout the AV and ventricular conduction systems with a preponderance in the circumferential transitional cell region. Beta2-adrenoreceptors were localised predominantly in AV and ventricular conduction systems with a paucity of expression in the circumferential transitional cell region. These results demonstrate that the overall uniform distribution of total nerve processes is comprised of nonuniformly distributed subpopulations of parasympathetic and sympathetic nerve processes. The observation that the midnodal cell region exhibits a differential spatial pattern of parasympathetic and sympathetic innervation suggests multiple sites for modulation of impulse conduction within this region. Moreover, the localisation of beta2-ARs in the AV conduction system, with an absence of expression in the circumferential transitional cell layer, suggests that subtype-specific pharmacological agents may have distinct effects upon AV nodal conduction.

Acetylcholinesterase↗

Comparison of late results of surgical or radiofrequency catheter modification of the atrioventricular node for atrioventricular nodal reentrant tachycardia.

AIMS: Although arrhythmia surgery and radiofrequency catheter ablation to cure atrioventricular nodal reentrant tachycardia differ in technical concept, the late results of both methods, in terms of elimination of the arrhythmogenic substrate and procedure-related new and different arrhythmias, have never been compared. This constituted the purpose of this prospective follow-up study. METHODS AND RESULTS: Between 1988 and 1992, 26 patients were surgically treated using perinodal dissection or 'skeletonization', and from 1991 up to 1995, 120 patients underwent radiofrequency modification of the atrioventricular node for atrioventricular nodal reentrant tachycardia. The acute success rates of surgery and radiofrequency catheter ablation were 96% and 92%, respectively. Late recurrence, rate in the surgical and radiofrequency catheter ablation groups was 12% and 17%, respectively. Mean follow-up was 53 months in the surgical group and 28 months in the radiofrequency catheter ablation group. The final success rate after repeat intervention was 100% in the surgical group and 98% in the radiofrequency catheter ablation group. Comparison of the initial and recent series of radiofrequency catheter ablated patients showed an increased initial success rate with fewer applications. In the radiofrequency catheter ablation group, a second- or third-degree block developed in three patients (2%), requiring permanent pacing, whereas in the surgical group no complete atrioventricular block was observed. Inappropriate sinus tachycardia needing drug treatment was observed in 13 patients (11%), mostly after fast pathway ablation, but was never observed after surgery. New and different supraventricular tachyarrhythmias arose in 27% of the patients in the surgical group and in 11% of the radiofrequency catheter ablation group, but did not clearly differ. CONCLUSION: This one-institutional follow-up study demonstrated comparable initial and late success rates as well as incidence of new and different supraventricular arrhythmias following arrhythmia surgery and radiofrequency catheter ablation for atrioventricular nodal reentrant tachycardia. Today radiofrequency catheter ablation has replaced arrhythmia surgery for various reasons, but the late arrhythmic side-effects warrant refinement of technique.

Adult↗

Origin of the sinoatrial node and atrioventricular node arteries in right, mixed, and left inferior emphasis systems.

The origin of the sinoatrial node artery (SAN) and atrioventricular node artery (AVN) was determined for 118 patients with normal coronary arteriograms. The coronary arteriograms of the 118 patients were divided into right (66.1%), mixed (26.3%), and left (7.6%) inferior emphasis systems. The SAN arose from the right coronary artery in 53%, the left coronary artery in 35%, and had a dual origin in 11%. The proximal right coronary artery was the origin of the SAN in 48.7% of right, 60.5% of mixed, and 55.6% of left inferior emphasis systems. The left coronary artery was the origin of the SAN in 38.5% of right, 25.8% of mixed, and 44.4% of left inferior emphasis systems. The AVN arose from the right coronary artery in 84%, the left coronary artery in 8%, and from both in 8% of the 118 patients. The right coronary artery was the origin of the AVN in 98.7% of right, 74.2% of mixed, and 0% of left inferior emphasis systems. The left coronary artery was the origin of the AVN in 0% of right, 25.8% of mixed, and 100% of left inferior emphasis systems.

Adult↗

Preoperative secundum atrial septal defect with coexisting sinus node and atrioventricular node dysfunction.

Sinus node dysfunction in patients after repair of the secundum atrial septal defect has been ascribed to surgical damage. We studied 15 consecutive patients with secundum atrial septal defect before operative intervention. Noninvasive testing included 34-hour electrocardiographic monitoring and a standard 13-lead ECG. Intracardiac electrophysiologic techniques included corrected sinus node recovery time, sinoatrial conduction time, His bundle recording to measure AH and HV intervals, the atrial pacing rate at which atrioventricular node Wenckebach occurred, and atrioventricular nodal refractory period. The ECG revealed an ectopic atrial rhythm in two patients. Intracardiac electrophysiology showed an abnormal corrected sinus node recovery time (range -40 to 800 msec) in 10 patients. Five patients had evidence of atrioventricular nodal dysfunction with prolonged AH interval or abnormal atrial pacing rate at which atrioventricular Wenckebach occurred. These data indicate that sinus node dysfunction or atrioventricular node dysfunction were present before surgical intervention.

Adolescent↗

[Different sensitivity of sinus node and atrioventricular node to adenosine triphosphate].

We showed that higher concentration of adenosine 5'-triphosphate (ATP) was required to prolong the spontaneous cycle length of the sinus node (SN) than that required to prolong the spontaneous cycle length of the atrioventricular node (AVN). Spontaneously beating preparations of SN and AVN of rabbit (n = 8) were superfused with Tyrode solution containing 10(-8)-10(-3)M ATP, and action potential was recorded. The negative chronotropic action of ATP was dependent on the concentration. The required concentration of ATP to prolong spontaneous cycle length significantly (p less than 0.01) was 10(-5)M in SN and 10(-6)M in AVN, respectively. At concentrations higher than 10(-6)M, the degree of prolongation was greater in AVN than in SN (p less than 0.01). 10(-7)M dipyridamole enhanced this effect of ATP, while 10(-4)M theophylline reduced it. Action potential duration of 50% repolarization was not changed significantly in either SN or AVN at concentrations up to 10(-3)M. Maximum diastolic potential (MDP) was hyperpolarized from 10(-8)M to 10(-4) M. Hyperpolarization of MDP induced by ATP was greater in AVN than in SN but it was not statistically significant. MDP was depolarized by 10(-3) M ATP in both SN and AVN. The maximum velocity of depolarization was slightly larger in both SN and AVN as the concentration of ATP was increased in the perfusate. However, it was not statistically significant. 10(-3) M ATP decreased the maximum velocity of depolarization.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

[Effect of nifedipine on sinus node and atrioventricular node function following autonomic blockade in the human].

The effect of intravenously administered nifedipine (7.5 micrograms/kg) on sinus node and atrioventricular (AV) node function was evaluated in 17 patients, 9 of whom had sinus node disease after autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg i.v.). The patients' ages ranged from 18 to 77 years. After nifedipine there was a nonsignificant increase in the median values for sinus cycle length from 750 ms to 760 ms, for sinus node recovery time from 1150 ms to 1240 ms, for corrected sinus node recovery time from 440 ms to 460 ms, and for sinoatrial conduction time from 63 ms to 75 ms. Nevertheless, nifedipine produced a significant increase in the AV node refractory periods (median values): the effective refractory period lengthened from 300 ms to 305 ms (rate 100/min) and from 290 ms to 300 ms (rate 120/min) respectively. The functional refractory period increased from 380 ms to 400 ms (rate 100/min) and from 385 ms to 410 ms (rate 120/min) respectively. The Wenckebach period was significantly prolonged from 370 ms to 390 ms. We conclude, therefore, that in the absence of autonomic control intravenous administration of nifedipine exerts a mild depressive effect on AV node but not on sinus node function.

Adolescent↗

Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade.

The effects of digoxin on sinus node and atrioventricular (AV) node function were studied in 18 patients (mean age 53.6 years) with normal intrinsic heart rates. Electrophysiologic testing was performed both during basal state and after autonomic blockade with propranolol and atropine. Full digitalization was achieved by intravenous administration of digoxin (0.02 mg/kg) given in three divided doses over a 24-hour period. The following day, after a basal recording, autonomic blockade was again induced and the study was repeated. During basal state, digoxin significantly prolonged the sinus cycle length (SCL) (p less than 0.01) and the AH interval (p less than 0.01). However, when the intrinsic sinus node functions were compared (i.e., the values obtained after autonomic blockade), digoxin did not produce significant changes in intrinsic SCL, corrected sinus node recovery time, and sinoatrial conduction time. No significant changes were noted even in the intrinsic AH interval and AV nodal refractory periods. These findings suggest that: (1) intravenous administration of digoxin in therapeutic doses does not produce any depression of the intrinsic functions of the sinus node and AV node; and (2) the depressant effects induced by digoxin during basal state appear to be mediated through the autonomic nervous system.

Adult↗

The use of two-dimensional echocardiography during catheter ablation of the atrioventricular node.

Atrioventricular nodal catheter ablation has proved an effective option in patients with drug-refractory, uncontrolled, supraventricular tachyarrhythmias; however, many complications in the immediate post ablative period relate to direct myocardial damage due to the electrical current generated by the catheter. The authors used two-dimensional echocardiography in a 57-year-old female patient with recurrent uncontrolled rapid ventricular rates despite multiple antiarrhythmic medications, in an attempt to identify the sequence of events responsible for complications of the ablation procedure. The echocardiographic images showed evidence of an explosion: microbubbles outlining an expanding force were seen which, if contained in a confined space such as the coronary sinus, might explain previously observed mechanical damage. Two-dimensional echocardiography may be useful for continual monitoring of catheter position during ablation.

Arrhythmias, Cardiac↗

Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node.

A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 +/- 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 +/- 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p less than 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 +/- 0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p less than 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.

Adenosine Triphosphate↗

Cx43 and dual-pathway electrophysiology of the atrioventricular node and atrioventricular nodal reentry.

Fluorescent imaging has revealed that posterior nodal extensions provide the anatomical substrate for the dual-pathway electrophysiology of the atrioventricular (AV) node during normal conduction and reentry. The reentry can be intranodal, or as well as the posterior nodal extensions, it can involve an endocardial layer of atrial/atrial-nodal (A/AN) cells as part of the AV nodal reentry (AVNR) circuit. Using fluorescent imaging with a voltage-sensitive dye and immunolabeling of Cx43, we mapped the electrical activity and structural substrate in 3 types of AVNR induced by premature atrial stimulation in 8 rabbit hearts. In 6 cases, the AVNR pathway involved (1) a fast pathway (FP), (2) the A/AN layer, and (3) a slow pathway (SP). In 4 cases, reentry took the path (1) SP, (2) A/AN layer, and (3) FP. In 2 cases, reentry was intranodal, propagating between the 2 posterior nodal extensions. Immunolabeling revealed that the FP and SP are formed by Cx43-expressing bundles surrounded by tissue without Cx43. Cx43-expressing posterior nodal extensions are the substrate of AVNR during both intranodal and extranodal reentry.

Animals↗