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At least 883 records · Page 49Linked to original sources
PubMed1981

Properties of an acetylcholine-induced conductance in the rabbit atrial myocardium.

Using a conventional microelectrode technique, action potentials (A.P.) recorded from the isolated left atrial trabeculae of the rabbit were analyzed. The membrane current during A.P. was reconstructed. In spite of an extracellular Ca2+-deficiency and the application of verapamil, acetylcholine (ACh) reduced the A.P. duration by inducing an outward current IACh. This current was blocked by atropine (10-6 M). A Nernst-plot of the reversal potential at different K+-concentrations showed a slope of 58.5 mV for a 10-fold change in concentration. After pacing pauses longer than 10 s an inward going (anomalous) rectification (A.R.) for IACh occurred. Increasing the duration of the pacing pauses the rectification was more accentuated. During a constant pacing the A.R. for IACh disappeared. ACh did not modify the A.R. The maximum slope conductance for IACh was dependent on the extracellular concentration of ACh (0.035 mS x cm-2 at 20 microM ACh, 0.012 mS x cm-2 at 0.2 microM ACh). The experimental results are discussed, using the model of an ACh-induced potassium channel. The channel should be related to the muscarinic receptor of the atrial myocardium.

Acetylcholine↗
PubMed2006

Narrow, slow-conducting isthmus dependent left atrial reentry developing after ablation for atrial fibrillation: ECG characterization and elimination by focal RF ablation.

INTRODUCTION: The complete circuit of reentrant left atrial tachycardias (LATs) occurring after ablation for atrial fibrillation (AF) has not been well described. Identifying discrete isthmuses critical to these LATs may simplify their elimination by catheter ablation. METHODS AND RESULTS: Fifteen patients (all male, 56 +/- 8 years) with 15 reentrant LATs following AF ablation underwent activation and entrainment mapping. Eleven patients (11 LATs) had a single localized site with low amplitude (0.16 +/- 0.05 mV), fractionated long duration (131 +/- 23 msec) electrograms coinciding with an isoelectric interval of 106 +/- 24 msec between flutter waves on all 12 ECG leads. Three-dimensional mapping and entrainment revealed this site to be a narrow markedly slowly conducting isthmus adjacent to ablated left (n = 8) or right (n = 3) pulmonary vein (PV) ostia, and critical to nine small diameter (15 +/- 3 mm) and two large diameter (49 +/- 2 mm) circuits. One radiofrequency (RF) application on this isthmus eliminated LAT in all 11 patients. Four patients (four LATs) with large circuits around the mitral annulus and/or PV ostia lacked isoelectric ECG intervals and slow-conducting isthmuses and required multiple RF applications across anatomically wide, rapidly conducting isthmuses. CONCLUSION: Focally ablatable narrow isthmuses of slow conduction are critical for the majority of reentrant LAT occurring after ablation for AF. The role and presence of these isthmuses can be anticipated by observing significant isoelectric intervals between flutter waves on all 12-surface ECG leads. Their distinctive electrophysiological characteristics allow their identification and elimination by simple RF ablation.

Atrial Fibrillation↗
PubMed1990

[Atrio-ventricular conduction in patients with permanent right-ventricular stimulation. I. Possibilities of evaluation by the method of trans-esophageal electrocardiogram].

UNLABELLED: We analyzed 214 patients with permanent, VVI mode stimulation divided in 5 groups. Group I 89 patients (pts) with sick sinus syndrome (sss) (mean age 60 +/- 14 yrs), group II 21 pts with sss and atrioventricular (a-v) conduction disturbances (mean age 54 +/- 19 yrs), group III 72 pts with a-v block, but without intraventricular conduction disturbances (mean age 68 +/- 11 yrs), group IV 20 pts with a-v block and registered bundle branch block (mean age 67 +/- 7) and group V 12 pts after His bundle ablation (mean age 51 +/- 20 yrs). In all pts we recorded leads I, II, III, V1, V6 and oesophageal (oe) on Mingophon 7 (Siemens-Elema) with paper speed 50 mm/s. All recordings were performed during basic and magnetic rate of the pulse generator. We could analyzed ventriculo-atrial (v-a) conduction in group I-IV respectively in 89.9%, 95.3%, 84.7%, 100%, 83.3% and in all population in 89.2% cases. In 23 pts (10.8%) we could not analyzed v-a conduction due to atrial flutter or fibrillation. V-a conduction was present in groups I-IV in 61.2%, 35%, 21.4%, 45% and 10% cases respectively. CONCLUSIONS: 1. In group patients with sick sinus syndrome and VVI stimulation ventriculo-atrial conduction was recorded in most cases. 2. Ventriculo-atrial conduction was recorded in part of the population with atrio-ventricular block. 3. Frequency of ventriculo-atrial conduction phenomenon is dependent on degree of a-v block. 4. Transesophageal recording of ventriculo-atrial conduction phenomenon in patients with implantable VVI pacemaker is simple, noninvasive and useful method for clinical practice.

Adolescent↗
PubMed1997

Effect of phasic vagal stimulation and atrial pacing site on atrioventricular conduction time.

We tested the hypothesis that the effect of phasic vagal stimulation on atrioventricular (AV) conduction time is affected by the site of atrial pacing in anesthetized dogs. We paced the right atrium at a constant cycle length from the interatrial septum (IAS), superior coronary sinus (SCS), or inferior coronary sinus (ICS) regions, and we evaluated the time-dependent effects of vagal stimulation on AV conduction at each pacing site. When we stimulated the vagi at stimulus (St)-A phases greater than 136 +/- 40 ms and less than the phase that blocked AV conduction (182 +/- 70 ms), IAS pacing prolonged A-V intervals by 8.6 +/- 8.2 ms more than ICS pacing. A change in pacing site affected the A-V intervals by up to 30 ms when we stimulated the vagus at those times that caused the A-V intervals to prolong maximally. Furthermore, the effect of atrial pacing site on A-V intervals was modulated by AV nodal recovery times during the second or third cycles after the vagal stimulus.

Animals↗
PubMedDate not supplied

[Interatrial aneurysm as a cause of supraventricular arrhythmia in a newborn infant].

Atrial septal aneurysm is a rare malformation that may occur as an isolated abnormality or in association with various cardiac defects or with connective tissue disease. The reported incidence in adults is 0.2% and in children 4.9% which suggests spontaneous regression with advancing age. Atrial septal aneurysm may be complicated by thromboembolism, valvular obstruction or arrhythmias. Supraventricular arrhythmias have been reported in as much as 16% of the cases, most commonly paroxysmal supraventricular tachycardia, supraventricular extrasystoles and atrial flutter. The relationship between the arrhythmias and the atrial septal aneurysm is still controversial. Two cases of atrial septal aneurysm in neonates are described, who presented with arrhythmias: supraventricular extrasystoles with aberrant conduction and atrial flutter with variable conduction, respectively. One of them required treatment with various anti-arrhythmia agents. During follow-up the arrhythmias remitted with spontaneous involution of the aneurysm. In the presence of the supraventricular arrhythmias in neonates, atrial septal aneurysm needs to be ruled out as a potential cause.

Age Factors↗
PubMed2001

Novel PRKAG2 mutation responsible for the genetic syndrome of ventricular preexcitation and conduction system disease with childhood onset and absence of cardiac hypertrophy.

BACKGROUND: We recently reported a mutation in the PRKAG2 gene to be responsible for a familial syndrome of ventricular preexcitation, atrial fibrillation, conduction defects, and cardiac hypertrophy. We now report a novel mutation in PRKAG2 causing Wolff-Parkinson-White syndrome and conduction system disease with onset in childhood and the absence of cardiac hypertrophy. METHODS AND RESULTS: DNA was extracted from white blood cells obtained from family members. PRKAG2 exons were amplified by polymerase chain reaction and were screened for mutations by direct sequencing. The genomic organization of the PRKAG2 gene was determined using inter-exon long-range polymerase chain reaction for cDNA sequence not available in the genome database. A missense mutation, Arg531Gly, was identified in all affected individuals but was absent in 150 unrelated individuals. The PRKAG2 gene was determined to consist of 16 exons and is at least 280 kb in size. CONCLUSIONS: We identified a novel mutation (Arg531Gly) in the gamma-2 regulatory subunit (PRKAG2) of AMP-activated protein kinase (AMPK) to be responsible for a syndrome associated with ventricular preexcitation and early onset of atrial fibrillation and conduction disease. These observations confirm an important functional role of AMPK in the regulation of ion channels specific to cardiac tissue. The identification of the cardiac ion channel(s) serving as substrate for AMPK not only would provide insight into the molecular basis of atrial fibrillation and heart block but also may suggest targets for the development of more specific therapy for these common rhythm disturbances.

AMP-Activated Protein Kinases↗
PubMed2000

The influence of right atrial septal pacing on the interatrial contraction sequence.

UNLABELLED: Right atrial septal pacing yields shorter interatrial conduction delays than conventional right atrial pacing at the free wall or the right atrial appendage. However, the hemodynamic effects of right atrial septal pacing are less well known. This study measured the delay between right and left atrial contractions during right atrial septal pacing (n = 21), conventional right atrial pacing (n = 32) and atrial multisite pacing (n = 6) by pulse Doppler echocardiography of transtricuspidal and transmitral blood flow. The effects of right atrial septal pacing (n = 14) versus conventional right atrial pacing (n = 22) on the optimal AV delay during dual chamber pacing was examined in patients with high degree atrioventricular (AV) block. Compared to sinus rhythm, conventional right atrial pacing increased P wave duration from 119 +/- 21 ms to 137 +/- 24 ms (P < 0.001), whereas both right atrial septal pacing (119 +/- 10 ms before, 106 +/- 13 ms during pacing, P = 0.002) and atrial multisite pacing (123 +/- 20 ms before, 112 +/- 11 ms during pacing, P = 0.5) shortened P wave duration. Atrial pacing caused a significant (P < 0.002) prolongation of atrial contraction [corrected] delays from 24 +/- 21 ms to 41 +/- 26 ms during conventional right atrial pacing, and reversed the right-to-left into a left-to-right contraction sequence in 20 of 21 patients during right atrial septal pacing (atrial conduction delay during sinus rhythm: 34 +/- 23 ms vs -37 [corrected] +/- 26 ms during atrial pacing, P < 0.0001). Atrial multisite pacing caused a nonsignificant shortening of the usual right-to-left contraction delay from 22 +/- 34 ms to 11 +/- 18 ms. The optimal left heart AV delay during AV sequential pacing was significantly (P = 0.002) shorter during right atrial septal pacing (108 +/- 38 ms) than during conventional right atrial pacing (152 +/- 33 ms). During conventional right atrial pacing the optimal right heart AV delay was significantly (P = 0.029) shorter than the optimal left heart AV delay. The opposite relation was observed for right atrial septal pacing (P = 0.033). CONCLUSIONS: Interatrial septal pacing does not synchronize right and left atrial contractions. It reverses the atrial mechanical timing from a right-to-left to a left-to-right contraction sequence, and requires the setting of shorter AV delays during dual chamber pacing if based on the optimization of left heart timing. Interatrial septal pacing is a technique which allows pacing of the left atrium from a right atrial site, rather than a single site approach to biatrial pacing.

Adolescent↗
PubMed1985

Improved method for evaluating ventriculoatrial conduction before implantation of atrial-sensing dual chamber pacemakers.

Pacemaker-mediated tachycardia may occur when a spontaneous ventricular premature depolarization is retrogradely conducted to the atrium with a ventriculoatrial (VA) interval that exceeds the atrial refractory period of an atrial-sensing dual chamber pacemaker. Previous methods for evaluating VA conduction have failed to predict clinical occurrences of pacemaker-mediated tachycardia. In this study, maximal VA intervals after ventricular extrastimuli during atrial or atrioventricular (AV) sequential pacing were compared with intervals measured by the standard method of ventricular pacing. VA intervals were 201 +/- 53 ms during ventricular pacing and 224 +/- 52 ms after ventricular extrastimuli during atrial pacing (p = NS). VA intervals were 305 +/- 77 ms after ventricular extrastimuli during AV sequential pacing and were longer than VA intervals during ventricular pacing (p less than 0.001) or after ventricular extrastimuli during atrial pacing (p less than 0.01). Thus, the ventricular extrastimulus technique during AV sequential pacing reveals substantially longer VA intervals than does ventricular pacing and explains why pacemaker-mediated tachycardia might occur when pacemaker atrial refractory periods are designed or programmed according to VA intervals measured only during ventricular pacing.

Adult↗
PubMed2003

Incisional atrial reentrant tachycardia: experimental study on the conduction property through the isthmus.

BACKGROUND: Incisional atrial reentrant tachycardia is a life-threatening tachyarrhythmia after surgery for congenital heart disease. Slow conduction through an isthmus between anatomical barriers, such as a right atriotomy or the sites for cannulation, has been shown to be a prerequisite for perpetuation of the incisional atrial reentrant tachycardia. However, the conduction property through the isthmus has not been examined in detail. METHODS: To examine the conduction property, 2 tandem incisions were made on the lateral right atrium with various distances (3 to 20 mm) between the incisions in 16 canines. Four weeks after the surgery, the lateral right atrium was mapped epicardially during pacing to examine the conduction property through the isthmus. The conduction property was characterized by approximated curves of the conduction velocity through the isthmus in accordance with the pacing cycle lengths. The atrial tissue at the isthmus was examined microscopically. RESULTS: The approximated curves of the conduction velocity were classified into 3 different types. Decremental conduction was observed only in the isthmi between 5 and 15 mm in width. A small amount of surviving myocardium between the scars formed the critical isthmus microscopically (decremental type). In the isthmi wider than 15 mm in width, slow conduction was not seen at any paced cycle length (nondecremental type). In the extremely narrow isthmi less than 5 mm in width, all of the atrial myocardium at the isthmus was replaced by fibrous tissue. Conduction was blocked at the isthmus and the activation detoured around the incisions (block type). There was a statistically significant difference in the approximated curves between the 3 different types of conduction properties (P <.01). CONCLUSION: The width of the isthmus determines the conduction property through the isthmus that contributes to the development of the incisional atrial reentrant tachycardia. Thus, the incisional atrial reentrant tachycardia may be preventable by leaving a sufficient amount of surviving myocardium between the incisions or by connecting the incisions by an ablative procedure.

Animals↗
PubMed1989

[Atrial arrest and intraventricular conduction disorders due to accidental hyperkalemia during kidney transplantation].

Besides anemia, coagulopathies, and hypertension, electrolyte disturbances are among the most significant features of end-stage renal disease. Although plasma potassium represents only 1.5%-2% of the whole-body content, hyperkalemia has definite effects on cardiac pacemaker cells and myocardial conduction. The typical ECG findings and therapeutic management will be discussed. Case report. A 64-year-old man with chronic renal failure due to phenacetin abuse was scheduled for transplantation of a 41-h-old cadaver kidney. The preoperative laboratory check revealed BUN 51 mg% and creatinine 11.5 mg%; serum sodium and potassium were within normal limits (sodium 141 mmol/l, potassium 5.11 mmol/l). A central-venous blood gas sample after induction of anesthesia and intubation revealed pH of 7.32, pCO2 43 mmHg, HCO3 22.1 mmol/l, base excess - 3.4 mmol/l, and venous oxygen saturation 84%. Plasma potassium (5.22 mmol/l) was within the normal range. As an endarterectomy of the left common and external iliac arteries had to be performed, the arterial cross-clamping time was longer than normal (73 min). After declamping an ECG pattern (modified V5 lead) typical of hyperkalemia (atrial arrest, idioventricular rhythm, right bundle-branch block-like QRS, AV dissociation, AV block I) was observed. Plasma potassium had increased to 6.77 mmol/l (+1.55 mmol/l). Immediate treatment was started with a bolus injection of 20 ml 10% calcium gluconate, rapid infusion of 200 ml 8.4% sodium bicarbonate, and glucose-insulin infusion (glucose 33 1/3%, 15 U regular insulin). After 25 min sinus rhythm was restored and potassium levels decreased to normal. Despite the observed ECG changes the cardiovascular status remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1992

Increased ventricular response rate during exercise in patients with atrial fibrillation treated with theophylline.

The effect of theophylline on atrioventricular conduction in atrial fibrillation was investigated by determining ventricular response rates at rest and during exercise treadmill tests in eight patients (mean [+/- SEM] age, 64.2 +/- 2.0 years) with chronic atrial fibrillation. Tests were performed before and after 7 days of oral theophylline treatment (plasma level, 87.7 +/- 7.8 mumol/L). There was no significant change in baseline ventricular rate or duration of exercise, but the maximum ventricular rate with theophylline treatment was 12.3% +/- 2.4% higher than that with placebo (176.3 +/- 7.5 vs 158.1 +/- 8.8 beats per minute), and, during each stage of exercise, the ventricular rate with theophylline exceeded that with placebo. The increased heart rate during theophylline administration occurred without a significant difference in the exercise-induced increase in circulating plasma catecholamine levels. We conclude that treatment with theophylline may contribute to difficulties with rate control in acutely ill patients with coexisting atrial fibrillation.

Aged↗
PubMed1987

Method for antegrade/retrograde conduction discrimination using a standard atrial bipolar lead.

Significant differences between morphology, magnitude, and relative timing of antegrade and retrograde conduction were demonstrated on unipolar electrograms from a standard atrial bipolar J lead positioned in the right atrium in dogs. The morphology of the P wave sensed from the tip was more or less biphasic while the morphology of the P wave sensed from the ring was monophasic only and of lower frequency content. The unipolar-ring P wave was attenuated in retrograde as compared with the antegrade. During retrograde conduction the unipolar-ring signal returned to baseline earlier in time relative to the peak of the unipolar-tip signal, than it did during antegrade conduction. Based on these differences a sensing circuit capable of discriminating between antegrade and retrograde conduction was built. This discriminator circuit, which relies on a standard lead and simple electronics, functioned reliably in trials in dogs and thus may prove to be practical for use in future pacemakers.

Algorithms↗
PubMed1992

[Atrial flutter with paroxysmal 1:1 atrioventricular conduction].

Three patients with "lone" paroxysmal atrial flutter complicated by paroxysms of 1:1 AV conduction are presented. One patient (42 years of age) had been misdiagnosed as an neurotic for 18 years. The mechanism, diagnosis and treatment of the condition are outlined. The most characteristic symptoms are dizzy spells and fainting. The recommended diagnostic procedures include long term ECG recording by telemetry or Holter, exercise-ECG and oesophageal-ECG.

Adult↗
PubMed2002

Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and the major cardiac cause of stroke. Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevailing theory is that multiple random wavelets of activation coexist to create an unorganized atrial rhythm. Experiments in isolated hearts have demonstrated that stable, self-sustained rotors can exist in the atria and that high frequency activation by such rotors results in the complex patterns of activation that characterize AF. Studies in animals and patients support the view that at least some cases of paroxysmal and chronic AF are the result of the uninterrupted periodic activity of discrete reentrant sites. In this brief review article, we examine historical data and more recent experimental evidence behind the hypothesis that AF may be organized by one, or a small number of high-frequency reentrant sources localized in the left atrium. We then discuss the potential implications and evidence supporting such a hypothesis for human AF. Finally, we suggest future studies designed to unravel the detailed molecular, cellular and pathophysiological mechanisms responsible for AF initiation and maintenance. The work discussed may open potentially exciting new diagnostic and therapeutic possibilities.

Acetylcholine↗