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PubMed1975

Wenckebach phenomenon within the atria.

A patient with a history of fainting and a bifacicular block (CRBBB plus LPH) was analyzed by His Bundle electrograms. During atrial pacing at a rate of 138/min, a Wenckebach type of block occurred within the atrium or at the electode-atrium junction, or both. The sinus intra-atrial conduction time (P-A inverval) was normal. During atrial pacing (pacing rate of 138 to 148/min), St-A interval progressively lengthened and ultimately a second degree Wenckebach type of block was obtained. The surface electrocardiogram (ECG) was normal and only electrical pacing brought on the intra-atrial conduction defect. Simultaneous with this atrial block, a second degree (Mobitz II) block developed.

Aged↗

PubMed2001

Effects of angiotensin-converting enzyme inhibition on the development of the atrial fibrillation substrate in dogs with ventricular tachypacing-induced congestive heart failure.

BACKGROUND: Atrial structural remodeling creates a substrate for atrial fibrillation (AF), but the underlying signal transduction mechanisms are unknown. This study assessed the effects of ACE inhibition on arrhythmogenic atrial remodeling and associated mitogen-activated protein kinase (MAPK) changes in a dog model of congestive heart failure (CHF). METHODS AND RESULTS: Dogs were subjected to various durations of ventricular tachypacing (VTP, 220 to 240 bpm) in the presence or absence of oral enalapril 2 mg. kg(-1). d(-1). VTP for 5 weeks induced CHF, local atrial conduction slowing, and interstitial fibrosis and prolonged atrial burst pacing-induced AF. Atrial angiotensin II concentrations and MAPK expression were increased by tachypacing, with substantial changes in phosphorylated forms of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38-kinase. Enalapril significantly reduced tachypacing-induced changes in atrial angiotensin II concentrations and ERK expression. Enalapril also attenuated the effects of CHF on atrial conduction (conduction heterogeneity index reduced from 3.1+/-0.4 to 1.9+/-0.2 ms/mm, P<0.05), atrial fibrosis (from 11.9+/-1.1% to 7.5+/-0.4%, P<0.01), and mean AF duration (from 651+/-164 to 218+/-75 seconds, P<0.05). Vasodilator therapy of a separate group of VTP dogs with hydralazine and isosorbide mononitrate did not alter CHF-induced fibrosis or AF promotion. CONCLUSIONS: CHF-induced increases in angiotensin II content and MAPK activation contribute to arrhythmogenic atrial structural remodeling. ACE inhibition interferes with signal transduction leading to the AF substrate in CHF and may represent a useful new component to AF therapy.

Angiotensin II↗

PubMed1980

[Hemodynamic and electrophysiologic effects of the new calcium antagonist Ro 11-1781 (author's transl)].

In a 3-part study the new calcium-antagonist Ro 11-1781 was investigated in respect to hemodynamic, electrophysiologic and antiarrhythmic effects. In the first part of the investigation, systolic time intervals were determined as an indicator of left ventricular performance in 10 patients without cardiac disease before and 5 min after i.v. injection of Ro 11-1781 (1 mg/kg/body weight). At the same time blood pressure was measured. There was a significant decrease in systolic and diastolic blood pressure (p < 0.01). Due to the resulting activation of the sympathetic nervous system by baroreflex, heart rate increased by 7 bpm (p < 0.01), there was a shortening of the pre-ejection period PEPc by 15 ms (p < 0.01), whereas left ventricular ejection time LVETc was not changed significantly. The ratio PEPc/LVETc decreased significantly (p < 0.01), reflecting the increase of left ventricular contractility, which results from the activation of the sympathetic nervous system. The PQ interval was increased (16 ms, p less than 0.01), an atrioventricular block however was not seen. In the second part of the investigation, sinus node function was studied in 8 patients by His-bundle electrography and programmed stimulation of the right atrium. There was no significant change in sinus-node recovery time, sinu-atrial conduction time, sinus-node rate and atrial conduction time in response to Ro 11-1781. However, in 2 patients with sinus-bradyarrhythmia a second-degree sinu-atrial block was provoked by the calcium-antagonist. The drug was shown to have a negative dromotrope effect to the AV node, reflected by an increase of the PQ interval (p < 0.01), AH interval (p < 0.01) and a decrease (p < 0.01) of the maximal 1:1 conduction of the AV node, whereas the HV interval was not changed significantly. The antiarrhythmic effects of Ro 11-1781 were studied in 13 patients with atrial flutter, atrial fibrillation or paroxysmal supraventricular tachycardia: In 10 patients the injection of the calcium-antagonist produced a marked decrease in ventricular rate for a short time reflecting a neagative dromotrope effect in the AV node. In 5 patients conversion to sinus rhythm was observed.

Adult↗

PubMed1977

[Intra-atrial excitation conduction and atrioventricular nodex conduction].

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Action Potentials↗

PubMed1997

Prevalence of retrograde accessory pathway conduction during atrial fibrillation.

INTRODUCTION: Although atrial fibrillation occurs frequently in patients with the preexcitation syndrome, its pathogenesis remains controversial. The purpose of this study was to test the hypothesis that retrograde conduction over the accessory pathway occurs during atrial fibrillation and can serve as an important source of new wavefronts in atrial fibrillation. METHODS AND RESULTS: Eight patients undergoing surgical division of their accessory pathway(s) were studied. A plaque electrode array containing 56 (7 x 8) bipolar electrodes (5-mm resolution) was placed epicardially at the AV junction over the accessory pathway and atrial fibrillation was electrically induced. Excluding one patient who had only preexcited QRS complexes during atrial fibrillation and another whose accessory pathway was outside the mapped region, 4 of the 6 patients studied showed retrograde conduction over the accessory pathway during atrial fibrillation (mean atrial cycle length 157 +/- 59 msec). In these patients, 186 atrial wavefronts near the accessory pathway were analyzed. Among 67 wavefronts immediately following nonpreexcited QRS complexes, 17 originated from retrograde conduction. This constituted 9% (17/186) of total atrial wavefronts near the accessory pathway. Estimated atrial refractory period during atrial fibrillation ranged from 81 to 165 msec. CONCLUSIONS: (1) In patients with the preexcitation syndrome and atrial fibrillation, retrograde conduction over the accessory pathway contributed up to 9% of total atrial wavefronts near the accessory pathway. (2) The presence of an excitable gap in human atrial fibrillation was suggested by atrial preexcitation during retrograde conduction.

Atrial Fibrillation↗

PubMed1984

[Effects of digitalis on the parameters of sinus function in sick sinus syndrome. Evaluation using a multiprogrammable permanent atrial pacemaker with temporary inhibition].

A non invasive electrophysiological study was performed in eight patients with sick sinus syndrome using a multiprogrammable AAI pacemaker (Medtronic Spectrax Sxt) with temporary pacing inhibition. We measured the corrected sinus node recovery time and sino-atrial conduction time (Narula method) before and after digoxin administration (acutely iv and orally for 10 days). Digitalis lengthened both the corrected sinus node recovery time and the sino-atrial conduction time; in particular, after the long-term oral treatment sinus function worsened markedly. The prolongation of the sino-atrial conduction time seems to be related to an indirect effect of the drug, since its disappears after atropine administration. Our results suggest that patients with the sick sinus syndrome need permanent pacing when long-term treatment with digitalis is requested; the pacemaker we used permits a non-invasive long-term evaluation of sinus function in such patients.

Administration, Oral↗

PubMedDate not supplied

[Effect of atrio-ventricular conduction on the appearance of supraventricular arrhythmia and thrombotic complications in patients with chronic stimulation of cardiac ventricles in sick sinus syndrome].

Two hundred three patients with sick sinus node disease were treated with continuous ventricular stimulation between 1981 and 1985. To 1988, 168 patients aged between 26 and 88 years were followed-up for 5.1 years on the average. All these patients were divided into two groups: I (93 patients) with sinusal bradycardia, and group II (93 patients) with brady-tachycardia. Ventriculo-atrial conduction was seen in 82.61% of patients of group I in whom the implantation of electric stimulator produced the attacks of atrial fibrillation, and in 44.23% of patients without such attacks (p < 0.01); in 80.77% of patients of group II in whom atrial fibrillation became stable with time, and in 50.57% with intermittent atrial fibrillation (p < 0.01) ventriculo-atrial conduction was noted. It may be concluded, that the presence of ventriculo-atrial conduction in patients with prolonged stimulation of the cardiac ventricles favor the occurrence and stabilization of the paroxysmal atrial fibrillation and thrombotic complications.

Adult↗

PubMed2002

Mechanisms for atrial fibrillation in patients with Wolff-Parkinson-White syndrome.

INTRODUCTION: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). METHODS AND RESULTS: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long-term follow-up (17+/-7 months). CONCLUSION: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP-dependent atrial vulnerability, and the other is intrinsic and AP-independent atrial vulnerability.

Adolescent↗

PubMed1979

Human electropharmacology of the calcium antagonist dimeditiapramine (Ro 11-1781) in coronary patients.

The electrophysiological effect of dimeditiapramine (Ro 11-1781), a Ca2+ antagonist, was evaluated in 20 patients with coronary heart disease. Electrophysiological measurements, including sinus cycle length, sinoatrial conduction time, intra-atrial conduction time, atrial, atrioventricular, nodal and ventricular refractory periods and intraventricular conduction time were recorded before and after the intravenous administration of Ro 11-1781. At a dose which is effective against cardiac arrhythmias, Ro 11-1781 produced no statistical significant changes in the sinoatrial and intraventricular conduction time. Similarly, neither the sinoatrial nor the ventricular refractory period was affected. Ro 11-1781, however, increased the atrioventricular conduction time and decreased the systolic blood pressure to a statistically significant extent. The tolerance was very good.

Adult↗

PubMed1997

Electrophysiological properties in patients undergoing atrial compartment operation for chronic atrial fibrillation with mitral valve disease.

AIMS: Surgical treatment for atrial fibrillation is now feasible in selective cases. The aim of this study was to assess the electrophysiological properties of patients undergoing atrial compartment operation for chronic atrial fibrillation. METHODS AND RESULTS: Electrophysiological studies were performed in 20 mitral valve patients with atrial fibrillation who had been maintained in sinus rhythm for more than 1 year after atrial compartment operation. Intra-cardiac recording and programmed electrical stimulation were performed in various atrial compartments. The parameters studied included sinus node function, atrial conduction and refractoriness, atrioventricular conduction function and inducible arrhythmias if any. Intra-cardiac recordings showed that the rhythm was of sinus origin in all cases, with the earliest atrial activity located in the high right atrium. The mean sinus cycle length was 750 +/- 110 ms, AH time 106 +/- 29 ms, and HV time 53 +/- 7 ms. The sinus node function was normal in 18 patients (90%), and only two patients had prolonged sinus node recovery and sino-atrial conduction. The right atrial appendage compartment was driven by the sinus node in all patients. However, the conduction time from the high right atrium to the right atrial appendage compartment was markedly prolonged in 12 of 15 patients (80%) undergoing the three-compartment operation in which an incision was placed between the high right atrium and right atrial appendage compartments. On the other hand, the electrical activities in the left atrial compartment were much more varied. In 13 of 20 patients (65%), the left atrial compartment was driven by the sinus node; 11 of the 13 patients had a normal or mildly prolonged conduction time (ranged 75 to 146 ms), whereas two patients had a marked delay in conduction (200 ms and 266 ms, respectively). In the remaining seven patients, the left atrial compartments were dissociated from the rest of the heart; five of them had a quiescent left atrium, one a fluttering left atrial rhythm, and one a slow left atrial rhythm. The effective refractory period was longer in the left atrial compartment (242 +/- 47 ms) as compared to that of the high right atrium (224 +/- 26 ms, P < 0.01) and right atrial appendage compartments (219 +/- 25 ms, P < 0.01). Programmed electrical stimulation could not induce atrial fibrillation in any patient, whereas two patients had inducible atrial flutter and three repetitive atrial responses. CONCLUSIONS: (1) Atrial compartment operation does not impair sinus node function in most cases. (2) Elimination of atrial fibrillation while maintaining the electrical connection between different atrial compartments is feasible.

Adolescent↗

PubMed2026

Association between plasma homocysteine levels and P-wave dispersion in pediatric patients with hyperhomocysteinemia.

UNLABELLED: Hyperhomocysteinemia has been recognized as a cardiovascular risk factor associated with endothelial dysfunction, oxidative stress, and vascular inflammation. Experimental and clinical studies suggest that elevated homocysteine levels may also influence myocardial electrophysiology and contribute to arrhythmogenesis. However, data regarding the relationship between homocysteine levels and electrocardiographic markers of atrial conduction in pediatric populations remain limited. This study aimed to evaluate the association between plasma homocysteine levels and electrocardiographic parameters, particularly P-wave dispersion, in children. This multicenter retrospective case-control study included pediatric patients evaluated in four tertiary pediatric metabolism centers between January 2023 and December 2025. A total of 47 patients with hyperhomocysteinemia (plasma total homocysteine ≥ 15 µmol/L) and 43 age- and sex-matched controls with normal homocysteine levels were included. Controls were selected from the screened population among children with available homocysteine measurements, electrocardiographic and echocardiographic evaluations, and no confirmed inherited metabolic disease or cardiac disorder. Clinical, biochemical, and electrocardiographic parameters, including maximum P-wave duration and P-wave dispersion, were retrospectively analyzed. A total of 90 participants were included, comprising 47 children with hyperhomocysteinemia and 43 healthy controls. P-wave dispersion and maximum P-wave duration were significantly higher in the hyperhomocysteinemia group compared with controls (48.96 [19.48-100.0] vs. 38.57 [10.57-71.19] ms, p < 0.001). Plasma homocysteine levels showed a moderate positive correlation with P-wave dispersion (ρ = 0.441, p < 0.001). These differences were more pronounced in children with higher homocysteine levels and in younger age groups (< 2 years and 2-14 years). In contrast, PR interval (p = 0.790) and QTc interval (p = 0.183) did not differ significantly between groups. Vitamin B12 levels were significantly lower in the hyperhomocysteinemia group (p = 0.013), while folate levels were comparable (p = 0.974). Although sodium, potassium, and magnesium levels differed significantly between groups, all values remained within normal physiological ranges. CONCLUSIONS: Children with hyperhomocysteinemia showed increased P-wave dispersion compared with controls. These findings suggest an association between elevated homocysteine levels and altered atrial conduction parameters in children. Further prospective studies are needed to determine the clinical significance of these findings. WHAT IS KNOWN: • Hyperhomocysteinemia is associated with cardiovascular risk and endothelial dysfunction. • Elevated homocysteine levels have been linked to cardiac electrophysiological alterations in adult populations. WHAT IS NEW: • Elevated homocysteine levels are associated with increased P-wave dispersion in children, with more pronounced effects observed in younger age groups. • These findings support an association between hyperhomocysteinemia and altered atrial conduction parameters in children.

Adolescent↗

PubMed1977

Effect of lidocaine and methyl lidocaine on cardiac conduction.

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.

Animals↗

PubMed1986

Influence of current strength on excitability and conduction of human atrium and atrioventricular node.

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.

Electric Stimulation↗

PubMed1999

[Clinical efficacy of non-invasive evaluation of intra- and interatrial conduction in patients with ischemic heart disease].

AIM: To try feasibility of non-invasive registration of intra- and interatrial conduction by means of simultaneous registration of echo-CG (in B and M modes) and ECG. MATERIALS AND METHODS: The time of intra- and interatrial conduction was measured at simultaneous registration of echo- CG (B and M modes) and ECG in standard lead II. The time of atrial conduction was registered in ms from the start of ECG wave "P" to beginning of echo-CG mechanical contractions. The results were compared to those obtained at the direct method (registration of atrial conduction by electrode fixed on the atrial myocardium). RESULTS: The data by the two above methods showed high correlation (for intraatrial conduction r = 0.93, for the interatrial one r = 0.85). The study confirmed the leading role of end-diastolic volume of the left ventricle and/or uneven wave movement along the atria in development of supraventricular arrhythmia in coronary heart disease. CONCLUSION: The proposed non-invasive method can find application for estimation of atrial conduction both in clinical practice and experiment. The time of exitation conduction through the atria measured by the new non-invasive method and the direct method is almost the same.

Animals↗

PubMed2004

Novel pore mutation in SCN5A manifests as a spectrum of phenotypes ranging from atrial flutter, conduction disease, and Brugada syndrome to sudden cardiac death.

OBJECTIVES: The purpose of this study was to determine the clinical and biophysical characteristics of a novel SCN5A mutation. BACKGROUND: Brugada syndrome and isolated cardiac conduction defect have been linked to SCN5A mutations. METHODS: Eleven members of a western European family underwent electrophysiologic investigations and mutation analysis of the SCN5A gene. Wild-type and mutant SCN5A channels were expressed in HEK293 cells, and whole cell currents were studied using patch clamp procedures. RESULTS: A novel mutation, R376H, in the first pore segment of SCN5A variably causes Brugada syndrome and/or conduction disease in a single family. Biophysical analysis demonstrated a significant current reduction for the mutant, a pathophysiologic profile consistent with Brugada syndrome and isolated cardiac conduction defect. Among 11 family members, 9 were carriers of the mutation. The proband's initial presentation was a saddleback Brugada ECG, atrial flutter, and diffuse conduction disturbances. He had no inducible ventricular arrhythmias but experienced sudden cardiac death. His brother was affected by atrial flutter and had a clear conduction disorder, but he did not display baseline or evocable ECG signs of Brugada syndrome. He received an implantable cardioverter-defibrillator that delivered one appropriate shock after 1 year of follow-up. The phenotype in the family members was highly variable and ranged from noninducible and inducible asymptomatic carriers of the mutations to isolated conduction disease and to symptomatic Brugada syndrome. CONCLUSIONS: We describe the functional characterization of a novel SCN5A pore mutation, R376H, with variable clinical expression in the same family. Differentiating between electrophysiologic entities (Brugada syndrome-isolated cardiac conduction defect) is more challenging. Recognition of factors modifying the clinical presentation may be important for clinical decision making.

Adolescent↗

PubMed1989

Transient complete AV block in Lyme disease. Electrophysiologic observations.

The findings in a patient with complete AV block and intra-atrial conduction disturbances due to Lyme disease are presented. The electrocardiographic follow-up and serial EP findings suggest that complete AV block in Lyme disease may signify a more extensive affection of the AV conduction system (with eventually attendant intra-atrial conduction disturbances) than described in earlier reports. An almost complete resolution of the considerable damage to the conduction system occurred within two weeks.

Adult↗

PubMed1979

[Systematic study of ventriculo-auricular conduction and its importance in the detection of aberrant conduction pathways].

Ventriculo-atrial conduction was studied by ventricular pacing in three groups of patients: 34 cases with the preexcitation syndrome on surface ECG, 35 cases with documented paroxysmal atrial tachycardia but with otherwise normal ECGs and 120 cases without either of these two conditions. This conduction time was unchanged up to pacing rates of over 160/min in 88 p. 100 cases with preexcitation and was thus a sign of a nodal short-circuit. This phenomenon was also observed in 85 p. 100 cases with isolated paroxysmal atrial tachycardia and in 20 p. 100 normal cases which suggests the presence of a latent accessory pathway in these patients.

Adolescent↗

PubMed1985

Electrophysiological effects of ethmozine in perfused rabbit hearts.

His-bundle electrocardiography was used to evaluate the effects of ethmozine on cardiac conduction in isolated perfused rabbit hearts electrically driven at cycle lengths of 320 and 250 ms. There was no significant change in conduction until high concentrations of ethmozine were reached. His-Purkinje and atrioventricular (AV) nodal conduction were slowed significantly at 0.1 microgram/mL and atrial conduction at 1.0 microgram/mL. Conduction block occurred at 10.0 micrograms/mL in all the hearts treated. Effects of the drug (0.1 and 0.01 microgram/mL) on conduction of extrasystoles were also studied in hearts driven at a basic cycle length of 270 ms. No significant change was observed in atrial conduction of extrasystoles throughout the coupling intervals tested at both concentrations. Ethmozine (0.01 and 0.1 microgram/mL) caused slowing of His-Purkinje conduction of extrasystoles but the effect of the drug did not change as a function of the coupling interval. An interval-dependent increase in AV-nodal conduction time was observed, with the maximum slowing of conduction occurring at coupling intervals close to the effective refractory period of the AV node. AV-nodal functional refractory period was increased significantly by ethmozine (0.01 and 0.1 microgram/mL). The effective refractory period was significantly increased only at the higher concentration.

Animals↗