Aberrant ventricular conduction during atrial fibrillation.
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Atrial Fibrillation↗
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[1:1 Conduction in atrial flutter through lidocaine].
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Adult↗
Arrhythmias and conduction disturbances following cardiac operation for the removal of left atrial myxomas.
Between September, 1971, and April, 1982, 11 patients (seven female) with left atrial myxomas underwent surgical resection at Cedars-Sinai Medical Center. The tumors ranged in size from 4 to 9 cm (mean 6.3 cm) and were attached to the interatrial septum (four superiorly, four inferiorly), the free atrial wall (one posteriorly, one at the dome), or both (one). Although all patients were symptomatic preoperatively, arrhythmias were uncommon; only one had chronic atrial fibrillation, and two others had had single episodes of paroxysmal atrial fibrillation in the immediate preoperative period. Early postoperatively, all but one patient had episodes of atrial fibrillation (eight patients), atrial flutter (four patients), junctional rhythm (six patients), sinus arrest (two patients), or complete heart block (three patients). Ten patients required antiarrhythmic therapy, and two required permanent pacemaker implantation. After a mean follow-up of 48 months (range 7 to 124), seven patients continue to have episodic or chronic supraventricular arrhythmias, with only three patients not using antiarrhythmic drugs regularly. The pathophysiological basis for these arrhythmias is unclear, but some patients appear to have sustained injury to the sinus node or atrioventricular node, while others have developed interatrial or intra-atrial conduction delays. Attention should be directed to the basis of these arrhythmias and conduction disturbances, as surgical technique may be the major determinant of this early and late postoperative complication.
Adult↗
[Mechanisms favoring and triggering atrial fibrillation].
Many experimental and clinical studies have demonstrated that it is possible to trigger atrial fibrillation (AF) by vagal stimulation which reduces and disperses the atrial refractory periods and decreases the threshold of fibrillation. In order to induce fibrillation, it is necessary to deliver a stimulation near to the refractory period. It has also been shown that, in these conditions, there is a delay in atrial conduction. A temporal relationship between the preceding diastole and the coupling interval increases atrial vulnerability and plays an equally important role. The decrease in the effective atrial refractory period, especially when the values are widely dispersed, and the delay in conduction predisposing to atrial reentry, may be considered to be the two most important electrophysiological mechanisms of AF. However, in order to maintain AF, the atrium must be dilated, especially when there is a concurrent cardiac disease. The presence of a shorter "wave length" of activation allowing multiple reentry circuits is an essential condition for sustaining AF. All conductions of induction and maintenance of AF may be observed without participation of S.N.A.. When no cause of AF (atrial pathology, etc.) is apparent, a short atrial refractory period with dispersion of its values and slowing of atrial conduction in presence of an extrastimulus are the probable inducing factors.
Atrial Fibrillation↗
Effects of hydrostatic pressure on conduction and excitability in rabbit atria.
The effects of hydrostatic pressure on cardiac conduction and excitability were studied in 39 rabbit right atrial preparations. Increases in pressure significantly increased atrial conduction time, i.e., 41% at 150 ATA. Excitability, determined from strength-duration (S-D) curves, was depressed by pressure. The slope constant of the S-D curve increased 64% at 150 ATA. Rheobase and the X-asymptote were not affected significantly. The depression of excitability partially accounted for the slowed conduction. Frequency stress and pressure had an additive effect to produce even greater decreases in excitability and increases in conduction time. Atrial refractoriness to premature stimuli also increased as a function of pressure. Nitrous oxide (2.5 ATA) partially reversed the effects of 150 ATA of pressure on conduction time and excitability. The results suggest that pressure acts by altering basic functional components of the myocardial cell membrane. Some of these changes, particularly when combined with frequency stress, i.e., rapid heart rate, may pose a serious threat to humans exposed to hyperbaric environments.
Animals↗
Right atrial free wall conduction velocity and degree of anisotropy in patients with stable sinus rhythm studied during open heart surgery.
AIMS: Although the perpetuation of several supraventricular arrhythmias is critically dependent upon intra-atrial conduction, the literature lacks detailed information on normal values of conduction velocity and degree of anisotropy. In order to explore these factors further, we have measured conduction velocities at the right atrial free wall during sinus rhythm and during atrial pacing in four directions parallel and perpendicular to the atrioventricular groove in patients with normal atria and stable sinus rhythm. METHODS AND RESULTS: Using a Bard Cardiac Mapping System, atrial ECGs were recorded using a 3 x 4 cm electrode array with 56 equally spaced bipolar electrodes in 12 patients undergoing open heart surgery due to ischaemic heart disease or Wolf-Parkinson-White syndrome. A bipolar pen probe connected to a Medtronic 5328 stimulator was used for pacing at a 10% higher rate than sinus rhythm. The local activation times were manually set and isochronal activation maps were created for each recording. The conduction velocities were calculated from the activation maps over a distance ranging from 2.2 to 4.2 cm. The majority of the activation maps showed no signs of anisotropy; the others had less than 15% spatial inhomogeneity of conduction. Mean conduction velocity, calculated from five consecutive beats, was 88 +/- 9 cm.s-1 (mean +/- SD), ranging between 68 +/- 4 and 103 +/- 3 cm.s-1 during sinus rhythm. Mean conduction velocity during atrial pacing was 81 +/- 16 cm.s-1 at a propagation direction of 0 degree, 74 +/- 14 cm.s-1 at a 90 degrees direction, 79 +/- 12 cm.s-1 at 180 degrees and 78 +/- 20 cm.s-1 at 270 degrees, where 0 degree was parallel to the atrioventricular groove in the cranial direction and the angle increased counter-clockwise. Mean conduction velocity during sinus rhythm was significantly higher (P < 0.05) than during atrial pacing at the 90 degrees and 180 degrees directions but not compared to atrial pacing at 0 degree or 270 degrees. There was no significant difference in mean conduction velocity in different directions during atrial pacing. CONCLUSION: Although anisotropy was documented during conduction velocity in individual cases, conduction velocity was not dependent on propagation direction at the epicardial right atrial free wall in patients with stable sinus rhythm. These findings do not exclude the presence of internodal preferential pathways as these are located sub-epicardially and a marked transmural discordance in activation has previously been documented in the vicinity of such pathways.
Adult↗
[Electrophysiologic effects of lorcainide (R 15889) in man].
The electrophysiological effects of lorcainide (R 15 899) were studied in 15 patients. Atrioventricular conduction was analysed by His bundle recording and cardiac refractory periods were determined by the extra stimulus method. The assessment of sino atrial function was performed by measuring sinus node recovery times and sino atrial conduction times. The electrophysiological data was recorded before and 10 minutes after a slow intravenous injection of 1,5 mg/Kg of lorcainide followed by a continuous infusion at 0,02 mg/Kg/min. The following results were obtained; 1) The HV interval increased in all cases (average : II ms) 2) The QRS and QT intervals were significantly prolonged 3) Lorcainide produced a slowing of conduction and an increase in the refractory periods at atrial level 4) AV nodal conduction was unaffected 5) The sinus rate slightly increased. There were no significant changes in sinus node recovery time or sino atrial conduction. It must be concluded that, in man, lorcainide produces electrophysiological effects of antiarrhythmic agents of the quinidine type.
Adolescent↗
Effects of halothane with and without histamine and/or epinephrine on automaticity, intracardiac conduction times, and development of dysrhythmias in the isolated guinea pig heart.
Histamine is released during allergic reactions, and is known to produce cardiac dysrhythmias. The authors compared the cardiac effects of histamine and epinephrine during exposure to halothane in the isolated perfused guinea pig heart. Responses studied were spontaneous sinus rate, intra-atrial conduction time, atrial-septal conduction time (ASCT), intraventricular conduction time (IVCT), and left ventricular pressure (LVP). The incidence and type of dysrhythmias with histamine and halothane and with epinephrine and halothane were analyzed from electrograms. The authors found that halothane alone (0.7 to 2.1 vol%) causes dose-dependent depressions of sinus rate and LVP, prolongs ASCT and IVCT, and produces atrioventricular (AV) block with junctional bradycardia. Histamine alone (.01-10 microM) increases sinus rate and LVP but, like halothane, prolongs ASCT. Halothane antagonizes the inotropic and chronotropic effects of histamine, but enhances ASCT compared with histamine alone. Histamine with halothane greatly increases the incidence of junctional tachycardia with AV dissociation from 0% with histamine alone up to 48%. Epinephrine alone (0.1-5 microM), like histamine, increases sinus rate and LVP, but does not cause a relative increase in ASCT. Halothane antagonizes the inotropic and chronotropic effects of epinephrine, but increases the incidence of ventricular tachycardia from 6% to 28%, and the incidence of premature ventricular excitations from 0% to 40%, compared with epinephrine alone. The authors' in vitro findings show that histamine and halothane, like epinephrine and halothane, can cause dysrhythmias, but that the genesis and type of dysrhythmias induced by these agents are dissimilar. Consequently, the release of histamine with an anaphylactoid reaction during halothane anesthesia, and the treatment of the reaction with epinephrine, could result in dangerous ventricular tachydysrhythmias.
Animals↗
Ventriculoatrial conduction metrics for classification of ventricular tachycardia with 1:1 retrograde conduction in dual-chamber sensing implantable cardioverter defibrillators.
The introduction of dual-chamber sensing in implantable cardioverter defibrillators (ICDs) has greatly reduced the incidence of false detection due to supraventricular tachycardias. The remaining arrhythmias which serve to confound classification are supraventricular tachycardias (SVTs) with 1:1 anterograde conduction and ventricular tachycardias (VT) with 1:1 retrograde conduction. An algorithm has been designed and tested (28 patients) which employs ventriculoatrial (VA) conduction measurements to separate 1:1 VTs from 1:1 SVTs. A study was conducted to assess realistic VA interval boundaries for classification of arrhythmias with 1:1 retrograde atrial conduction. Intracardiac atrial and ventricular recordings of 7 passages of VT with retrograde conduction, 12 passages of atrioventricular nodal reentrant tachycardia (AVNRT), 3 passages of atrial tachycardia (AT), 8 passages of sinus tachycardia (ST), and 2 passages of orthodromic reentrant tachycardia (ORT) were analyzed. Automated real-time atrial and ventricular waveform recognition was performed on each passage and VA intervals were measured. Separation of VT with retrograde conduction from other 1:1 supraventricular tachycardias was effected by imposing discrete VA interval boundaries. VA boundaries of 80 ms to 234 ms classified 1:1 VT with 100% sensitivity (SENS) and 80% specificity (SPEC). In addition, the lower boundary completely classified AVNRT with 100% SENS and 100% SPEC, and all passages of ST were contained above the upper boundary. These findings could be of importance in algorithms for next-generation implantable cardioverter defibrillators which include two-chamber (atrial and ventricular) sensing and two-chamber interval measurements.
Algorithms↗
[Effects of oxyfedrine on sino-atrial function and on conduction in patients with sinus node and/or atrial dysrhythmias (author's transl)].
The electrophysiological effects of Oxyfedrine on sino-atrial function and on A-V junctional and subjunctional conduction have been studied in 16 patients with sinus node and/or atrial dysrhythmias. The following effects have been observed: --a positive chronotropic effect on the sinus node; --an essentially indirect (rate-dependent) shortening of the Functional and Effective Refractory Periods (FRP and ERP) of the atria without variation of the Intra-Atrial Conduction Time (HRA-LRA). There was no significant shortening of the Maximal Atrial Latency (max AL), of the Corrected Sinus Node Recovery Time (CSNRT) and of the Sino-Atrial Conduction Time (SACT). The limits of Zones I, II, III of the sinus node response to atrial extra-stimuli were reduced with no significant change in their duration, expressed as percentage of the Sinus Cycle Length (SCL); --an improvement in the A-V junctional conduction (shortening of the A-H interval for comparable cycle lengths) due to a relatively shortened A-V junctional ERP. The use of the drug in patients with sinus bradycardia and/or atrial dysrhythmias and conduction disturbances, is proposed.
Adult↗
[Cryosurgical treatment of atrial tachyarrhythmia with atrial flutter].
Two cases of atrial tachyarrhythmias with atrial flutter requiring cryosurgical treatment are reported. In two cases, preoperative electrophysiological studies revealed supraventricular reentrant tachyarrhythmias during atrial flutter and showed enhanced conduction through the AV node that conducted atrial impulses rapidly to the ventricle. Based on intraoperative endocardial mapping, the earliest excitation site was localized along the AV node and His bundle during supraventricular tachyarrhythmias in one case. The cryosurgical treatment was administered at Koch's triangles and in one case additionally at coronary sinus. After the operation, supraventricular tachyarrhythmias were not inducible and no clinical recurrences have occurred. Normal atrioventricular conduction was preserved in two cases. We concluded that cryosurgical treatment is useful for the treatment of the atrial tachyarrhythmias.
Adult↗
Disparate effects of deficient expression of connexin43 on atrial and ventricular conduction: evidence for chamber-specific molecular determinants of conduction.
BACKGROUND: Myocardial conduction depends on intercellular transfer of current at gap junctions. Atrial myocytes express three different gap junction channel proteins-connexin43 (Cx43), connexin45 (Cx45), and connexin40 (Cx40)-- whereas ventricular myocytes express only Cx43 and Cx45. However, the physiological roles of individual connexins are unknown. We have previously shown that mice heterozygous for a null mutation in the gene encoding Cx43 (Cx43(+/-) mice) express 50% of the normal amount of Cx43 in ventricular myocardium and exhibit marked slowing of ventricular conduction. METHODS AND RESULTS: To determine whether atrial conduction is affected in Cx43(+/-) mice, we measured atrial conduction velocity in isolated hearts, performed detailed ECG and electrophysiological studies in intact animals, and determined the amount of cardiac connexins in atrial and ventricular tissue. Ventricular conduction velocity was reduced by 38% in Cx43(+/-) mice compared with wild-types, but atrial conduction velocity in the same hearts was normal. QRS duration was significantly greater in Cx43(+/-) mice than in wild-types, but P-wave duration and amplitude did not differ. Atrial expression of Cx43 was reduced by 50%. CONCLUSIONS: These results indicate that Cx43 is a principal conductor of intercellular current in the ventricle because ventricular conduction is significantly slowed when Cx43 content is reduced by only 50%. In contrast, a similar reduction in Cx43 content in atrial muscle has no effect on atrial conduction, suggesting that Cx40 (which is expressed in atrial but not ventricular myocytes) is a major electrical coupling protein in atrial muscle. Thus, Cx43 and Cx40 may be chamber-specific determinants of myocardial conduction.
Animals↗
Electrophysiology of atropine.
The effect of atropine on the refractory periods of the human atrium, A-V node, and His-Purkinje system was studied. The A-V node in man appears more sensitive to atropine than the atria as evidenced by a reduction in the effective and functional refractory periods of the A-V node without alteration of atrial conduction. Although atropine does not directly alter the refractory periods of the His-Purkinje system, atropine-induced facilitation of A-V nodal conduction results in block of premature atrial impulses in the His-Purkinje system, demonstrating an indirect effect of atropine on His-Purkinje conduction. Rarely, atropine may precipitate re-entrant atrial tachycardia (one patient) through facilitation of A-V nodal conduction.
Adult↗
Atypical termination of simultaneous sino-atrial and atrio-ventricular Wenckebach type conduction caused by atrial premature beats.
This is a case report of a patient with group beating characterized by progressively shortening P-P intervals and at the same time gradually increasing P-R intervals showing R-P/P-R interval reciprocity due to the simultaneous occurrence of sino-atrial (S-A) Wenckebach and atrio-ventricular (A-V) Wenckebach-like periodicities. All group beatings are terminated by atrial premature beats elicited by a critical P-P interval shortening during S-A Wenckebach type conduction preventing the typical termination of Wenckebach periods.
Aged↗
[Electrophysiological properties of atrial fibrillation with WPW syndrome and the role of procainamide in conversion].
Fifty one patients with recurrent episodes of atrial fibrillation associated with WPW syndrome were studied by pre-operative clinical electrophysiogical testing. The results showed that: these patients had an markedly prolonged intra-atrial conduction time (PA intervals: 42.22 +/- 10.93 ms) than the patients only with attack of atrioventricular reentry tachycardia (AVRT) (PA intervals: 17.21 +/- 9.68ms, P less than 0.001). The attack of atrial fibrillation related to an markedly prolonged atrial vulnerable phase and the retrograde conduction of accessory pathway (AP). The clinical results of atrial fibrillation were decided by the antegrade effective refractory period (AERP) of AP. When the shortest R-R (V-V) intervals during attack of atrial fibrillation was shorter than 180ms, the atrial fibrillation spontaneously turned to the ventricular fibrillation. The conversion of atrial fibrillation to sinus rhythm showed that procainamide not only prolonged AERP of AP, which were 248.57 +/- 15.74ms and 388.57 +/- 63.9 ms (P less than 0.001) respectively before and after intravenous procainamide infusion, but also prolonged intra-atrial conduction time significantly, the PA interval before and after intravenous procainamide infusion were 42.22 +/- 10.93 ms and 57.14 +/- 11.12 ms (P less than 0.025) respectively.
Adolescent↗
Mechanism for atrial tachyarrhythmia in chronic volume overload-induced dilated atria.
UNLABELLED: Mechanism of chronic volume overload-induced AT. INTRODUCTION: Atrial dilatation associated with chronic volume overload (CVO) plays an important role in the development of atrial fibrillation (AF). However, the underlying mechanisms are unknown. METHODS AND RESULTS: CVO-induced atrial dilatation was created in Japanese white rabbits using arteriovenous shunt formation for 6 weeks. Epicardial action potentials were measured from both atria in Langendorff-perfused sham-operated control hearts (n=8) and in CVO hearts (n=8) using high-resolution optical mapping techniques. The left atrial diameter was greater in CVO hearts (16.0+/-0.4 mm) compared to control hearts (11.0+/-0.8 mm). During steady-state pacing, right and left atrial conduction velocities were significantly lower in CVO hearts compared to control hearts (P<0.01). Rapid atrial pacing did not induce atrial tachyarrhythmia (AT) in any control hearts. However, in seven of eight CVO hearts 16 episodes of AT were induced, of which 9 exhibited a single reentrant circuit. The remaining 7 episodes exhibited a focal pattern of excitation without evidence of reentry. Interestingly, the activation rate was higher during reentry (16.1+/-1.5 Hz) compared to focal AT (9.8+/-1.0 Hz). In addition, 15 of 16 episodes occurred in the posterior left atrium (PLA). In all seven CVO hearts, AT was self-sustained for more than 10 minutes. CONCLUSION: CVO caused atrial dilatation, conduction slowing, and AT associated with reentrant and focal excitation originating from the PLA. These results suggest that the PLA may play an important role in AT induction associated with CVO-induced atrial dilation.
Animals↗
Inappropriate detection of supraventricular arrhythmias by implantable dual chamber defibrillators: a comparison of four different algorithms.
Inappropriate therapy of supraventricular tachyarrhythmias by an ICD is still a common problem. Dual chamber (DDD) ICDs provide additional atrial sensing and should result in higher specificity for detection of supraventricular tachyarrhythmias. However, a direct comparison of different dual chamber algorithms has not been reported. The detection algorithms of four different DDD ICDs were tested: Phylax AV, Defender IV, Ventak AV III DR, and Gem DR 7271. Based on arrhythmias recorded from patients undergoing invasive electrophysiological studies and in many cases of catheter ablation at our institution, a library consisting of 71 supraventricular and 15 ventricular tachyarrhythmias was created. The library consists of episodes of atrial fibrillation, atrial flutter with different AV conduction, typical and atypical AV nodal reentrant tachycardia, AV reentrant tachycardia, sinus tachycardia, and ventricular tachycardia with and without ventriculoatrial conduction. Atrial fibrillation was appropriately classified by all four algorithms. However, the specificity for detection of other supraventricular tachyarrhythmias achieved by the Biotronik (12%) and the Guidant (11%) devices was significantly lower compared to the specificity of the ELA (28%) and the Medtronic DDD ICD (20%). This is due to the fact that the Biotronik and the Guidant algorithm classified all supraventricular tachyarrhythmias resulting in a stable ventricular rate as ventricular tachycardia, whereas the ELA and Medtronic algorithms performed a more detailed analysis by assessment of PR association, atrial onset, or timing of the atrial event relative to the ventricular event, respectively. Atrial fibrillation, the most common supraventricular tachyarrhythmia in patients with ICD, was detected by all devices.
Algorithms↗
Atrial pacing for the prevention and termination of atrial fibrillation.
Atrial fibrillation (AF) affects about 2% of the general population and 8%-11% of those older than 65 years. The demand for effective therapeutic strategies for AF is anticipated to increase substantially as the proportion of the elderly population increases. Atrioventricular nodal ablation accompanied by permanent pacemaker implantation is an established option in elderly patients with intractable arrhythmia and poor ventricular rate control. However, it renders most patients pacemaker dependent and does not eliminate symptoms associated with loss of atrial transport or reduce the risk of stroke. The considerable limitations of rhythm or rate control strategies prompted interest in preventative atrial pacing, which may reduce the incidence of AF by either eliminating the triggers and/or by modifying the substrate of AF. Atrial or dual-chamber pacing has been proven to prevent or delay progression to permanent AF in elderly patients with sinus node dysfunction as compared with ventricular pacing. Patients with advanced atrial conduction delay may benefit from atrial resynchronization pacing. There may be additional benefits associated with the use of particular sites of pacing, specific pacing algorithms designed to target potential triggers of AF, and pace-termination of atrial tachycardia. Preventive and antitachycardia pacing algorithms incorporated in implantable cardioverter-defibrillators and pacemakers are currently under investigation and may offer a valuable alternative to antiarrhythmic drug therapy in elderly patients with left ventricular dysfunction at high risk of proarrhythmia or worsening heart failure. The evolution of hybrid therapy, in which two or more different strategies are employed in the same patient, may be the most effective approach to management of AF.
Age Factors↗