Atrial Vulnerability Research Articles

Étude échographique prospective : hypertrophie lipomateuse du septum inter-auriculaire

Within this one-year echocardiographic prospective study, we collected 11 cases of lipomatous hypertrophy of the inter atrial septum (LHIS) (prevalence : 2.2 %). 45 % of them had inter-atrial block at ECG and we found a strong link with atrial arythmias. This link implies a search for atrial vulnerability in case of stroke without any other cause than LHIS.

Relation between Spontaneous Atrial Fibrillation and Atrial Vulnerability in Patients with Wolff‐Parkinson‐White Pattern

An intracavitary electrophysiological study was carried out on 103 patients with Wolff-Parkinson-White (WPW), 23 symptomatic patients had documented episodes of atrial fibrillation, 54 symptomatic patients had atrioventricular reentrant tachycardias, and 26 asymptomatic. Patients were examined for the relation between spontaneous atrial fibrillation and atrial vulnerability, defined as the possibility to induce sustained (greater than 1 minute) episodes of atrial fibrillation with a stimulation protocol excluding atrial bursts. Atrail fibrillation induction was attempted by single and double atrial extrastimuli during pacing at two different cycle lengths and incremental atrial pacing. Sustained atrail fibrillation was induced in 65% of the patients with spontaneous atrial fibrillation, and in 13% of the symptomatic patients with documented episodes of atrioventricular reentrant tachycardias and in 15% of the asymptomatic patients (P less than 0.0005). Atrial vulnerability was higher in patients with spontaneous atrial fibrillation than in patients without this arrhythmia. No significant difference was observed between symptomatic without atrial fibrillation and asymptomatic patients.

Electrophysiologic effects and efficacy of cibenzoline on stimulation-induced atrial fibrillation and flutter and implications for treatment of paroxysmal atrial fibrillation

The effects of intravenous cibenzoline (1.5 mg/kg) on atrial vulnerability and electrophysiology were assessed in 25 patients with documented paroxysmal atrial fibrillation (AF), in whom sustained (> 30 seconds) AF was induced by atrial stimulation with up to 2 extrastimuli and paced rates between 100 and 180 beats/min. In 7 patients AF persisted despite the application of cibenzoline, and in 8 patients induction of AF was not prevented. In 10 patients the induction of sustained AF was prevented by cibenzoline. Intraatrial conduction time, flutter cycle length and shortest ventricular cycle length during AF were increased by cibenzoline (p ≤ 0.01). Sinus cycle length was decreased (p ≤ 0.05), whereas sinus node recovery time remained unchanged. The effective refractory period of the right atrium was not significantly affected. Eight patients with frequent episodes of paroxysmal AF received oral cibenzoline for control of paroxysmal AF irrespective of the efficacy of intravenous cibenzoline. Prevention of stimulation-induced AF predicted successful treatment of paroxysmal AF (p = 0.018). Cibenzoline could be effective in the treatment of atrial arrhythmias, and selection of an antiarrhythmic therapy for recurrent AF seems to be useful.

Atrial fibrillation and atrial vulnerability in the Wolff-Parkinson-White syndrome

To explore the etiology of paroxysmal atrial fibrillation (AF) in the Wolff-Parkinson-White (WPW) syndrome, we examined the rates of AF episodes and performed electrophysiologic studies in 58 patients with WPW syndrome. They were classified into three patient groups depending on the property of antegrade conduction over accessory pathways: manifest WPW, intermittent WPW, and concealed WPW. Atrial vulnerability was defined as the inducibility of AF or repetitive atrial responses. The three groups were: 24 patients in manifest WPW, aged 42 +/- 15 yrs, 38% with AF; 12 patients in intermittent WPW, aged 40 +/- 15 yrs, 25% with AF; 22 patients in concealed WPW, aged 44 +/- 16 yrs, 9% with AF. There were no significant differences in the mean age between the groups. The incidences of atrial vulnerability detected in electrophysiologic studies in each group were 54%, 42%, and 27% respectively. The incidence of AF was well correlated with that of atrial vulnerability (p less than 0.01). The effective refractory periods (ERP) of the atrium and the retrograde ERP of the accessory pathway did not differ significantly between the three groups. Atrial conduction delay was more prominent in manifest WPW than in concealed WPW. The incidence of AF and atrial vulnerability was highest in the manifest WPW group, intermediate in the intermittent WPW group, and lowest in those patients with concealed WPW. The difference in incidence between the manifest WPW group and the concealed WPW group was significant (p less than 0.05). Therefore, the property of antegrade conduction over accessory pathways may be related to the genesis of AF in the WPW syndrome.

Correlation Between Modification of Electrophysiologic Parameters by Hydroquinidine (Chlorhydrate) and Its Effects on Atrial Vulnerability

Correlation Between Modification of Electrophysiologic Parameters by Hydroquinidine (Chlorhydrate) and Its Effects on Atrial Vulnerability

Paroxysmal atrial fibrillation with and without primary atrial vulnerability: Clinical and electrophysiological differences

Primary atrial vulnerability defined as induction of repetitive atrial firing by a single atrial extrastimulus cannot always be demonstrated in patients with paroxysmal atrial fibrillation. The authors studied the electrophysiological differences between paroxysmal atrial fibrillation with and without primary atrial vulnerability. In 14 of 31 patients with documented history of atrial fibrillation, single extrastimulation at the high right atrium initiated repetitive atrial firing defined as rapid disorganized atrial activity continuing longer than 1 second. In the 14 patients with vulnerable atrium, the atrial effective and functional refractory were periods significantly shorter and the duration of the local atrial electrogram of the premature beat was longer and was fractionated. The % sinus node recovery time was longer in patients without vulnerability. Nine of the 17 patients without atrial vulnerability had sinus node dysfunction, and 4 of the remaining 8 patients had a repetitive type of atrial automatic tachycardia. In contrast, only 3 (21%) of the 14 patients with vulnerability had sinus node dysfunction, and none showed repetitive atrial tachycardia. The high prevalence of sinus node dysfunction or repetitive type of atrial automatic tachycardia in patients without primary atrial vulnerability suggests that these transient electrophysiological modifications which are not dealt with in the basic conditions may have a role in the enhancement of atrial vulnerability.

Arrhythmias in the elderly

Longitudinal Cohort Study: Electrocardiogram and blood pressure were taken biannually along with history taking, physical examination and other laboratory studies. 6,690 subjects were included in this study in whom at least 7 out of 9 biannual check up examinations were performed. At the end of the study period, their ages ranged from about 40 to 90 years. The incidence of atrial fibrillation was about 0.2% in the forties and early fifties and increased to 0.6% by the late fifties. The incidence of atrial fibrillation was then increased almost linearly up to 2.5% at the end of the eighties. Likewise, incidence of CRBBB and LBBB was also increased with age even after the age of sixty; 1.0% at the fifties to 7.5% at the eighties in CRBBB and 0.05% at the fifties to 1.4% at the eighties in LBBB, respectively. Holter ECG Study: Holter ECG was recorded in 164 healthy subjects aged 14 to 87 years in whom no arrhythmias were found in the routine 12 leads ECG at entry to the study. In 96.9% of the subjects APC was recorded in the 24-hour Holter ECG irrespective of their age. The total number of APCs in 24 hours significantly increased with age, especially after age sixty. The incidence of couplet or short run APCs was 21.4% under age sixty and 74.2% above age sixty. Electrophysiologic Studies in Patients with Paroxysmal Atrial Fibrillation (Paf): Repetitive atrial firing (RAF) elicited by premature atrial stimulation, and prolonged intra-atrial electrogram (PAE) with multiple (more than 7) spikes recorded during sinus rhythm were taken as indicators of atrial vulnerability. RAF and PAE was observed in more than 60% of Paf patients with or without sick sinus syndrome (SSS), but only approximately 25% in the control group (without SSS). It was also noted that in patients with SSS, who were generally of old age, RAF was observed in about 63% even without Paf. These results suggest that the atrial vulnerability might be an expression of the common electrophysiologic properties of the atrial muscle in the elderly with atrial arrhythmias and/or SSS. Syncopal Episodes due to Transient Severe Hyperkalemia in the Elderly: Two patients with mild to moderate chronic renal failure developed transient severe hyperkalemia (9.9, 7.3 mEq/L, respectively), severe sinus bradycardia with sinus arrest and syncopal episodes. These transient findings almost completely improved in a few days by kayexatete and bicarbonate, and temporary back-up atrial pacing. Hyperkalemia was disproportionately severe compared to BUN and serum creatinine.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability in patients with paroxysmal supraventricular tachycardia

To assess the effects of β-adrenergic stimulation on atrial latency and atrial vulnerability, the electrophysiologic properties of the atrium were studied before and during intravenous infusion of isoproterenol at 2 to 5 μg/min in 11 patients with paroxysmal supraventricular tachycardia exhibiting atrial latency during programmed atrial extrastimulation. In all patients, the isoproterenol infusion reduced the extent of maximum atrial latency (from 86 ± 19 to 62 ± 16 ms, p < 0.001). This was accompanied by a significant shortening of both effective and functional refractory periods of the atrium (from 213 ± 31 to 174 ± 40 ms, p < 0.005 and from 259 ± 31 to 215 ± 29 ms, p < 0.001, respectively). The intraatrial and interatrial conduction times were also significantly reduced (from 24 ± 15 and 63 ± 17 to 15 ± 10 and 48 ± 15 ms, p < 0.005, respectively). In 3 patients with demonstrable atrial vulnerability, the isoproterenol infusion abolished the inducibility of repetitive atrial responses or atrial flutter, or both. Although the clinical significance of the suppressive action of β-adrenergic stimulation on atrial vulnerability remains to be determined, the present study has demonstrated that β-adrenergic stimulation significantly reduces atrial latency.

Relation Between clinical presentation and induced arrhythmias in the Wolff-Parkinson-White syndrome

Electrophysiologic testing is warranted in patients with the Wolff-Parkinson-White (WPW) syndrome presenting with rapid atrial fibrillation (AF) or ventricular fibrillation. Indications are less clear in patients presenting only with atrioventricular reentrant tachycardia (ART). A knowledge of propensity of this latter group to show a rapid ventricular response in the event of AF and the ability of electrophysiologic testing to reproduce the type and rate of clinical arrhythmias are relevant to this decision. The records of 126 symptomatic patients with manifest WPW syndrome were reviewed and separated into 4 groups according to presentation: group 1—AF; group 2—ART; group 3—palpitations suggesting ART; and group 4—AF and ART. All patients except those in group 3 had electrocardiographically documented clinical arrhythmias, and these arrhythmias were compared with those induced during electrophysiologic testing. The shortest RR interval during induced AF and the cycle length of induced ART correlated well with those occurring clinically (r = 0.72, p < 0.00001), as did the cycle length of induced ART (r = 0.79, p < 0.00001). Patients presenting with AF (65%) had a higher incidence of atrial vulnerability (48%) and sustained AF at electrophysiologic testing than those presenting with ART (16% and 5%) or undocumented palpitations (27% and 21%). Forty-one percent of patients with ART and 51% with undocumented palpitations had potentially lethal rates (shortest RR interval <250 ms) during induced AF. The ability to reproduce clinical arrhythmias and the frequency of rapid rates during AF induced in patients presenting with only ART or undocumented palpitations supports the recommendation for electrophysiologic testing in symptomatic patients with WPW.

Data on the proarrhythmic action of liooflazine (clinium): Effects ofthe drug on atrial and ventricular vulnerability

Data on the proarrhythmic action of liooflazine (clinium): Effects ofthe drug on atrial and ventricular vulnerability

Electrophysiologic profile of asymptomatic Wolff-Parkinson-White pattern

Electrophysiologic testing in patients with asymptomatic Wolff-Parkinson-White syndrome (WPW) may be useful in defining arrhythmic substrates and predictors of fatality. Forty-two patients with asymptomatic WPW, mean age 36 years, underwent electrophysiologic studies and were followed prospectively. They were compared with a matched control group of patients studied within the same period for documented tachycardia associated with the WPW syndrome. Asymptomatic patients had longer anterograde effective refractory periods of the accessory pathway, longer minimum cycle lengths maintaining 1:1 conduction over the accessory pathway, longer minimum RR intervals between consecutive preexcited beats during atrial fibrillation (AF) and longer mean RR intervals during AF than their symptomatic counterparts. Sustained reciprocating tachycardia could not be induced in most patients and induction of AF required rapid atrial pacing in all patients. Nine patients had an anterograde effective refractory period of less than 270 ms and 17% had minimum cycle length less than 250 ms during induced AF. Over a follow-up of 29 ± 18 months, 1 patient died of noncardiac causes and the rest remained asymptomatic. Thus, patients with asymptomatic WPW have deficient electrophysiologic substrates to maintain orthodromic reciprocating tachycardia under baseline conditions and do not have atrial vulnerability. Seventeen percent of patients had potentially lethal ventricular rates during induced AF.

Effect of sotalol on human atrial action potential duration and refractoriness: cycle length dependency of class III activity.

Using intracardiac electrophysiological techniques the effects of sotalol hydrochloride were studied in the right atrium in eight patients with paroxysmal supraventricular atrial arrhythmias. Atrial action potential duration was recorded from two well separated standard sites via endocardial contact electrodes before and for 30 minutes after intravenous sotalol (1 mg X kg-1). Atrial effective refractory period and vulnerability to atrial arrhythmia initiation were assessed by premature extrastimulation. All patients developed a prolonged action potential duration (mean +6%, p less than 0.01 in high atrial site; +8%, p less than 0.01 in low atrial site), with similar increases in atrial effective refractory period (mean +9%, p less than 0.01). The small regional difference in action potential duration detected between these well separated recording sites was minimally decreased, indicating no tendency towards increased regional inhomogeneity of repolarisation. The relatively refractory zone as denoted by the gap between atrial effective refractory period and action potential duration was slightly reduced, and transient repetitive atrial depolarisations, initially provoked by extrastimuli in two patients, were abolished. The relation between atrial interval and duration, investigated using two modes of paced cycle length modification, showed that a gradual reduction in pacing cycle length was more potent in shortening action potential duration than was isolated premature extrastimulation. Sotalol was significantly more effective in opposing shortening of the action potential duration caused by progressive cycle length reduction than that caused by isolated extrastimulation. The class III antiarrhythmic activity of sotalol, confirmed in the atrium, is dependent on cycle length and mode of cycle length alteration. Under study conditions, there was no tendency to increase atrial vulnerability or regional non-uniformity of repolarisation.

Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: incidence after surgical ablation of the accessory pathway.

The effect of surgical ablation of ablation of atrioventricular accessory pathways on the incidence of atrial fibrillation in patients with Wolff-Parkinson-White syndrome was examined and the results of preoperative electrophysiologic testing were studied to determine factors predictive of outcome. Among 50 consecutive surgical cases, 19 patients were identified with a past history of at least one episode of spontaneous atrial fibrillation documented by electrocardiogram before surgery. The mean number of episodes of atrial fibrillation was 1.97/patient/year during a mean symptomatic period of 6.9 years before surgery. These patients were compared with 19 consecutive patients undergoing surgery during the same time period who had a history of only reciprocating tachycardia. Patients with atrial fibrillation had a significantly shorter antegrade accessory pathway effective refractory period (270 +/- 39 vs 330 +/- 107 msec; p less than .05) and much faster ventricular rates during induced atrial fibrillation (shortest RR interval 219 +/- 73 vs 294 +/- 60 msec, p less than .005; average RR interval 324 +/- 109 vs 405 +/- 127 msec, p less than .01). Patients with atrial fibrillation also had longer PA intervals (47 +/- 13 vs 37 +/- 7 msec; p less than .02). At preoperative electrophysiologic testing, 18 patients with atrial fibrillation had atrial fibrillation induced and 14 sustained the arrhythmia for longer than 10 min. In contrast, atrial fibrillation, although induced in 14 of 19 patients with reciprocating tachycardia, was not sustained in any. Thus electrophysiologic testing suggested that both accessory pathway properties and atrial vulnerability may predispose to atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial vulnerability in the immature canine heart

The induction of repetitive atrial responses during atrial extrastimulation (atrial vulnerability) was studied in 3 groups of dogs. Group I consisted of 19 neonatal puppies (age 3 to 15 days), group II of 10 older puppies (age 5 to 11 weeks) and group III of 10 adult dogs. In all dogs, atrial extrastimulation was performed coupled to a constant paced rhythm that was 85 ± 7 % of the sinus cycle length at rest in group I,86 ± 6% in group II and 83 ± 10% in group III. In all groups, atrial repetitive responses were observed as the atrial functional refractory periods were approached during extrastimulation; however, the number of repetitive atrial responses was greater and the duration of repetitive firing longer in the neonates. In the neonatal group as many as 28 repetitive atrial responses were induced (9.4 ± 8.2 beats) and the duration of repetitive atrial firing averaged 838 ms (range 120 to 2,425). In contrast, in only 1 of 20 older puppies and adult dogs were more than 2 repetitive atrial beats observed (number of repetitive atrial beats in group II, 1.7 ± 1; in group III, 1.2 ± 0.5). Thus, the normal neonatal atrium is more susceptible to intraatrial reentry in response to premature extrastimulation than the more mature canine atrium. This enhanced atrial vulnerability may be related to the shorter atrial refractory periods of the neonate and may be of importance in understanding the genesis of certain dysrhythmias in the human neonate.

Effect of intravenous flecainide on atrial vulnerability in man.

Sixteen patients were investigated by means of programmed atrial stimulation at 2 different driving rates: 100/min and 120/min. All patients had an increased atrial vulnerability at both driving rates. After the administration of intravenous flecainide (1 mg/kg bodyweight as a bolus, followed by the same amount infused over a period of 20 minutes), the increased vulnerability was abolished in 11 and 9 patients, respectively. In the remaining patients the rate of induced atrial tachyarrhythmia decreased. These findings correlate with a significant prolongation of the effective refractory period of the right atrium and a corresponding significant shortening of its relative refractory period. It is concluded that flecainide may be effective in the treatment of atrial arrhythmias in humans.

Effect of intravenous flecainide on atrial vulnerability in man.

Sixteen patients were investigated by means of programmed atrial stimulation at two different driving rates: 100 and 120/min. All patients had an increased atrial vulnerability at both driving rates. After intravenous flecainide application (1 mg/kg body weight as a bolus followed by the same amount given by infusion over a period of 20 min) the increased vulnerability was abolished in 11 and 9 patients respectively. In the remaining patients the rate of induced atrial tachyarrhythmia decreased. These findings correlate with a significant prolongation of the effective refractory period of the right atrium and a significant shortening of the relative refractory period of the right atrium. It is concluded that flecainide may be effective in the treatment of atrial arrhythmias in man.

Effect of whiskey on atrial vulnerability and “holiday heart”

Vulnerability to atrial fibrillation and flutter was examined in 11 alcohol abusers who did not have cardiomyopathy or manifest heart failure. Atrial extrastimulation was done with rapid pacing (drive cycle length 500 ms) to facilitate induction of atrial vulnerability, seen in four alcohol abusers. The remaining seven were retested 30 minutes after drinking 60 to 120 ml of 86 proof whiskey (ethanol blood levels were 49 to 101 mg/100 ml but pulmonary capillary wedge pressure remained normal in all) and atrial fibrillation or flutter was induced in three of the drinkers. Three nondrinkers, symptomatic with sinus bradycardia but not in heart failure, were found not to be vulnerable to atrial fibrillation or flutter, but flutter was induced in two of the three after drinking whiskey. Whiskey did not alter atrial functional refractory periods (mean +/- standard error of the mean 297 +/- 14 to 290 +/- 12 ms) or widen the dispersion among three disparate right atrial sites (57 +/- 13 to 47 +/- 12 ms). Thus, whiskey enhanced vulnerability to atrial fibrillation and flutter in patients without heart failure or cardiomyopathy, substantiating the "holiday heart" syndrome.

Failure in the rate adaptation of the atrial refractory period: its relationship to vulnerability

We evaluated the relationship of rate-dependent changes in atrial refractoriness to atrial vulnerability in 39 patients. Vulnerability was considered present when sustained atrial tachyarrhythmias, lasting longer than 1 minute, could be provoked with one to three extra stimuli. Adaptation of atrial refractory period duration to rate was defined as: normal: steep rate reduction with a linear correlation slope value of 0.08 or more; non-adaptation: absence of rate reduction, the slope value being 0 to 0.01; poor adaptation: slight reduction with rate, the slope having values of 0.02 to 0.07. Increased vulnerability was demonstrable in 16 of 17 patients with non-adaptation of the effective refractory period (ERP), and in 10 of 10 with a similar defect of the functional refractory period (FRP); in the intermediate category (poor adaptation) the results for ERP and FRP were 7 11 and 5 6 . By way of contrast when both measurements showed normal adaptation, vulnerability was elicited in 2 9 patients. The significance between these groups showed P < 0.005. Of 17 patients with atrial arrhythmia by Holter, 14 showed poor or non-adaptation of the ERP. It is suggested that poor or absent rate adaptation of the atrial refractory period, and a propensity to atrial fibrillation or flutter, constitute a clinical entity not previously described.

Atrial and ventricular vulnerability in a patient with the Wolff-Parkinson-White syndrome.

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter. The atrial and ventricular effective refractory periods were 180 ms and less than 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atrial or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal by-pass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.

A microcomputer-controlled 3-channel stimulator for investigating atrial and ventricular vulnerability of the heart (author's transl)

Article Mikrocomputer-gesteuerte 3-Kanal-Stimulationseinrichtung zur Analyse der atrialen und ventrikulären Vulnerabilität des Herzens - A Microcomputer-Controlled 3-Channel Stimulator for Investigating Atrial and Ventricular Vulnerability of the Heart was published on January 1, 1981 in the journal Biomedical Engineering / Biomedizinische Technik (volume 26, issue 6).