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PubMed2004

Catheter ablation of atrial tachycardia due to recipient-to-donor transatrial conduction after orthotopic heart transplantation.

Atrial arrhythmias occur frequently after orthotopic heart transplantation. In some cases, they may depend on atrio-atrial conduction across the surgical suture line. We report an unusual case of a heart transplant recipient who had recipient atypical atrial flutter with 2:1 transatrial conduction and a resulting tachycardia in the donor atrium. Electroanatomical mapping identified the site of transatrial conduction and guided successful catheter ablation.

Aged↗
PubMed1998

Electrical-anatomic correlations between typical atrial flutter and intra-atrial re-entry following atrial surgery.

It is well known that in typical (or type I) atrial flutter, conduction proceeds counterclockwise, up the interatrial septum and down the right atrial wall anterior to the crista terminalis (CT). Recent careful mapping studies using entrainment pacing have clearly shown the importance of the CT and the eustachian valve ridge (EVR), which act as fixed barriers to intra-atrial conduction and interact with other barriers, including the tricuspid valve, inferior vena cava (IVC), and coronary sinus os, to create a long macroreentrant circuit. Ablative lesions are directed at the isthmus between the tricuspid valve and the IVC or between the tricuspid valve and the EVR. Patients who have had cardiac surgery may have typical atrial flutter, either counterclockwise or clockwise, and prior surgery may act to stabilize the circuit. Such patients may also have atypical flutter, which does not utilize this circuit. Surgical closure of septal defects requires a long anterior oblique atriotomy. Commonly, reentrant circuits are identified that use this barrier, as well as the tricuspid valve and CT, and are confined to the anterior atrial wall and do not involve the typical flutter isthmus. These may be ablated at the lower or the upper end of the atriotomy, extending the block to the tricuspid valve, IVC, or superior vena cava. After the Senning or Mustard procedure, typical flutter is common, and the baffle bisects the isthmus at the site of the EVR, perhaps enforcing block. Anterior atriotomy-mediated reentry also is seen, and both circuits need to be approached in a retrograde manner. After the Fontan atriopulmonary connection, atriotomies and atrial dilation may interact to make reentry more likely. After the "lateral tunnel" Fontan (cavopulmonary connection) suture lines are similar to those of the Senning procedure, but nearly all right atrial anatomy is in the pulmonary venous atrium. Such circuits may need to be approached via an atrial fenestration.

Adult↗
PubMed1995

Effect of flecainide on atrial and ventricular refractoriness and conduction in patients with normal left ventricle. Implications for possible antiarrhythmic and proarrhythmic mechanisms.

We studied the effects of intravenous flecainide (2 mg.kg-1) on atrial and ventricular refractoriness and conduction during sinus rhythm, induced atrial fibrillation and atrial pacing at rates of 100, 120 and 150 ppm, in 14 patients with normal left ventricle. Flecainide caused a significant increase in QRS duration during sinus rhythm (mean +/- SD: 87.2 +/- 8.4 ms vs 102.8 +/- 9.1 ms, P < 0.001), atrial fibrillation (87.8 +/- 10.0 ms vs 108.8 +/- 13.7 ms, P < 0.001) and at all paced rates. The duration of the atrial electrogram was significantly increased during sinus rhythm (54.9 +/- 13.2 ms vs 64.8 +/- 16.6 ms, P = 0.003) and at all pacing rates. The PA interval was also significantly prolonged, as was the pacing stimulus-to-atrial-electrogram interval at all pacing rates. There was increased QRS duration and atrial electrogram prolongation at higher pacing rates. Atrial refractoriness was prolonged during sinus rhythm (216.4 +/- 28.2 vs 228.6 +/- 36.1, P = 0.02), but not during atrial pacing at any rate. The QT interval, but not the JT interval or ventricular refractoriness, was significantly prolonged during sinus rhythm and at all pacing rates. Flecainide slows atrial conduction in a use dependent manner and increases atrial refractoriness during sinus rhythm but not during faster atrial pacing, thus not displaying a use-dependent effect. QRS duration is prolonged in a use-dependent manner without a commensurate increase in ventricular refractoriness. In the presence of rapidly conducted atrial fibrillation, which was not found to be slowed by flecainide, this effect may constitute a proarrhythmic mechanism even in patients with no apparent myocardial abnormality.

Adult↗
PubMed1999

Radiofrequency ablation of atrioventricular junction and pacemaker implantation versus modulation of atrioventricular conduction in drug refractory atrial fibrillation.

Modulation of atrioventricular (AV) node conduction and radiofrequency ablation of AV junction are alternative approaches to control ventricular rate in drug refractory atrial fibrillation (AF). In 2 centers, 120 patients were treated either with AV junction ablation (center 1, group 1, 60 patients [30 men, aged 64 +/- 11 years], paroxysmal AF in 24 patients) or with modulation (group 2, 60 patients [32 men, aged 58 +/- 12 years], paroxysmal AF in 43 patients). In group 1, complete AV block was achieved in all patients. In group 2, the procedure was performed in sinus rhythm (30 patients), prolonging the Wenckebach cycle length from 328 +/- 85 to 466 +/- 80 ms (p <0.01) or during AF (30 patients), decreasing ventricular rate from 178 +/- 35 to 96 +/- 35 beats/min (p <0.01), and to <100 beats/min in 17 patients (61%). Complete AV block was induced in 9 of 60 patients (15%). In groups 1 and 2, at a follow-up of 27 +/- 7 and 26 +/- 6 months, there were 2 deaths (1 cardiac, 1 sudden death) and 1 death for end-stage heart failure, respectively. Hospital readmissions decreased from 3.2 to 0.2 and from 4.2 to 0.2/year; late AF recurrences at of >120 beats/min were documented in 6% and 12%, respectively. Symptom score analysis including effort and rest dyspnea, exercise intolerance, weakness, and palpitation showed a significant improvement in both treatment groups, when acutely effective, in patients with paroxysmal and/or chronic AF. In conclusion, ablation of the AV junction shows a higher acute success rate compared with modulation of the AV node conduction in patients with drug refractory AF. Depending on the acute success, both approaches therefore were similarly effective in achieving long-term ventricular rate control and symptom score improvement.

Aged↗
PubMed1998

Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells.

The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the "compact" node. Optical APs (124) were recorded from 5 x 5 mm (approximately 0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third (peaks I and III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike (peak II) represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of tau 1 (49.5 +/- 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and tau 2 (57.57 +/- 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 +/- 3.21 ms, indicating an apparent conduction velocity (theta N) of 0.162 +/- 0.02 m/s (n = 9) that was insensitive to TTX. In contrast, tau 1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that theta N is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Acetylcholine↗
PubMed1991

[Successful high-frequency catheter ablation of an accessory atrioventricular conduction pathway in atrial fibrillation].

This report describes the case of a 41-year-old patient with Wolff-Parkinson-White syndrome and recurrent, highly symptomatic episodes of atrial fibrillation (with rapid heart rates of a mean of 250 beats/min) in whom transvenous catheter ablation of the accessory pathway was successfully performed in a relatively short time during the arrhythmia. The feasibility of an abbreviated approach to the relatively time-consuming ablation procedure in Wolff-Parkinson-White syndrome is discussed.

Adult↗
PubMed2001

What is cardiac resynchronization therapy?

Cardiac resynchronization refers to pacing techniques that change the degree of atrial and ventricular electromechanical asynchrony in patients with major atrial and ventricular conduction disorders. Atrial and ventricular resynchronization is usually accomplished by pacing from more than one site in an electrical chamber--atrium or ventricle--and occasionally by stimulation at a single unconventional site. Resynchronization produces beneficial hemodynamic and antiarrhythmic effects by providing a more physiologic pattern of depolarization. Atrial resynchronization may prevent atrial fibrillation in selected patients with underlying bradycardia or interatrial block. Its antiarrhythmic effect in the absence of bradycardia is unclear. Ventricular resynchronization is of far greater clinical value than atrial resynchronization. Biventricular (or single-chamber left ventricular) pacing is beneficial for patients with congestive heart failure, severe left ventricular systolic dysfunction, dilated cardiomyopathy (either ischemic or idiopathic), and a major left-sided intraventricular conduction disorder, such as left bundle branch block. The change in electrical activation from resynchronization, which has no positive inotropic effect as such, is translated into mechanical improvement with a more coordinated left ventricular contraction. Several recent randomized trials and a number of observational studies have demonstrated the long-term effectiveness of ventricular resynchronization in the above group of patients. The high incidence of sudden death among these patients has encouraged ongoing clinical trials to evaluate the benefit of a system that combines biventricular pacing and cardioversion-defibrillation into a single implantable device.

Arrhythmias, Cardiac↗
PubMed1998

Circadian rhythms of atrioventricular conduction properties in chronic atrial fibrillation with and without heart failure.

OBJECTIVES: We examined the circadian variations in atrioventricular (AV) conduction properties during atrial fibrillation (AF) by a technique based on the Lorenz plot of successive ventricular response (VR) intervals and analyzed their relations with clinical features. BACKGROUND: The VR interval in chronic AF shows circadian variation, which is attenuated in patients with an increased risk of death. Although the VR interval is determined by the dynamic processes in the AV node randomly stimulated by rapid atrial activity, the circadian variations of the AV conduction properties related to this mechanism are unknown. METHODS: In 48 patients with chronic AF, Lorenz plots were generated on overlapping sequential segments of 512 VR intervals in 24-h ambulatory electrocardiograms. For each scatter plot, the 1.0-s intercept of the lower envelope (LE1.0) of the plot and the degree of scatter above the envelope (root mean square difference from the envelope [scattering index]) were measured for estimating AV node refractoriness and concealed AV conduction, respectively. RESULTS: In all patients, a significant circadian rhythm was observed for the average VR interval, LE1.0 and scattering index, with an acrophase occurring at night. The mesor, amplitude and acrophase of LE1.0 and the scattering index closely and independently correlated with the corresponding rhythm variables of the average VR interval (partial r2 0.98, 0.86 and 0.68 for LE1.0 and 0.98, 0.92 and 0.92 for scattering index). The amplitudes of these measures were lower in patients with congestive heart failure (CHF) even after adjustment for the effects of age, duration of AF, medications, left atrial diameter and blood pressure (p < 0.01 for all). CONCLUSIONS: These results suggest that 1) both AV node refractoriness and the degree of concealed AV conduction during AF may show a circadian rhythm; 2) the circadian rhythms of these properties may independently contribute to the circadian variation of the VR interval; and 3) these circadian rhythms may be attenuated in patients with CHF.

Aged↗
PubMed1981

The mechanism of AV junctional reentry: role of the atrionodal junction.

Mapping of atrial-AV nodal (AVN) activation patterns was performed in 10 superfused rabbit AVN preparations utilizing 3 bipolar electrodes placed simultaneously at the crista terminalis (CT), interatrial septum (IAS) and His bundle (H) regions in close proximity to the AVN, along with two or three microelectrodes in the AN, N and NH regions of the AVN. Basic and premature stimuli were introduced at either or both the CT and IAS regions of the AVN. The timing of the premature stimuli was varied to induce close interaction of inputs to the AVN. Summation and/or cancellation, as evidenced by changes in the morphology of the action potentials and alteration of H1-H2 intervals, were observed. Apparent reentry phenomena could be induced or terminated by appropriately timed stimulation at the CT and IAS inputs. Reentry was critically related to both the patterns and timing of the spread and excitation within AVN and surrounding atrial tissue. Slow conduction and unidirectional block were observed in various portions of the reentry circuit. It is concluded that 1) interaction between input waves engaging the AVN produced either summation or fragmentation; 2) slow conduction and reentry resulted from a critical collision of wavefronts; 3) in this preparation, AVN reentry circuits always appeared to involve conduction through atrial tissue immediately surrounding AVN; and 4) remarkably, reentry confined to the intranodal region was never observed.

Action Potentials↗
PubMed2001

Ventricular arrhythmia vulnerability in cardiomyopathic mice with homozygous mutant Myosin-binding protein C gene.

BACKGROUND: Homozygous mutant mice expressing a truncated form of myosin-binding protein C (MyBP-C(t/t)) develop severe dilated cardiomyopathy, whereas the heterozygous mutation (MyBP-C(t/+)) causes mild hypertrophic cardiomyopathy. Adult male MyBP-C(t/t) and MyBP-C(t/+) mice were evaluated for arrhythmia vulnerability with an in vivo electrophysiology study. METHODS AND RESULTS: Surface ECGs were obtained for heart rate, rhythm, and conduction intervals. Atrial, atrioventricular, and ventricular conduction parameters and refractoriness were assessed in 22 MyBP-C(t/t), 10 MyBP-C(t/+), and 17 wild-type MyBP-C(+/+) mice with endocardial pacing and intracardiac electrogram recording. Arrhythmia induction was attempted with standardized programmed stimulation at baseline and with isoproterenol. Heart rate variability and ambient arrhythmia activity were assessed with telemetric ECG monitors. Quantitative histological characterization was performed on serial sections of excised hearts. MyBP-C(t/t) and MyBP-C(t/+) mice have normal ECG intervals and sinus node, atrial, and ventricular conduction and refractoriness. Ventricular tachycardia was reproducibly inducible in 14 of 22 MyBP-C(t/t) mice (64%) during programmed stimulation, compared with 2 of 10 MyBP-C(t/+) mice (20%) and 0 of 17 wild-type controls (P<0.001). Ventricular ectopy was present only in MyBP-C(t/t) mice during ambulatory ECG recordings. There were no differences in heart rate variability parameters. Interstitial fibrosis correlated with genotype but did not predict arrhythmia susceptibility within the MyBP-C(t/t) group. CONCLUSIONS: MyBP-C(t/t) mice, despite prominent histopathology and ventricular dysfunction, exhibit normal conduction and refractoriness, yet are vulnerable to ventricular arrhythmias. Somatic influences between genetically identical mutant mice most likely account for variability in arrhythmia susceptibility. A sarcomeric protein gene mutation leads to a dilated cardiomyopathy and ventricular arrhythmia vulnerability phenotype.

Animals↗
PubMed1997

Effect of phenylephrine infusion on atrial electrophysiological properties.

OBJECTIVE: To determine the effect of changes in autonomic tone induced by phenylephrine infusion on atrial refractoriness and conduction. DESIGN: Left and right atrial electrophysiological properties were measured before and after a constant phenylephrine infusion designed to increase sinus cycle length by 25%. SUBJECTS: 20 patients, aged 53 (SD 6) years, undergoing electrophysiological study for investigation of idiopathic paroxysmal atrial fibrillation (seven patients) or for routine follow up after successful catheter ablation of supraventricular tachycardia (13 patients). MAIN OUTCOME MEASURES: Changes in left and right atrial effective refractory periods, atrial activation times, and frequency of induction of atrial fibrillation. RESULTS: Phenylephrine (mean dose 69 (SD 18) mg/min) increased mean blood pressure by 22 (12) mm Hg (range 7 to 44) and lengthened sinus cycle length by 223 (94) ms (20 to 430). Left atrial effective refractory period lengthened following phenylephrine infusion from 250 (25) to 264 (21) ms (P < 0.001) but there was no significant change in right atrial effective refractory period: 200 (20) v 206 (29), P = 0.11. There was a significant relation between the effect of phenylephrine on sinus cycle length and on right atrial refractoriness (r = 0.6, P = 0.005) with shortening of right atrial refractoriness in patients with the greatest prolongation in sinus cycle length. During phenylephrine infusion, the right atrial stimulus to left atrial activation time at the basic pacing cycle length of 600 ms was unchanged, at 130 (18) v 131 (17) ms, but activation delay with a premature extrastimulus increased: 212 (28) v 227 (38) ms, P = 0.002. Atrial fibrillation was induced by two of 58 refractory period measurements at baseline and by 12 of 61 measurements during phenylephrine infusion (P < 0.01). Phenylephrine increased the difference between left and right atrial refractory periods by 22.8 (19.4) ms in the five patients with induced atrial fibrillation after phenylephrine compared to 0.9 (16.2) ms in the 13 patients without induced atrial fibrillation after phenylephrine infusion (P = 0.02). CONCLUSIONS: Phenylephrine infusion increased left atrial refractoriness and intra-atrial conduction delay following a premature right atrial extrastimulus. Induction of atrial fibrillation during phenylephrine infusion was associated with non-uniform changes in atrial refractoriness. These data support the concept that changes in autonomic tone may precipitate atrial fibrillation in susceptible individuals.

Adult↗
PubMed2001

Predictors of atrial flutter with 1:1 conduction in patients treated with class I antiarrhythmic drugs for atrial tachyarrhythmias.

OBJECTIVES: The purpose of the study was to look for the predictor factors of atrial proarrhythmic effects of class I antiarrhythmic drugs. BACKGROUND: Class I antiarrhythmic drugs may induce or exacerbate cardiac arrhythmias. The predictors of ventricular proarrhythmia are known. The predictors of atrial flutter with 1:1 conduction are unknown. METHODS: Clinical history, EGG, signal-averaged EGG (SAECG) and electrophysiologic study were analysed in 24 cases of 1:1 atrial flutter with class I AA drugs and in 100 control patients without history of 1:1 atrial flutter with class I AA drugs. RESULTS: The ages of patients varied from 46 to 78 years. Underlying heart disease was present in nine patients. The surface EGG revealed the presence of a short PR interval (PR<0.13 ms), visible in leads V5, V6 in eight (35%) patients with normal P wave duration; in other patients with prolonged P wave duration, PR seemed normaL On SAECG recording, there was a pseudofusion between P wave and QRS complex. The electrophysiologic study revealed some signs indicating a rapid AV nodal conduction (short AH interval or rate of 2nd degree AV block at atrial pacing >200 beats/mm) in 19 of the 23 studied patients. All patients, except one, had at least one sign indicating a rapid AV nodal conduction (short PR and/or P wave-QRS complex continuity on SAECG). In the control group, seven patients (7%) had a short PR interval (P<0.01) and 11 (11%) had a pseudofusion between P wave and QRS complex on SAECG (P<0.001). The P wave-QRS complex pseudofusion on SAECG had a sensitivity of 100% and a specificity of 89% for the prediction of an atrial proarrhythmic effect with class I antiarrhythmic drug. CONCLUSION: We recommend avoiding class I AA drugs in patients with a short PR interval on surface EGG and to record SAECG in those with apparently normal PR interval to detect a continuity between P wave and QRS complex, which could indicate a rapid AV nodal conduction, predisposing to 1:1 atrial flutter with the drug.

Adult↗
PubMed2005

High incidence of sudden cardiac death with conduction disturbances and atrial cardiomyopathy caused by a nonsense mutation in the STA gene.

BACKGROUND: The STA gene encodes emerin and is one of the genes that is affected in Emery-Dreifuss muscular dystrophy (EDMD). Although it has been reported that EDMD caused by the STA gene mutation is associated with X-linked recessive inheritance, the genotype-phenotype correlations, with special reference to cardiac manifestations, are not well defined. METHODS AND RESULTS: We identified 16 carriers (7 male and 9 female) with a nonsense mutation in exon 6 of the STA gene in 2 EDMD families. Pacemakers were required for treatment of bradyarrhythmias in all 7 male carriers and in 2 of the 9 female carriers. In addition, 2 of the 9 female carriers displayed atrial fibrillation. In these 2 families, 3 males without pacemaker implantation, who were not tested genetically, had died suddenly. In these family members, the majority of carriers with the mutation had not been clinically diagnosed as having EDMD before genetic testing because of extremely mild or nonexistent skeletal myopathy. CONCLUSIONS: EDMD caused by this mutation is characterized by atypical clinical features and incomplete penetrance of the clinical phenotype and may result in serious cardiac complications, including sudden death. Approaches to preventing possible sudden death in carriers with the STA gene mutation require further study.

Adolescent↗