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[Atrial electrophysiologic properties in paroxysmal atrial fibrillation. Study conducted with the stimulation of 5 atrial sites].

Programmed atrial stimulation at five atrial sites was performed to evaluate electrophysiologic atrial properties in 17 control patients (14 M, 3F, mean age 61 +/- 9 years) (Group A) and in 18 patients with paroxysmal atrial fibrillation (13 M, 5 F, mean age 61 +/- 5 years) (Group B) with normal sinus node function. The mean value of the P wave duration was similar in both groups. Programmed atrial stimulation was performed at five atrial sites: high, medium and low lateral wall, and high and low medial wall. We evaluated the following parameters: A) local conduction delay measured at the functional refractory period as the difference between A1-A2 and S1-S2 intervals; B) widening of local electrogram measured at the functional refractory period as the difference between A1-A2 interval measured at the end of each local electrogram and A1-A2 interval measured at the beginning of each local electrogram. We evaluated the mean and the maximum value of the two above-mentioned parameters; C) dispersion of effective refractory period and functional refractory period, determined as the longest minus the shortest refractory period from the range of refractory periods measured in each patient; D) the mean of effective refractory periods and functional refractory periods observed at five atrial sites. Mean and maximum local conduction delay, mean effective and functional refractory periods did not present significant differences in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Influence of basic atrial rhythm on intraatrial conduction of extrastimuli.

Atrial arrhythmias appear to be related to the genesis of intraatrial conduction delays by extrastimuli. To clarify the effects of the basic atrial cycle on intraatrial conduction of extrastimuli, atrial conduction delays and conduction delay zones were measured in 22 patients with and without atrial arrhythmias. Basic cycles were (A) sinus rhythm; (B) paced at the right atrial (RA) appendage with maximum cycle length possible; (C) paced at the RA appendage with cycle length of 600 ms; and (D) paced at the proximal coronary sinus at the same cycle length as B. Extrastimuli were always delivered at the RA appendage. Conduction delays and conduction delay zones were 5- to 7-fold longer when driving stimuli and extrastimuli were delivered through the same electrodes than when the basic cycle was sinus or driven at a distance from the extrastimuli (p less than 0.001). This effect must be considered when groups of patients or the results of interventions are compared.

Atrial Fibrillation↗

Electrophysiology and endocardial mapping of induced atrial fibrillation in patients with spontaneous atrial fibrillation.

We analyzed the patterns of atrial activation and characterized the electrophysiologic properties of regional atrial sites in the, right atrium and left atrium at the onset of atrial fibrillation (AF) induced with programmed right atrial (RA) stimulation. Intraatrial conduction, atrial electrogram return cycle lengths for the first AF cycle, RA and left atrial (LA) activation maps during AF, and the stability and reproducibility of atrial activation sequences at AF onset and maintenance were analyzed in 23 patients with AF. Correlation of intracardiac electrograms with surface electrocardiographic morphology was attempted. Maximum intraatrial conduction delay for high RA premature beats was observed at the coronary sinus ostium (n = 15), His bundle region (n = 13) or interatrial septum (n = 15). The return cycle lengths for the first AF cycle showed increasing conduction delay with increasing prematurity of the last extrastimulus in most patients. Suprisingly, discrete atrial electrograms with regular or irregular cycle lengths were present at the onset of electrocardiographic documented coarse AF in 13 of 15 patients (87%). Fragmented or chaotic atrial activity were present in 2 of 15 patients (13%) in coarse AF but observed at > or = 1 atrial sites in 7 of 8 patients (88%) with fine AF (p = 0.001). The atrial activation sequence at the onset of the induced AF elicited by high RA extrastimuli usually showed the earliest activation site at the crista terminalis (9 patients) or interatrial septum (9 patients). In contrast, induced AF elicited from other RA sites usually showed earliest atrial activation at the septum (3 patients) or coronary sinus ostium (3 patients). Atrial activation sequences for the first induced AF cycle were usually reproducible in most patients. Atrial activation patterns during the first 10 cycles for AF were stable in RA and LA regions in 6 of 23 patients (260%) but demonstrated significant change(s) at > or = 1 region in 17 of 23 patients (74%) (p <0.05). We conclude that pacing induced AF elicited by RA premature beats commences as a regular or irregular rapid atrial tachycardia consistent with a transitional, but often organized, arrhythmia. The activation sequence and electrophysiologic behavior of the first induced AF cycle is consistent with intraatrial reentry and reproducible in most patients. More than 1 atrial activation sequence can sometimes be observed, emphasizing the dynamic nature of the initial RA reentrant circuits.

Aged↗

Familial atrial septal defect with atrioventricular conduction defects.

Atrial septal defect of the ostium secundum type is almost always sporadic, with multifactorial inheritance. We report a case of a family in which atrial septal defects of the ostium secundum type with atrioventricular conduction defects were observed in four generations: five proven cases and two probable cases. Ten families have been reported as showing atrial septal defect of the ostium secundum type and atrioventricular conduction defects with dominant inheritance. Moreover, in our family the transmission model can also confirm autosomal dominant inheritance. We believe that cardiologists should take a familial approach to atrial septal defect of the ostium secundum type for both research and genetic counseling purposes. In a patient with ASD II, the AV conduction defects should prompt a detailed family history and clinical evaluation of first-degree relatives.

Adult↗

His electrogram alternans reveal dual atrioventricular nodal pathway conduction during atrial fibrillation: the role of slow-pathway modification.

BACKGROUND: Traditional tools to study dual-pathway atrioventricular nodal (AVN) electrophysiology are not applicable in subjects with permanent atrial fibrillation (AF). The presence of fast-pathway (FP) and slow-pathway (SP) wavefronts and their possible modification remain uncertain in this condition. We demonstrated previously that His electrogram (HE) alternans can determine whether the FP or the SP reaches the His bundle on a beat-by-beat basis. We have now applied this novel index to monitor dual-pathway conduction and the effects of SP modification during AF. METHODS AND RESULTS: In 12 rabbit AVN preparations, HE alternans were confirmed during a standard A(1)A(2) pacing protocol. During AF, in 9 of the 12 hearts, HE alternans indicated the presence of dual pathways. Successful SP modification guided by the HE alternans eliminated the SP, resulting in a predominantly FP conduction during AF in all hearts. This increased the average His-His interval (204+/-14 versus 276+/-51 ms, P<0.001). Morphological studies revealed that SP modification damaged only the posterior extension of the AVN. CONCLUSIONS: We have demonstrated for the first time in rabbits that HE alternans permit "visualization" of dual-pathway electrophysiology and confirmed the presence of both FP and SP wavefronts during AF. This novel index has been used in a selective SP ablation that resulted in a significant slowing of the ventricular rate. HE alternans provide a new insight into the mechanisms of AVN conduction and could guide AVN modification for ventricular rate control in AF clinically.

Animals↗

[Intra-sinus echo: demonstration using direct intracavitary recording of the sinus potential].

The authors searched for intra-sinusal echos during electrophysiological investigation of 53 patients (41 men, 12 women, average age: 61 +/- 12 years). Cycles of sinus echos were recorded in 8 patients (15 per cent). The period during which sinus echos could be recorded was 125 ms (average 40.6 +/- 34 ms). Indirect assessment of sinus node function in patients with sinus echos was normal (corrected sinus node recovery time, estimated atrio-sino atrial conduction times using Narula's technique). A valid and reproducible direct recording of the sinus node potential was only possible in one patient. In this case the echo cycles were provoked by stimulation periods of between 440 and 320 ms (echo zone of 120 ms). All the echos obtained were preceded by a sinus node potential with a different duration and morphology to that observed during basal sinus cycles (respective sino-atrial conduction times 105 and 115 ms). In this patient we were also able to induce sinus echos after a single extrastimulus during the spontaneous rhythm. the echo zone was 130 ms and with a shorter coupling interval (310 ms) two successive sinus echos were recorded. The demonstration of intrasinusal echos by direct recording of the sinus node potential supports the experimental data of Allessie and Bonke on isolated right atrial tissues of the rabbit. Improvements in the technique of endocavitary direct recording of the sinus node potential in man should complete this data by showing the possibility of sinoatrial tachycardias due to reentry.

Action Potentials↗

Dual AV nodal pathways and conduction during atrial fibrillation.

OBJECTIVE: AV node modification reduces ventricular rate during atrial fibrillation (AF). We induced AF in patients with dual AV nodal pathways before and after radiofrequency ablation (RFA) of AV nodal reentry tachycardia (AVNRT) and examined the role of the two pathways in the transmission of impulses during AF. DESIGN AND RESULTS: AF was induced in 30 patients before and after slow pathway ablation. Before RFA mean (AF CLmean) and shortest (AF CLshort) ventricular cycle lengths correlated significantly to ERPf, ERPs, and antegrade Wenckebach block (r = 0.53-0.67). Ablation eliminated slow pathway conduction completely in 10 patients (group A), whereas in 20 patients some slow pathway conduction was still present (group B). After RFA there was a 10% increase in AF CLmean (20%, p < 0.05 in A and 5%, p = NS in B) and 7% in AF CLshort (11%, p = NS in A and 6%, p = NS in B). During isoproterenol infusion after RFA AF CLmean increased 8% (p < 0.05) (14% in A and 6% in B; p < 0.05 in both groups). The effects of RFA were mainly confined to patients with ERPs less than the median value (13% vs 3% in those above median, respectively; p < 0.05). CONCLUSION: The refractory periods of the AV nodal pathways are the main determinants of ventricular rate during induced AF. Slow pathway ablation reduces ventricular rate during AF. This effect was greatest when slow pathway conduction was completely eliminated. A short ERPs predicted a greater reduction in ventricular rate.

Adrenergic beta-Agonists↗

[Study of sinus function and nodal conduction using transesophageal recordings].

Transoesophageal pacing is mainly used for treatment of supraventricular tachycardias and assessment of refractory periods of accessory pathways. It has been proposed for the study of sinus node function and A-V nodal conduction. The aim of this study was to know if transoesophageal pacing could modify the vago-sympathetic tone, therefore the results of the tests, knowing it can be discomfortable and that endodigestive procedures can induce vagal responses. Furthermore, the stimulation is elicited near the left atrium, and not in the right atrium as during endocavitary tests. We have compared in 20 patients (age 68 +/- 12) the results obtained by both endocavitary and transoesophageal pacing (tension 21.2 +/- 4.5 V, duration 16 msec, interelectrode spacing 30 mm). We measured sino-atrial conduction time (SACT), sinus node recovery time (SNRT), Wenckebach's point and nodal refractory periods. After introduction of the oesophageal lead we observed a significant (p less than 0.01) but slight and transitory tachycardia. The results of A-V nodal conduction parameters were not significantly different and were significantly correlated (r = 0.94 for Wenckebach's point and effective refractory period). For the sinus node function, there was no significant difference between the parameters if the oesophago-atrial delay (mean 104.4 +/- 25.9 msec) is taken into account. The correlation is poor for sino-atrial conduction time (corrected SACT, r = 0.55), tighter for sinus node recovery time (maximal corrected SNRT, r = 0.92).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Gaps in anterograde conduction in patients with the short PR interval, normal QRS complex syndrome.

Of 8 patients with the short PR interval, normal QRS complex syndrome studied recently, 3 reported here displayed gaps in anterograde conduction. Atrial premature beats at decreasing coupling intervals conducted with minimal AH prolongation until a zone within the cardiac cycle was reached where conduction failed at a supra-Hisian level. Conduction resumed at earlier atrial coupling intervals and was associated with a sudden increase in the AH interval and the appearance of atrial echo beats with earliest atrial activation on the proximal coronary sinus electrogram. It is suggested that the failure of anterograde conduction at relatively late atrial coupling intervals was caused by a short AH functional refractoriness produced by the pre-excitation of the lower AV junction by a partial AV nodal bypass. Conduction resumed only when early atrial premature beats found the extranodal pathway refractory and were transmitted with decremental delay through the AV node.

Adult↗

[Effects of practolol on A-V conduction during atrial stimulation in 50 patients with and without coronary heart disease].

Practolol was injected intravenously at 3 dose levels (5, 15 and 25 mg total dose) in patients with ischemic heart disease and in non-cardiac cases. The influence of practolol on the P-Q interval at rest and at paced rates (atrial stimulation) of 110, 125 and 140 beats/min was studied: only the 15 mg dose produced a significant prolongation of the P-Q interval of normal patients at rest and at paced rates. No significant P-Q changes were found in patients with ischemic heart disease at all dose levels. It is concluded that practolol has no measurable direct effect on A-V conduction and that patients with ischemic heart disease are not more sensitive as regards A-V conduction.

Adolescent↗

The HMG-CoA reductase inhibitor atorvastatin prevents atrial fibrillation by inhibiting inflammation in a canine sterile pericarditis model.

OBJECTIVE: It has been recently reported that AF is associated with tissue inflammation. Statins reduce C-reactive protein (CRP) levels. However, the effect of statin on atrial fibrillation (AF) is unclear. The purpose of the present study was to evaluate the effect of statin on AF in a canine sterile pericarditis model. METHODS: Sterile pericarditis was created in 20 dogs randomly assigned to two groups: a control group (10 dogs) and an atorvastatin treatment group (10 dogs). Atorvastatin was administered orally (2 mg/kg/day) beginning 1 week before the operation until the end of the study. Before and 2 days after the operation, CRP levels, the duration of induced AF, the atrial effective refractory period (AERP), and intra-atrial conduction time were determined. RESULTS: Before the operation, there were no significant differences in any of the parameters between the two groups. On the second postoperative day, the atorvastatin group had a lower CRP level (7.6+/-0.5 versus 11.7+/-1.3 mg/dl, P<0.0001), a shorter AF duration (177+/-57 versus 534+/-189 s, P<0.0001), a longer AERP (138+/-6 versus 130+/-6 ms, P<0.01), and a shorter intra-atrial conduction time (46+/-3 versus 51+/-5 ms, P<0.01) than the control group. CONCLUSIONS: Atorvastatin can prevent maintenance of AF by inhibiting inflammation in the canine sterile pericarditis model. Atorvastatin may thus be a novel therapeutic agent for AF.

Animals↗

Recording of spike potentials of heart atria and His bundle using microcatheterization via subclavian vein.

The authors describe their own method of right heart microcatheterization by means of transcutaneous introduction of an original unipolar microcatheter into the left subclavian vein. The method makes possible recording of th His bundle electrogram as well as of spike potentials of the sinus node and atrial conduction pathways. His bundle electrograms were recorded in 237 subjects, of whom 72 had ischaemic heart disease and 115 suffered from other cardiopathies, 50 persons with non-cardiac diseases constituted the control group. The high diagnostic value of His bundle electrogram was confirmed, especially in appraising the degree of A-V block, differentiation between aberrant QRS complexes and ventricular extrasystolia, and in other arrhythmias. Recording of spike potentials of the sinus node, atrial conduction pathways, and His bundle, and determination of the interposed intervals allow selective assessments of the impulse propagation velocities in individual segments of heart conduction system, especially on drug administration, and offer valuable information on the genesis of various types of arrhythmias and conduction disturbances.

Action Potentials↗

Comparative effects of thiopental and propofol on atrial vulnerability: electrophysiological study in a porcine model including acute alcoholic intoxication.

BACKGROUND: Atrial tachyarrhythmias (AT) frequently complicate the perioperative period. Alcohol intoxication is a recognized causative factor for dysrrhythmias. We studied the effects of propofol and thiopental on atrial electrophysiology and vulnerability to AT in a closed-chest porcine model in which AT are facilitated by ethanol. METHODS: Thirty-eight pigs were randomly assigned to thiopental (T-group, n=19) or propofol (P-group n=19). All animals were assigned to undergo a right atrial electrical stimulation protocol (RASP) at baseline. Thirty pigs were assigned to undergo additional RASP during ethanol infusion, while the remaining eight were assigned to undergo additional RASP during saline infusion (control group). We analysed effective refractory period (ERP), and intra-atrial conduction interval (ICI) (between atrial sites 4 cm apart), at several cycle lengths (CL). RESULTS: There were no significant differences at baseline. During ethanol infusion, propofol produced a greater rate-dependent decrease in excitability, manifested by a longer minimum paced CL with 1:1 atrial capture: 145 (11) vs 164 (27) ms in the T- and P-group, respectively (P=0.01). Propofol was associated with a greater rate-related slowing in conduction: difference between ICI at CL of 300 ms and ICI at minimum CL: 30 ms in P-group and 22 ms in T-group (P<0.03). In the P-group we observed a longer duration of induced arrhythmias (145 (131) vs 74 (91) s, P<0.03) and a higher proportion with atrial flutter (AFl) (76 vs 19%, P<0.001). CONCLUSIONS: Propofol in this model was more arrhythmogenic than thiopental, as manifested by a longer duration of induced arrhythmias, particularly AFI.

Alcoholic Intoxication↗

Clinical-electrocardiographic correlates of newly acquired left bundle branch block: the Framingham Study.

To determine whether any associated electrocardiographic findings in persons with newly acquired complete left bundle branch block (LBBB) correlate with the prevalence of associated clinically apparent cardiovascular abnormalities, electrocardiograms (ECGs) from all 55 members of the Framingham Study cohort in whom LBBB developed during 18 years of routine prospective biennial examinations were reviewed. A QRS axis left of or equal to 0 degrees, left atrial conduction delay and an inverted T wave in lead V6 on the first ECG with LBBB, and an abnormal ECG in the Framingham examination preceding the appearance of LBBB each correlated with the prevalence of systemic hypertension, cardiomegaly, coronary heart disease and congestive heart failure. However, neither the PR interval nor the duration of the QRS complex on the first ECG with LBBB correlated with the prevalence of any of the associated cardiovascular abnormalities. The 8 patients with neither left atrial conduction delay nor a QRS axis left of or equal to 0 degrees on the first Framingham ECG with LBBB nor an abnormal ECG on the examination preceding the appearance of LBBB were 6 times more likely to remain free of all of the clinical cardiovascular abnormalities than the 47 patients with 1 or more of these 3 electrocardiographic findings (p less than 0.001).

Adult↗

Comparative mechanisms of antiarrhythmic drug action in experimental atrial fibrillation. Importance of use-dependent effects on refractoriness.

BACKGROUND: Antiarrhythmic drugs are considered to terminate atrial fibrillation by prolonging refractoriness, but direct experimental evaluation of this concept has been limited. The atria are activated rapidly during atrial fibrillation, and antiarrhythmic drugs are known to have important rate-dependent actions. The potential role of such properties in determining drug effects during atrial fibrillation has not been evaluated. METHODS AND RESULTS: We evaluated the effects of representative class Ia (procainamide), Ic (propafenone), and III (sotalol) antiarrhythmic drugs on sustained cholinergic atrial fibrillation and atrial electrophysiological properties in anesthetized, open-chest dogs. Loading and maintenance doses were used to produce stable plasma concentrations, and computer-based 112-electrode epicardial mapping was used to study atrial conduction and activation during atrial fibrillation. Clinically used doses of procainamide and propafenone terminated atrial fibrillation in 13 of 13 (100%) and 7 of 10 (70%) dogs, respectively, but a dose of sotalol (2 mg/kg IV) in the clinical range terminated atrial fibrillation in only 2 of 8 (25%) dogs (P = .0005 vs procainamide, P = .08 vs propafenone). Procainamide and propafenone prevented atrial fibrillation induction in 13 of 13 (100%) and 7 of 10 (70%) dogs, respectively, compared with none of 8 dogs for 2 mg/kg sotalol (P < .0001 vs procainamide, P = .004 vs propafenone). A larger dose of sotalol (cumulative dose, 8 mg/kg) was uniformly effective in terminating atrial fibrillation and preventing its induction. All drugs significantly increased atrial refractory period, with effects that were use dependent for propafenone but reverse use dependent for sotalol. Effective doses of all drugs significantly increased the wavelength for reentry at rapid atrial rates in the presence of vagal stimulation into the range observed under drug-free conditions in the absence of vagal input. The inefficacy of clinical doses of sotalol was explained by the reverse use dependence of its effects on refractoriness, which resulted in reduced effects on wavelength at rapid rates. The effects of propafenone on refractoriness were significantly increased at rapid rates, contributing to its ability to increase wavelength and terminate atrial fibrillation. Activation mapping showed that drugs terminated atrial fibrillation by reducing the number and increasing the size of reentry circuits, leading to termination by mechanisms related to block in the remaining circuit(s). CONCLUSIONS: We conclude that antiarrhythmic drugs terminate experimental atrial fibrillation by increasing the wavelength for reentry at rapid rates, leading to a reduction in the number of functional reentry circuits and, eventually, failure of reentrant excitation. Use-dependent effects on refractoriness can limit (in the case of the reverse use dependence of sotalol) or contribute (in the case of propafenone) to antiarrhythmic drug efficacy against atrial fibrillation by determining drug-induced changes in wavelength at rapid atrial rates.

Animals↗