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PubMed1979

Relationship of atrial fibrillatory wave amplitude to left atrial size and etiology of heart disease. An old generalization re-examined.

It is commonly stated that coarse f waves in atrial fibrillation suggest the presence of rheumatic heart disease and large left atrial size, whereas fine f waves indicate non-rheumatic disease and small left atrial size. Using echocardiography as a more reliable indicator of left atrial size, 37 consecutive patients with chronic atrial fibrillation were evaluated. The correlation coefficients between left atrial size and maximum f wave amplitude was -0.12 and -0.07, using average f wave amplitude. Only 53 per cent (9 of 17) of patients with rheumatic heart disease had f wave greater than 1 mm. and 56 per cent (10 of 18) of patients with f wave size less than or equal to 1 mm. had non-rheumatic disease. This study refutes the contention that the f wave amplitude in atrial fibrillation is correlated with either left atrial size or etiology of heart disease. It is possible that an intra-atrial conduction defect is responsible for coarse f wave morphology.

Atrial Fibrillation↗
PubMed2004

Increased vulnerability to atrial fibrillation in transgenic mice with selective atrial fibrosis caused by overexpression of TGF-beta1.

Studies on patients and large animal models suggest the importance of atrial fibrosis in the development of atrial fibrillation (AF). To investigate whether increased fibrosis is sufficient to produce a substrate for AF, we have studied cardiac electrophysiology (EP) and inducibility of atrial arrhythmias in MHC-TGFcys33ser transgenic mice (Tx), which have increased fibrosis in the atrium but not in the ventricles. In anesthetized mice, wild-type (Wt) and Tx did not show significant differences in surface ECG parameters. With transesophageal atrial pacing, no significant differences were observed in EP parameters, except for a significant decrease in corrected sinus node recovery time in Tx mice. Burst pacing induced AF in 14 of 29 Tx mice, whereas AF was not induced in Wt littermates (P<0.01). In Langendorff perfused hearts, atrial conduction was studied using a 16-electrode array. Epicardial conduction velocity was significantly decreased in the Tx RA compared with the Wt RA. In the Tx LA, conduction velocity was not significantly different from Wt, but conduction was more heterogeneous. Action potential characteristics recorded with intracellular microelectrodes did not reveal differences between Wt and Tx mice in either atrium. Thus, in this transgenic mouse model, selective atrial fibrosis is sufficient to increase AF inducibility.

Action Potentials↗
PubMed1990

Demonstration of an area of slow conduction in human atrial flutter.

Ten patients with chronic atrial flutter were studied prospectively using electrophysiologic mapping and pacing techniques to assess the mechanism of atrial flutter and the presence of an area of slow conduction in the atria. Electrograms recorded from greater than or equal to 30 right atrial sites for each patient during atrial flutter demonstrated that right atrial free wall activation was craniocaudal and that the interatrial septum activation was caudocranial, consistent with a reentrant circuit involving the right atrium. In six patients, slow conduction occurred during atrial flutter in the inferior right atrium and was spatially associated with fractionated electrographic recordings. In the other four patients, a "missing" interval of electrical activity occurred in the inferior right atrium for an average of 40% of the atrial flutter cycle. Transient entrainment criteria were demonstrated in each patient during rapid high right atrial pacing. The mean activation time from the high right atrial pacing site to the coronary sinus (inferior left atrial) recording site was long (228 ms) and consistent with activation through an area of slow conduction. During rapid pacing of atrial flutter from the coronary sinus site, no transient entrainment criteria could be demonstrated. The mean activation time from the coronary sinus pacing site to the high right atrial recording site was relatively short (134 ms) and consistent with orthodromic activation of the high right atrium not through an area of slow conduction. High right atrial pacing during sinus rhythm at rates similar to atrial flutter demonstrated a short activation time to the coronary sinus and low right atrial sites (mean 169 and 88 ms, respectively), indicating activation that did not traverse an area of slow conduction. Coronary sinus pacing during sinus rhythm demonstrated the same phenomena. Low right atrial electrograms recorded during sinus rhythm and during rapid pacing of sinus rhythm were not fractionated, although they were during atrial flutter. Thus, atrial mapping and pacing data were complementary, indicating that human atrial flutter in the patients studied was generated by a reentrant circuit in the right atrium, with an area of slow conduction in the low right atrium present only during atrial flutter.

Atrial Flutter↗
PubMed2000

Abnormal cardiac conduction and morphogenesis in connexin40 and connexin43 double-deficient mice.

Connexin40-deficient (Cx40(-/-)/Cx43(+/+)) and connexin43-heterozygous knockout mice (Cx40(+/+)/Cx43(+/-)) are viable but show cardiac conduction abnormalities. The ECGs of adult double heterozygous animals (Cx40(+/-)/Cx43(+/-)) suggest additive effects of Cx40 and Cx43 haploinsufficiency on ventricular, but not on atrial, conduction. We also observed additive effects of both connexins on cardiac morphogenesis. Approximately half of the Cx40(-/-)/Cx43(+/+) embryos died during the septation period, and an additional 16% died after birth. The majority of the latter mice had cardiac hypertrophy in conjunction with common atrioventricular junction or a ventricular septal defect. All Cx40(-/-)/Cx43(+/-) progeny exhibited cardiac malformations and died neonatally. The most frequent defect was common atrioventricular junction with abnormal atrioventricular connection, which was more severe than that seen in Cx40(-/-)/Cx43(+/+) mice. Furthermore, muscular ventricular septal defects, premature closure of the ductus arteriosus, and subcutaneous edema were noticed in these embryos. Cx40(+/-)/Cx43(-/-) embryos showed the same phenotype (ie, obstructed right ventricular outflow tract) as reported for Cx40(+/+)/Cx43(-/-) mice. These findings demonstrate that Cx43 haploinsufficiency aggravates the abnormalities observed in the Cx40(-/-) phenotype, whereas Cx40 haploinsufficiency does not worsen the Cx43(-/-) phenotype. We conclude that the gap-junctional proteins Cx40 and Cx43 contribute to morphogenesis of the heart in an isotype-specific manner.

Animals↗
PubMedDate not supplied

[Sequential pattern of the propagation of excitation in the heart of the sheep Ovis brachyurae].

With the aid of intramural multipolar technique, the earliest focus of the depolarization is revealed in the myocard thickness of the cranioventral region of the right atrium of the sheep. From there the depolarization wave with a saw-edged front is spread along the thickness of the atria. The chronotopography of the intramural activation wave front shows a more complicated picture of the atrial excitation than a smiply radial one. Apparently it is connected with the presence of the atrial conduction system. The main mass of myocardium of free ventricle walls and the lower two thirds of the septum are activated by means of multifocal depolarization. The base third of the septum is the last to be activated. These features of excitation of the ovine ventricle myocardium can be explained by special character of distribution of the Purkinje fibers in myocardium ventricles.

Animals↗
PubMed1975

The role of an accessory atrioventricular pathway in reciprocal tachycardia. Observations in patients with and without the Wolff-Parkinson-White syndrome.

To study the pathway of tachycardia in patients with the Wolff-Parkinson-White (WPW) syndrome and reciprocal tachycardias, results from intracavitary recordings and atrial and ventricular stimulation were reviewed in 71 patients with the WPW syndrome and 54 patients without pre-excitation. In all patients a reproducible tachycardia could be initated and terminated by appropriately timed electrical stimuli. The following findings were accepted as suggesting the participation of an accessory pathway in the tachycardia circuit: 1) no increase in ventriculo-atrial conduction (V-A C) time following ventricular stimuli given with increasing prematurity; 2) activation of right or left atrium (depending upon the location of the atrial end of the accessory pathway) prior to activation of atrium in the His bundle lead; 3) slowing of tachycardia following bundle branch block to the ventricle in which the accessory pathway inserts; 4) V-A C time of early stimuli on the ventricle during the tachycardia equal to or less than the V-A c time following QRS complexes during tachycardia; 5) inability to initiate tachycardia or slowing of tachycardia following the administration of drugs affecting the accessory pathway. Accepted as suggestive for atrioventricular (A-V) nodal re-entry were the following factors: 1) activation of atrium following initiation of tachycardia by a single atrial premature beat after activation of the bundle of His but before or simultaneous with ventricular activation in first and subsequent beats of tachycardia; 2) initiation of tachycardia following a gradual increase in V-A C time with the appearance of a His bundle electrogram in between the premature beat and retrograde atrial activation; 3) gradual increase in V-A C time with the appearance of a His bundle electrogram following ventricular premature beats given with increasing prematurity; 4) two-to-one block distal to the A-V node or His bundle with persistance of tachycardia. If only positive findings were accepted, 51 patients of the WPW group used their accessory pathway during tachycardia. In eight patients re-entry was confined to the A-V node. In the remaining 12 patients the mechanism was not clear. Of the patients not showing pre-excitation in A-V direction, 47 patients seemed to have their re-entry circuit in the A-V node, five patients used an accessory pathway in V-A direction, and in two patients the pathway of tachycardia could not be identified.

Adolescent↗
PubMed1977

Electrophysiologic study of the condition system in normal children.

Values for cardiac conduction intervals obtained from normal children are reported so that the data will be available for comparison with patients who are suspected of having abnormalities. Sinus node recovery time correlated linearly with the resting PP interval. The mean intra-atrial conduction was considerably shorter in children (less than 25 msec) than in adults (42 msec). The atrioventricular node had similar electrophysiologic properties in the child and adult. With aging, the His bundle to Purkinje fiber time increased significantly (P less than .01).

Adolescent↗
PubMed2006

Pirfenidone prevents the development of a vulnerable substrate for atrial fibrillation in a canine model of heart failure.

BACKGROUND: Atrial fibrosis is an important substrate in atrial fibrillation (AF), particularly in the setting of structural heart disease. In a canine model, congestive heart failure (CHF) produces significant atrial fibrosis and the substrate for sustained AF. This atrial remodeling is a potential therapeutic target. The objective of the present study is to evaluate the effects of the antifibrotic drug pirfenidone (PFD) on arrhythmogenic atrial remodeling in a canine CHF model. METHODS AND RESULTS: We studied 15 canines, divided equally into 3 groups: control, CHF canines not treated with PFD, and CHF canines treated with PFD. CHF was induced by ventricular tachypacing (220 bpm for 3 weeks), and oral PFD was administered for the 3-week pacing period. We performed electrophysiology and AF vulnerability studies, atrial fibrosis measurements, and atrial cytokine expression studies. Only canines in the untreated CHF group developed sustained AF (>30 minutes, 4 of 5 canines; P<0.05). Treatment of CHF canines with PFD resulted in an attenuation of arrhythmogenic left atrial remodeling, with a significant reduction in left atrial conduction heterogeneity index (median [25% to 75% interquartile range] 4.96 [3.53 to 5.64] versus 2.52 [2.11 to 2.82], P<0.01; pacing cycle length 300 ms), left atrial fibrosis (16.0% [13.0% to 17.5%] versus 8.7% [5.7% to 10.6%], P<0.01), and AF duration (1800 [1020 to 1800] seconds versus 6 [5 to 22] seconds, P<0.01). Immunoblotting studies demonstrated the drug's effects on multiple cytokines, including a reduction in transforming growth factor-beta1 expression. CONCLUSIONS: Treatment of CHF canines with PFD results in significantly reduced arrhythmogenic atrial remodeling and AF vulnerability. Pharmacological therapy targeted at the fibrotic substrate itself may play an important role in the management of AF.

Animals↗
PubMed2002

Electrophysiological properties of the human atrium in atrial fibrillation.

It has been reported that ectopic foci from the pulmonary veins can initiate atrial fibrillation (AF) and can also act as drivers for maintaining AF. However, not all patients with atrial arrhythmias initiate AF. A substrate for atrial propensity to AF is required for AF initiation and maintenance. Thus, we reviewed and discussed mainly the electrophysiological properties observed in AF. Abnormal atrial electrograms during sinus rhythm and abnormal responses of the atrium elicited by programmed stimulation have been observed more frequently in patients with paroxysmal AF than in those without. A shorter atrial effective refractory period, greater dispersion of the atrial refractoriness and atrial conduction delay are also of electrophysiologic significance in the genesis of AF. Electrical remodeling is likely to be a final common pathway that ultimately supervenes. Even if atrial electrical remodeling facilitates AF initiation and AF perpetuation, the initiation of AF requires a trigger. Further investigation into the electrophysiological properties in AF will be needed in order to contribute to the future development of an appropriate treatment.

Aging↗
PubMed1996

Influence of ECG measurement accuracy on ECG diagnostic statements.

Computer analysis of electrocardiograms (ECGs) provides a large amount of ECG measurement data, which may be used for diagnostic classification and storage in ECG databases. Until now, neither error limits for ECG measurements have been specified nor has their influence on diagnostic statements been systematically investigated. An analytical method is presented to estimate the influence of measurement errors on the accuracy of diagnostic ECG statements. Systematic (offset) errors will usually result in an increase of false positive or false negative statements since they cause a shift of the working point on the receiver operating characteristics curve. Measurement error dispersion broadens the distribution function of discriminative measurement parameters and, therefore, usually increases the overlap between discriminative parameters. This results in a flattening of the receiver operating characteristics curve and an increase of false positive and false negative classifications. The method developed has been applied to ECG conduction defect diagnoses by using the proposed International Electrotechnical Commission's interval measurement tolerance limits. These limits appear too large because more than 30% of false positive atrial conduction defect statements and 10-18% of false intraventricular conduction defect statements could be expected due to tolerated measurement errors. To assure long-term usability of ECG measurement databases, it is recommended that systems provide its error tolerance limits obtained on a defined test set.

Arrhythmias, Cardiac↗
PubMed1998

Rapid drug infusion for termination of atrial fibrillation in an experimental model.

Episodes of paroxysmal atrial fibrillation (PAF) in the ambulatory patient might be terminated promptly by intravenous infusion from an implanted drug delivery system. We have explored this concept in a series of experiments using rapid intra-atrial infusions in dogs. In the acute studies, rapid intra-atrial infusions of procainamide were delivered during continual measurements of epicardial monophasic action potentials (MAP), atrial effective refractory periods (ERP), and right to left atrial conduction times (CT) in 9 dogs. In the chronic studies, 20 episodes of sustained PAF were induced in 4 dogs after six weeks of rapid or burst atrial pacing from a specially programmed implanted pacemaker. Rapid infusions of procainamide were then delivered to the right atrium through a previously implanted catheter connected to a subcutaneous access port. Procainamide significantly increased the duration of the atrial MAP, ERP and CT in the acute experiments. It also terminated induced PAF within five minutes of the end of infusion in all twenty of the chronic experiments. We conclude that rapid intra-atrial infusion of procainamide is very effective in this animal model of PAF, and that such infusion prolongs atrial MAP, ERP and CT.

Action Potentials↗
PubMed1975

Electrophysiologic properties of perhexiline.

Perhexiline maleate (Pexid), a promising clinical antiarrhythmic and antianginal drug, was evaluated for its electrophysiologic effects on the entire conduction system of the intact canine heart throughout a wide range of therapeutic and potentially toxic doses. Intracardiac conduction times were measured by bipolar intramyocardial and transvenous endocardial electrodes before and following the intravenous administration of each dose of perhexiline maleate, 3 mg/kg every 30 min for a total of 4 doses in 7 open-chest anesthetized dogs. Eight animals served as controls in which similar operative technique and electrophysiologic variables were recorded after infusion of the maleate diluent. In addition, the effects of perhexiline on atrial and ventricular thresholds to electrical stimulation were recorded, as well as the QRS and QT intervals, sinus rate, and rhythm disorders. It was observed that perhexiline did not significantly (p greater than .05) alter sinus rate, QT interval, QRS duration, PR interval, intra-atrial conduction time, atrioventricular nodal conduction time, and His-Purkinje conduction velocity. The drug did not affect the cardiac threshold to electrical stimulation of less than 0.1 ma. No ectopic atrial or ventricular activity emerged during the accumulated influence of the agent. From this study, it is concluded that perhexiline does not exert deleterious actions on the conduction system of the intact canine heart. In view of the negligible toxic effects and its efficacy in treating ventricular tachyarrhythmias in patients, the drug deserves further clinical evaluation.

Animals↗
PubMed1999

Relationships among electrophysiological findings and clinical status, heart function, and extent of DNA mutation in myotonic dystrophy.

BACKGROUND: Impulse-conduction abnormalities and arrhythmias are common in myotonic dystrophy (MD). This study was performed to determine whether a correlation exists between electrophysiological (EP) testing data and clinical status, heart function, or size of the DNA abnormality (cytosine-thymine-guanine sequence repeat). METHODS AND RESULTS: Eighty-three MD patients underwent invasive EP studies prompted primarily by the presence of asymptomatic conduction abnormalities. AV conduction disturbances were common and mainly distal (HV interval, 66.2+/-14 ms). AV conduction observed from the surface ECG was generally concordant with endocardial measurements. However, 11 of 20 patients with normal surface ECGs had abnormal subhisian conduction. Atrial arrhythmias were inducible in 41% of cases and correlated with prolongation of the AH interval (P=0.02) and a shorter atrial refractory period (P=0.04). Induction of ventricular arrhythmias (18%) correlated strongly with age (P=0. 0003). After adjustment for age, the extent of DNA mutation correlated with the Walton score (P=0.0018) but not with conduction abnormalities or induction of arrhythmias. CONCLUSIONS: Prolongation of the HV interval is the most common conduction abnormality in MD and can be reliably recognized only by invasive EP testing. It raises the issue of prophylactic pacing to limit the incidence of sudden death in MD. Atrial and ventricular arrhythmias are often inducible, although their predictive value remains to be determined. Young age emerged as the most powerful predictor of inducible ventricular tachyarrhythmias. Conversely, we found no relationship between ECG or EP abnormalities recorded during invasive testing and the DNA mutation size or severity of peripheral muscle involvement.

Adult↗
PubMed1998

Altered pattern of connexin40 distribution in persistent atrial fibrillation in the goat.

INTRODUCTION: Since altered expression of gap junction proteins (connexins) in diseased myocardial tissue may lead to abnormal electrical coupling between cardiomyocytes and hence contribute to arrhythmogenesis, the expression of connexin(Cx)40 and Cx43 was studied in atrial appendage from goats in sinus rhythm (SR) and persistent atrial fibrillation (AF). METHODS AND RESULTS: Biopsies were taken from the left and right atrial appendages from goats in SR or after pacing-induced persistent AF. Analyses of Cx40 and Cx43 mRNA and protein levels, using quantitative (competitive) polymerase chain reaction and western blotting, respectively, revealed no significant changes in the overall expression of Cx40 and Cx43 as a result of persistent AF. At the cellular level, immunohistochemistry and confocal laser scanning microscopy showed a homogeneous distribution of either connexin in atrial sections taken during SR. After induction of AF, the distribution of Cx43 gap junctions was unchanged whereas the Cx40 pattern showed marked inhomogeneities with small areas (0.15 to 0.6 mm in diameter, 25% of section surface area) of low-density Cx40 located between larger areas of normal (unchanged) Cx40 density. Activation mapping (244 electrodes, spatial resolution 2.25 mm) of the right atrial wall did not reveal changes in atrial conduction velocity. CONCLUSION: Pacing-induced persistent AF in the goat gave rise to changes in the spatial organization of Cx40 gap junctions. Although the overall conduction velocity appeared not to have changed, microheterogeneities in conduction due to the local redistribution of Cx40 gap junctions might have contributed to the initiation and maintenance of AF.

Animals↗
PubMed1992

Effects of physiological aging on cardiac electrophysiology in perfused Fischer 344 rat hearts.

Aging effects on heart rate and atrioventricular (AV) conduction were studied in Langendorff-perfused hearts from 18 mature (4-6 mo), 12 middle-aged (12-14 mo), and 18 senescent (24-26 mo) Fischer 344 rats. Heart rate decreased with increasing age from 218 +/- 18 in mature to 196 +/- 27 (mean +/- SD) beats/min in middle-aged rats to 183 +/- 22 beats/min in senescent rats (analysis of variance, P less than 0.001). Spontaneous AV conduction time increased from 43 +/- 7 to 49 +/- 5 to 62 +/- 9 ms with aging (P less than 0.0001). Paced AV conduction time also lengthened with aging, and AV Wenckebach block cycle length increased from 122 +/- 10 to 133 +/- 9 to 152 +/- 16 ms (P less than 0.005). Intra-atrial conduction time was unaffected by age. Age differences in heart rate and AV conduction responses to isoproterenol (0.5 x 10(-9) to 1 x 10(-7) M) were noted with greater sensitivity at lower doses in hearts from younger rats. In separate experiments, 18 mature and 19 senescent Fischer 344 rats received reserpine (0.25 mg.kg-1.day-1 ip) for 6 days before study. Age differences in heart rate and AV conduction persisted (P less than 0.0001). Histopathological examination of AV nodal and His-bundle tissues in three hearts from each age group showed increased intercellular collagen with advancing age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1997

[Auricular vulnerability: what information can be obtained from the study of auricular vulnerability? How to perform this study?].

The factors involved in atrial vulnerability are the presence of intra-atrial conduction disorders and abnormalities of refractory periods which are short, dispersed and poorly adapted to heart rate. All these factors are arrthythmogenic. The main value of the study of atrial vulnerability consists of investigation of unexplained ischaemic cerebrovascular accidents in young subjects. In practice, atrial vulnerability can be measured in the context of a classical endocavitary electrophysiological investigation. The stimulation and recording parameters must be standardized. Latent atrial vulnerability can be considered to be present when at least one of the following elements are found: significant inducibility, very short and poorly adapted effective refractory periods, decreased latent atrial vulnerability index.

Atrial Fibrillation↗
PubMed1996

Separation of cardiac conduction system and atrial activities by spatial regression.

Multiple channel magnetocardiography is potentially useful for the study of the cardiac conduction system. However, normal atrial repolarization occurs simultaneously and obscures the interpretation of the net signal. Magnetocardiographic data in four normal subjects at rest and mild exercise were found to exhibit high spatial correlation during atrial activation. Based on measured channel-to-channel covariances, the atrial repolarization signals as measured in channels in the null zone of conduction system activity were used to estimate atrial repolarization in all channels. A linear prediction method was used which based on the "kriging" estimator of geostatistical theory. Due to high spatial correlations in the limited thoracic region studied, predictions based on a single null channel were found to be adequate. Removal of the atrial component facilitates the beat-by-beat estimation of conduction system changes during rest and exercise using the multiple channel biomagnetometer.

Atrial Function↗
PubMed1999

Dispersion of filtered P wave duration by P wave signal-averaged ECG mapping system: its usefulness for determining efficacy of disopyramide on paroxysmal atrial fibrillation.

INTRODUCTION: Although it is desirable to know drug efficacy before initiating antiarrhythmic therapy, there have been no methods for this evaluation. P wave signal-averaged ECG (P-SAECG) is useful to detect subtle changes in disturbance of atrial conduction. The purpose of this present study was to test whether P-SAECG mapping system would give any information on the efficacy of disopyramide on the prevention of paroxysmal atrial fibrillation (PAF). METHODS AND RESULTS: P-SAECG was performed before disopyramide treatment, at 3 hours after a single dose of oral disopyramide (200 mg), and after 4 weeks of disopyramide treatment (300 mg/day). After measuring the filtered P wave duration by the vector magnitude and mapping methods, we calculated filtered P wave duration dispersion, difference between the maximal and minimal filtered P wave duration within 16 chest leads at these three time points. Filtered P wave duration and filtered P wave duration dispersion before treatment were longer in 32 patients with symptomatic PAF than in 31 healthy volunteers. Disopyramide was effective for suppression of PAF in 17 patients and ineffective in 15 patients after 4 weeks of treatment. Filtered P wave duration was similarly prolonged at 3 hours in the two groups, whereas filtered P wave duration dispersion at 3 hours after the disopyramide administration behaved differently; it decreased in all of the effective group and increased in all of the ineffective group. The effective patients were prospectively followed with the same treatment for 6 months. In 16 (94%) of these 17 effective patients, no PAF was documented and they remained to be asymptomatic. CONCLUSIONS: Thus, measuring filtered P wave duration dispersion with the P-SAECG mapping method after a single administration may predict the long-term efficacy of disopyramide in patients with PAF.

Administration, Oral↗