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 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated dog hearts perfused with blood from a donor dogand driven at two heart rates were used to compare the effects of propranolol with those of its quaternary ammonium derivative on atrial, atrioventricular (AV) nodal, and His-Purkinje conduction. Propranolol slowed only AV-nodal conduction, increasing the minimal conduction time and the effect of prematurity, without affecting fatigue. Practolol did not have this effect. Dimethylpropranolol had similar but not identical effects on the AV node, but also slowed atrial and ventricular conduction. In contrast with the quaternary derivative of lidocaine, dimethylpropranolol's effect on atrial and ventricular conduction was not dependent on the heart rate. The effect of dimethylpropranolol on ventricular conduction was observed at doses lower than those reported by others to be antiarrhythmic.
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PMID:The effect of propranolol and dimethylpropranolol on cardiac conduction. 48 71

The effects of lidocaine and methyl lidocaine on cardiac conduction were studied using His bundle recordings from isolated blood perfused dog hearts. The input and output characteristic of the atrioventricular (AV) node can be described as consisting of three components, namely, minimal conduction time, fatigue, and the effect of prematurity (deltaCT). Lidocaine (2.5-10.0 mg/kg) increased minimal conduction time but not fatigue. Methyl lidocaine (1.25-5.0 mg/kg) increased both. A dose of 5 mg/kg or less of either drug caused a nonparallel shift of the deltaCT curve to the right. High doses of lidocaine (10 mg/kg) cause deltaCT to become rate-dependent. Lidocaine slowed atrial conduction only slightly. Atrial block prevented the observation of the effect of methyl lidocaine in doses higher than 5.0 mg/kg. Both drugs showed greater effect on atrial conduction at fast heart rate. Lidocaine did not affect ventricular conduction time at slow heart rates and had only minimal effects at fast heart rates. Methyl lidocaine increased ventricular conduction time at all heart rates. The results of this study indicate that lidocaine and methyl lidocaine have entirely different spectra of activity on cardiac conduction, in that their effect on AV nodal conduction do not differ greatly whereas the quaternary analog has a much stronger depressant effect on atrial and ventricular conduction.
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PMID:Effect of lidocaine and methyl lidocaine on cardiac conduction. 85 Jan 38

To study the pathway of tachycardia in patients with the Wolff-Parkinson-White (WPW) syndrome and reciprocal tachycardias, results from intracavitary recordings and atrial and ventricular stimulation were reviewed in 71 patients with the WPW syndrome and 54 patients without pre-excitation. In all patients a reproducible tachycardia could be initated and terminated by appropriately timed electrical stimuli. The following findings were accepted as suggesting the participation of an accessory pathway in the tachycardia circuit: 1) no increase in ventriculo-atrial conduction (V-A C) time following ventricular stimuli given with increasing prematurity; 2) activation of right or left atrium (depending upon the location of the atrial end of the accessory pathway) prior to activation of atrium in the His bundle lead; 3) slowing of tachycardia following bundle branch block to the ventricle in which the accessory pathway inserts; 4) V-A C time of early stimuli on the ventricle during the tachycardia equal to or less than the V-A c time following QRS complexes during tachycardia; 5) inability to initiate tachycardia or slowing of tachycardia following the administration of drugs affecting the accessory pathway. Accepted as suggestive for atrioventricular (A-V) nodal re-entry were the following factors: 1) activation of atrium following initiation of tachycardia by a single atrial premature beat after activation of the bundle of His but before or simultaneous with ventricular activation in first and subsequent beats of tachycardia; 2) initiation of tachycardia following a gradual increase in V-A C time with the appearance of a His bundle electrogram in between the premature beat and retrograde atrial activation; 3) gradual increase in V-A C time with the appearance of a His bundle electrogram following ventricular premature beats given with increasing prematurity; 4) two-to-one block distal to the A-V node or His bundle with persistance of tachycardia. If only positive findings were accepted, 51 patients of the WPW group used their accessory pathway during tachycardia. In eight patients re-entry was confined to the A-V node. In the remaining 12 patients the mechanism was not clear. Of the patients not showing pre-excitation in A-V direction, 47 patients seemed to have their re-entry circuit in the A-V node, five patients used an accessory pathway in V-A direction, and in two patients the pathway of tachycardia could not be identified.
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PMID:The role of an accessory atrioventricular pathway in reciprocal tachycardia. Observations in patients with and without the Wolff-Parkinson-White syndrome. 113 22

Of 67 patients with reciprocal atrioventricular (A-V) nodal tachycardia consecutively studied by programmed electrical stimulation of the heart, nine patients showed second degree block toward the ventricle and one patient toward the atrium during tachycardia. In four patients the occurrence of block was critically related to the prematurity of the test stimulus initiating the tachycardia. In three patients block developed following increase in rate of tachycardia. In two patients block could be elicited by introducing premature ventricular stimuli during tachycardia. Our observations indicate that different mechanisms may be responsible for second degree block during reciprocal supraventricular tachycardia. The finding of second degree block during reciprocal supraventricular tachycardia excludes a tachycardia with A-V conduction over the A-V node - His pathway and V-A conduction over an accessory A-V pathway.
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PMID:Second degree block during reciprocal atrioventricular nodal tachycardia. 125 79

Sinoatrial conduction time (SACT) was estimated from the delay in the atrial recovery period after premature depolarization applied in that portion of atrial diastole when increasing prematurity resulted in a constant recovery interval. In 20 normal patients SACT was 169 msec. +/- 91 (2 S.D.). At least nine of 19 patients with "sick-sinus syndrome" (SSS) demonstrated SACT that were longer than seen in these normal subjects. SACT was prolonged in seven of nine SSS patients with abnormal A-V nodal conduction. Among 10 SSS patients with normal A-V conduction, only two had prolonged SACT. This study identifies first-degree sinoatrial block as a frequent manifestation of SSS associated with the presence of A-V node conduction abnormalities.
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PMID:First-degree sinoatrial heart block: sinoatrial block in the sick-sinus syndrome. 125 28

The AV node of those mammalian species in which it has been thoroughly investigated (rabbit, ferret, and humans) consists of various cell types: transitional cells, midnodal (or typical nodal cells), lower nodal cells, and cells of the AV bundle. There are at least two inputs to the AV node, a posterior one via the crista terminalis and an anterior one via the interatrial septum, where atrial fibers gradually merge with transitional cells. The role of a possible third input from the left atrium has not been investigated. Since the transition from atrial fibers to nodal fibers is gradual, it is very difficult to define the "beginning" of the AV node, and gross measurements of AV nodal length may be misleading. Histologically, the "end" of the AV node is equally difficult to define. At the site where macroscopically the AV node ends, at the point where the AV bundle penetrates into the membranous septum, typical nodal cells intermingle with His bundle cells. A conspicuous feature, found in all species studied, is the paucity of junctional complexes, most marked in the midnodal area. The functional counterpart of this is an increased coupling resistance between nodal cells. An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart. In those studies in which activation patterns, transmembrane potential characteristics, and histology have been compared, a good correlation has been found between AN and transitional cells, N cells and the area where transitional cells and cells of the beginning of the AV bundle merge with midnodal cells, and NH cells and cells of the AV bundle. Dead-end pathways correspond to the posterior extension of the bundle of lower nodal cells and to anterior overlay fibers. During propagation of a normal sinus beat, activation of the AN zone accounts for at least 25% of conduction time from atrium to His bundle, the small N zone being the main source of AV nodal delay. Cycle length-dependent conduction delay is localized in the N zone. Conduction block of premature atrial impulses can occur both in the N zone and in the AN zone, depending on the degree of prematurity. Several factors determining AV nodal conduction delay have been identified.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Morphology and electrophysiology of the mammalian atrioventricular node. 245 33

Rosenblueth's hypothesis states that atrioventricular (AV) nodal conduction delay and Wenckebach periodicity of AV transmission are not due to overall decremental conduction within the AV node but are due to a single step delay which is caused by a special element or layer of the AV nodal tissue. This paper discusses some theoretical considerations which allow detailed evaluation of the original hypothesis. Two artificial conduction structures which incorporate the Rosenblueth phenomenon are presented and tested by theoretical experiments that consider the potential of these structures to produce (a) basic pattern of Wenckebach periods, (b) decremental shortening of RR intervals during Wenckebach periods. These experiments are also employed to test whether or not the Rosenblueth concept can be used to explain (c) appropriate dependence of AV conduction changes on the prematurity of atrial depolarizations, and of (d) alternating cycle lengths such as may be seen with atrioventricular reentrant tachycardia. The results of the theoretical considerations show that the original concept of the Rosenblueth hypothesis is sufficient to explain (a) but it cannot be used for realization of (b), (c) and (d). A modification of the original concept complying with both (a) and (b) is proposed. This modified structure can also reproduce (c), but not simultaneously with (b). The experiments show that anisotropy of intra AV nodal conduction may create an electrophysiological mechanism of single-step delay. Different anisotropic conduction structures have to be considered to reproduce phenomenon (d).
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PMID:Theoretical evaluation of the Rosenblueth hypothesis. 246 Aug 28

We postulated that comparison of ventriculoatrial intervals during junctional tachycardia and during right ventricular apical pacing may provide similar diagnostic information to that obtained from the insertion of ventricular extrasystoles during tachycardia. We studied 39 patients with either atrioventricular reentrant tachycardia (AVRT) (23 patients) using a single atrioventricular accessory pathway or atrioventricular nodal reentrant tachycardia (AVNRT) (16 patients). Ventriculoatrial [VA] intervals were measured during tachycardia, during right ventricular apical pacing at the same rate as that of the tachycardia and following a ventricular extrasystole delivered at the minimum reset interval (minimum prematurity of a ventricular extrasystole required to advance the subsequent atrial complex by more than 10 msec). The difference between the minimum VA interval during tachycardia and during ventricular pacing was closely related to both the minimum reset interval (r = 0.92, P less than 0.001) and the difference between the minimum VA interval during tachycardia and following a ventricular extrasystole delivered at the minimum reset interval (r = 0.97, P less than 0.001) in the 23 patients in whom the minimum reset interval could be determined. The ratio between the minimum ventriculoatrial interval during tachycardia and ventricular pacing could be determined in all cases and was between 1.53 and 1.68 in AVRT with right free wall (two patients), 0.94 and 1.29 with anteroseptal (three patients), 0.91 and 1.08 with posteroseptal (five patients) and 0.48 and 0.71 with left free wall (13 patients) pathways, while it was between 0.32 and 0.27 in AVNRT (16 patients). The ratio was more discriminative when corrected for ventricular latency and was also useful when calculated from the high right atrial electrogram. We concluded that comparison of ventriculoatrial intervals during junctional tachycardia and during right ventricular apical pacing can discriminate between the mechanisms of tachycardia and the site of pathway. It provides similar information to that obtained from ventricular extrasystoles during tachycardia with the advantage that it can be determined in all cases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diagnostic value of comparison of ventriculoatrial interval during junctional tachycardia and right ventricular apical pacing. 247 22

The well-known paradoxic behavior of atrioventricular conduction, the so-called gap phenomenon, that occurs when impulses within a certain range of coupling intervals are blocked while impulses with shorter coupling intervals are conducted is attributed to differences in properties of refractoriness in neighboring regions of the conduction system. In contrast, in the present study a model was developed showing a similar phenomenon, dependent on different electrophysiologic mechanisms and localized within the atrioventricular node in an isolated rabbit heart tissue preparation (n = 11). The hearts were paced at cycle length of 400-500 msec, and atrioventricular nodal conduction times (A2H2) were measured versus atrial extrastimulus (A1A2) coupling intervals by standard extrastimulus techniques. Postganglionic vagal stimulation was applied in the atrioventricular node as short bursts of subthreshold (for myocardium) stimuli with duration of 50-150 msec, amplitude of 20-800 microA, and absolute phase (delay after A1) of 0-500 msec. Vagal bursts with appropriate parameters consistently produced bimodal conduction curves. Initially, gradual shortening of the A1A2 coupling interval was associated with an increasing A2H2, with an accentuated increase (or even atrioventricular block) within an intermediate A1A2 range. However, further shortening of the A1A2 coupling interval produced a decrease in A2H2, which subsequently was followed by a block at the effective refractory period. Microelectrode recordings indicated that this characteristic bimodal pattern of conduction curves, demonstrating a gap, reflected transient vagally induced hyperpolarization in the N region of the node. In those instances where conduction block occurred and gap was manifest, the most marked hyperpolarization coincided with the time of arrival of midcycle premature extrastimuli, whereas the conduction of extrastimuli with either more or less prematurity was under less-marked vagal influence. Thus, this study demonstrates a new electrophysiologic mechanism producing anomalous conduction curves and the gap phenomenon within the atrioventricular node based on vagal-induced nonuniform recovery of diastolic excitability.
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PMID:A new mechanism for atrioventricular nodal gap-vagal modulation of conduction. 291 54

The influence of current strength on excitability and conduction of atrium and atrioventricular node was assessed in 25 patients using different current strengths (2, 3, 4, 5, 7, 10, 15 mA) and introducing extrastimuli (parasinusal zone) after the eighth paced complex of a basic drive (100 beats X min-1). Bipolar stimulation with the distal pole as cathode was performed so that effective and functional refractoriness of atrium and atrioventricular node, and the maximum value of atrial latency (interval between the extrastimulus and the beginning of atrial activity), intra-atrial conduction time, and AH interval could be determined at each current strength. In some patients atrioventricular nodal effective refractoriness could or could not be determined at each current strength, whereas in others the determination was possible only at the highest or the lowest current strengths. Moreover, the increase in current strength induced a progressive parallel reduction in both atrial effective and functional refractoriness; induced a progressive lengthening of intra-atrial conduction time (this was seen only in patients with a history of atrial arrhythmias); allowed the maximum possible lengthening of AH interval; and did not visibly influence atrioventricular nodal refractoriness and atrial latency. By altering atrial refractoriness and intra-atrial conduction time current strength affects the prematurity of the atrial impulse and the time at which it reaches the atrioventricular node. These findings should be taken into account when diagnostic and therapeutic electrophysiological procedures are performed.
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PMID:Influence of current strength on excitability and conduction of human atrium and atrioventricular node. 370 42


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