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PubMed2000

Atrial automaticity and atrioventricular conduction in athletes: contribution of autonomic regulation.

Little is known about the sinoatrial automatism and atrioventricular conduction of trained individuals who present a normal resting electrocardiogram. We used transesophageal atrial stimulation, a minimally invasive technique, to evaluate aerobically trained athletes (n = 10) and sedentary individuals (n = 10) with normal resting electrocardiograms, to test the hypothesis that parasympathetic tone, as detected by heart rate variability, could be associated with changes in sinoatrial automatism and atrioventricular conduction. Corrected sinus node recovery time tended to be longer in athletes than in sedentary individuals, but this difference did not reach statistical significance. The Wenckebach point occurred at a lower rate in athletes than in the controls. Over a 24-h period of measurement, the mean RR interval was longer in the athletes than in the sedentary individuals. The mean square root of successive differences (rMSSD) tended to be higher in athletes than in controls, but this difference did not reach statistical significance. There was a moderate correlation (r = 0.48, P < 0.05) between the index of atrioventricular conduction, the rate at the Wenckebach point, and the logarithmically transformed rMSSD. Thus, as a corollary to its effects on the sinus node, where increased parasympathetic tone, decreased sympathetic tone, and non-autonomic components may contribute to sinus bradycardia, it is possible that athletic training may also induce intrinsic adaptations in the conduction system, which could contribute to the higher prevalence of atrioventricular conduction abnormalities observed in athletes.

Adult↗
PubMed2003

Three-dimensional noncontact mapping defines two zones of slow conduction in the circuit of typical atrial flutter.

The cavotricuspid isthmus (CTI) is a slow conduction area in the circuit of typical atrial flutter. However, conventional methods are limited by the inaccuracy of measurements of distance on the surface of the heart. The aim of the study was to define the conduction properties of the atrial flutter circuit along the tricuspid annulus by using a three-dimensional noncontact mapping system. In 34 atrial flutter patients (30 men, 4 women; mean age 54 +/- 14; 27 counter-clockwise, 4 clockwise, and 3 both), a noncontact multielectrode array was used to reconstruct electrograms in the right atrium. Isochronal and isopotential propagation mapping was performed during atrial flutter. The conduction velocity was calculated by dividing conduction time by surface distance. The right atrium along the tricuspid annulus was divided into five regions: lateral wall, superior right atrium, septum, septal CTI, and lateral CTI. Conduction velocities were 0.99 +/- 0.85, 1.67 +/- 1.21, 1.58 +/- 1.05, 0.82 +/- 0.72, and 1.68 +/- 1.00 m/s in counter-clockwise and 0.81 +/- 0.71, 2.61 +/- 1.90, 1.52 +/- 0.91, 0.91 +/- 0.80 and 1.91 +/- 0.83 m/s in clockwise, respectively. Conduction velocities were significantly slower in the septal CTI and lateral wall than in the lateral CTI, the septum, and the superior right atrium (P < 0.05). No significant difference was found between the septal CTI and the lateral wall. Conduction within the septal CTI was slower in patients treated with antiarrhythmic agents than in untreated patients (P < 0.05). The septal part of the CTI (but not the lateral CTI) and the lateral wall are slow conduction zones in the atrial flutter circuit, and both may, therefore, be mechanically important for the development of atrial flutter.

Atrial Flutter↗
PubMed1994

Substance P nerve terminals synapse upon negative chronotropic vagal motoneurons.

Previous data indicate that there are anatomically segregated and physiologically independent parasympathetic ganglia on the surface of the heart which are capable of selective control of sino-atrial rate, atrio-ventricular conduction, and atrial contractility. We have injected a retrograde tracer into the cardiac ganglion which selectively regulates heart rate (the SA ganglion). Medullary tissues were processed for the histochemical visualization of retrogradely labeled neurons and for the immunohistochemical detection of the neurotransmitter substance P (SP) by dual labeling light and electron microscopic methods. Negative chronotropic retrogradely labeled cells were found in a long slender column in the ventrolateral nucleus ambiguous (NA-VL) which enlarged somewhat at the level of the area postrema. These cells were found bilaterally, but they were asymmetrically distributed. Half the animals showed a pronounced right side predominance in retrograde labeling, while the other half of the animals showed a lesser left side predominance. These observations may help to explain some of the controversy in the literature concerning the relative influence of the right and left vagus nerves on sinus rate. Ultrastructural examination demonstrated axo-somatic and axo-dendritic contacts between SP nerve terminals and retrogradely labeled negative chronotropic NA-VL neurons. SP immunoreactivity was often associated with large dense-core vesicles in terminals forming either symmetric or asymmetric synapses. These observations provide a potential anatomical substrate for the centrally mediated bradycardia elicited by microinjections of SP into the NA. SP immunoreactive terminals were also observed to make axo-somatic, axo-dendritic, and axo-axonic synapses with unlabeled neurons in NA-VL.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effects of intravenous lidocaine on cardiac sympathetic nerve activity and A-V conduction in halothane-anesthetized cats.

To study neural contributions to the alterations in intracardiac conduction induced by i.v. lidocaine, we measured cardiac sympathetic nerve activity (CSNA) simultaneously with sinus cycle length (SCL) and A-V cats. Sixteen cats were anesthetized with halothane in oxygen and mid-sternotomized. The His-bundle electrogram and CSNA were recorded from an electrode placed in the interatrial septum and from the left ventrolateral or ventromedial nerve, respectively. Atrium-His (A-H), His-Purkinje (H-V), and total intraventricular (H-S) conduction times were measured during atrial pacing conducted at a cycle length of 300 ms. In eight cats, 1 MAC, 2 MAC, and 3 MAC halothane were given during i.v. lidocaine (Groups H-1, H-2 and H-3). In the other eight cats, anesthesia was switched from halothane to i.v. alpha-chloralose (30-50 mg.kg BW-1; Group C). A significant decrease in CSNA with i.v. lidocaine, 2 mg.kg BW-1 was recognized in Groups C and H-1, but not in Groups H-2 and H-3. Prolongations of SCL during the spontaneous cycle, A-H and H-V in the paced mode following i.v. lidocaine were significant in Groups C, H-1 and H-2, but not significant in Group H-3. We conclude that i.v. lidocaine induces a significant decrease in CSNA during alpha-chloralose or 1 MAC halothane anesthesia which partly contributes to the control of intracardiac conduction.

Anesthesia, Inhalation↗
PubMed1999

Promotion of atrial fibrillation by heart failure in dogs: atrial remodeling of a different sort.

BACKGROUND: Studies of atrial fibrillation (AF) due to atrial tachycardia have provided insights into the remodeling mechanisms by which "AF begets AF" but have not elucidated the substrate that initially supports AF before remodeling occurs. We studied the effects of congestive heart failure (CHF), an entity strongly associated with clinical AF, on atrial electrophysiology in the dog and compared the results with those in dogs subjected to rapid atrial pacing (RAP; 400 bpm) with a controlled ventricular rate (AV block plus ventricular pacemaker at 80 bpm). METHODS AND RESULTS: CHF induced by 5 weeks of rapid ventricular pacing (220 to 240 bpm) increased the duration of AF induced by burst pacing (from 8+/-4 seconds in control dogs to 535+/-82 seconds; P<0.01), similar to the effect of 1 week of RAP (713+/-300 seconds). In contrast to RAP, CHF did not alter atrial refractory period, refractoriness heterogeneity, or conduction velocity at a cycle length of 360 ms; however, CHF dogs had a substantial increase in the heterogeneity of conduction during atrial pacing (heterogeneity index in CHF dogs, 2. 76+/-0.16 versus 1.46+/-0.10 for control and 1.51+/-0.06 for RAP dogs; P<0.01) owing to discrete regions of slow conduction. Histological examination revealed extensive interstitial fibrosis (connective tissue occupying 12.8+/-1.9% of the cross-sectional area) in CHF dogs compared with control (0.8+/-0.3%) and RAP (0. 9+/-0.2%) dogs. CONCLUSIONS: Experimental CHF strongly promotes the induction of sustained AF by causing interstitial fibrosis that interferes with local conduction. The substrates of AF in CHF are very different from those of atrial tachycardia-related AF, with important potential implications for understanding, treating, and preventing AF related to CHF.

Animals↗
PubMed1992

[Secretion of atrial natriuretic peptide during artificial pacing: assessments including the influence of ventriculoatrial conduction].

Secretion of atrial natriuretic peptide (ANP) depends on the atrial wall distension which may be caused by ventricular pacing. This study was designed to assess the differences in plasma ANP level between DDD and VVI pacing. We measured ANP from venous blood samples using radio-immunoassay in patients with the sick sinus syndrome (n = 8) and atrioventricular block (n = 2) following DDD implantation. Measurement was made under control conditions during DDD and 15-180 min after the pacing mode was changed to VVI and 60 min after returning to DDD. Serum epinephrine (E), norepinephrine (NE), renin (R) and aldosterone (A) levels were also measured prior to and every 30 min after pacing mode changes. The plasma ANP concentration changed from 71.3 pg/ml (normal value) with DDD to 126.8 (15 min), 180.6 (30 min), 221.8 (60 min), 219.2 (90 min), 270.1 (120 min), 145.4 (150 min) and 115.1 pg/ml (180 min) with VVI. It increased markedly, then gradually decreased. It returned to the control value (66.6 pg/ml) in 60 min with DDD, and it reached the peak level with VVI within 60-120 min, and the peak was significantly higher than that for DDD. The increase related to the retrograde ventriculoatrial conduction during VVI pacing. There was no significant change in the NE, E, R and A concentrations. Systolic blood pressure decreased 15 mmHg in VVI and returned to normal by DDD. These results indicated that plasma ANP levels is elevated by VVI pacing, though it was not explained by ventricular pacing alone.

Aged↗
PubMed1983

Identical QRS complexes during atrial fibrillation with aberrant conduction and ventricular tachycardia. The value of a His bundle recording.

In a patient with chronic congestive heart failure, right bundle branch block-shaped QRS complexes occurred in salvos during atrial fibrillation. The site of origin of these complexes could not be determined from the 12-lead ECG alone. Recording of a His bundle electrogram showed that both intraventricular aberrant conduction and ventricular tachycardia were responsible for salvos having the same QRS complexes in the 12-lead ECG.

Aged↗
PubMed1993

Effects of diltiazem on concealed atrioventricular nodal conduction in relation to ventricular response during atrial fibrillation in anesthetized dogs.

By means of a new quantitative index for concealed conduction, we evaluated the effects of diltiazem on atrioventricular (AV) node concealment and correlated this index with the variability of the ventricular response during atrial fibrillation in 16 anesthetized mongrel dogs. After determination of the atrial effective refractory period (ERP), AV nodal ERP (AVNERP), concealment zone, and concealment index (AVNERP of blocked atrial extrasystole/AVNERP of conducted atrial extrasystole), the R-R intervals during atrial fibrillation induced by electrical stimulation were measured. Both low (0.1 mg/kg) and medium (0.2 to 0.4 mg/kg) doses of diltiazem prolonged the AVNERP and increased the mean R-R interval during atrial fibrillation. Only medium doses of diltiazem increased the degree of concealed conduction in the AV node and accentuated the variability of R-R intervals. There was a good positive correlation between the variability of the ventricular response during atrial fibrillation and the concealment index. In conclusion, medium doses of diltiazem are more effective in reducing heart rate during atrial fibrillation than a low dose. However, medium doses also increase the degree of concealed conduction in the AV node and enhance the irregularity of the ventricular response during atrial fibrillation. Measurement of the concealment index is useful for quantitating the degree of concealed conduction in the AV node, which is actually an important determinant of the ventricular response during atrial fibrillation.

Animals↗
PubMed1979

[Quantitative description of a calcium induced potassium conductance of the rabbit atrial myocardium by variation of the Ca++ concentration].

Action potentials of trabeculae from the left rabbit atrium were studied using a modified sucrose gap method. A mathematical treatment of the action potential time course and the phase plane trajectories gives an approximation of a potassium conductance of gK.GK increases be action potential shows a maximum at 1 s.gK reaches a steady state level after 40 s. The experimental findings are interpreted by means a mathematical model of a Ca++-induced K+-conductance.

Action Potentials↗
PubMed1993

Anatomy, histology, and pathology of the cardiac conduction system: Part I.

Normal anatomic and histologic features of the sinus node, atrial myocardium, and interatrial conduction of the cardiac impulse are reviewed. The controversy surrounding atrial conduction via specialized atrial cells versus specific internodal tracts (between sinus and atrioventricular nodes) is discussed.

Age Factors↗
PubMed1993

Adenosine induced intraatrial block.

Adenosine, an endogenous nucleoside with potent negative chronotropic and dromotropic effects on the sinus and AV nodes, is thought to have little if any antiarrhythmic effect on normal atrial tissue. However, there may be an electrophysiological basis for an adenosine effect on atrial tissue with atypical conduction properties. We examined the electrophysiological effects of adenosine in a patient with decremental atrial conduction properties. During incremental pacing from the high right atrium there was gradual prolongation of the intraatrial interval between the high right atrium and the low septal atrium, from 180 to 280 msec, until 2:1 intraatrial block occurred at a pacing cycle length of 280 msec. Adenosine (6 mg IV) resulted in transient intraatrial block followed by prolonged intraatrial conduction during high right atrial pacing at a cycle length of 400 msec. Thus, similar to its effects on the AV node and decremental AV accessory pathways, adenosine may also slow and abolish conduction in decremental atrial issue, an effect that is likely attributed to adenosine induced hyperpolarizing K+ current in partially depolarized atrial tissue.

Adenosine↗
PubMed1991

Distribution of atrial natriuretic peptide in the conduction system and ventricular muscles of the human heart.

Atrial natriuretic peptide (ANP), a cardiac hormone, is known to be located in the atrial specific granules, but its presence and localization in the ventricular muscle of the human heart has not been examined fully. Using a specific antibody to human ANP, we studied the conduction system and ventricular muscle with immunohistochemical and ultrastructural methods in 30 hearts obtained at autopsy. These included 12 normal and 18 diseased hearts. In the normal hearts, ANP-positive granules, which were regularly observed in the atrial myocytes, were found in small quantities in the cells of the penetrating and branching bundles in 4 of 12, and in the cells of the ventricular free walls in 2 of the 12 hearts. In the diseased hearts, the positivity increased significantly (P less than 0.05), being found in 13 of 18 (72.2%) conduction systems and 10 of 18 (55.6%) ventricular muscles. The granules were confirmed to be immunoreactive with ANP by ultrastructural examination. Furthermore, the presence of ANP mRNA in the conduction system as well as in the ventricular myocytes was demonstrated by Northern blot hybridization for which we used the complementary DNA of human ANP. Thus, a small quantity of ANP appears to be synthesized and stored in the conduction system and ventricles of some normal hearts. However, ANP was shown to be present in a larger percentage of the diseased hearts.

Aged↗
PubMed1988

Atrial natriuretic peptides inhibit conductive sodium uptake by rabbit inner medullary collecting duct cells.

The inner medullary collecting duct (IMCD) effects net sodium reabsorption under the control of volume regulatory hormones, including atrial natriuretic peptides (ANP). These studies examined the mechanisms of sodium transport and its regulation by ANP in fresh suspensions of IMCD cells. Sodium uptake was inhibited by amiloride but insensitive to furosemide, bu-metanide, and hydrochlorthiazide. These results are consistent with uptake mediated by a sodium channel or Na+/H+ exchange. To determine the role of sodium channels, cells were hyperpolarized by preincubation in high potassium medium followed by dilution into potassium-free medium. Membrane potential measurements using the cyanine dye, Di(S)-C3-5 verified a striking hyperpolarization of IMCD cells using this protocol. Hyperpolarization increased the apparent initial rate of sodium uptake fourfold. Amiloride and ANP inhibited potential-stimulated sodium uptake 73% and 65%, respectively; the two agents together were not additive. Addition of 5 mM sodium to hyperpolarized cells resulted in a significant amiloride-sensitive depolarization. Half-maximal inhibition of potential-driven sodium uptake occurred at 3 X 10(-7) M amiloride, and 5 X 10(-11) M ANP. We conclude that sodium enters IMCD cells via a conductive, amiloride-sensitive sodium channel, which is regulated by ANP. ANP inhibition of luminal sodium entry in the IMCD appears to contribute to the marked natriuretic effect of this hormone in vivo.

Amiloride↗