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PubMedDate not supplied

Electrophysiologic evaluation of intravenous verapamil in man.

The acute electrophysiological effects of intravenous verapamil (0.15 mg/kg body weight) were studied in 21 subjects with estimated normal impulse formation and conduction. Significant effects were sinus cycle shortening, depression of intranodal conduction and prolongation of AV node refractory periods. Sinus node recovery time, sinoatrial conduction time, atrial refractory periods, infranodal conduction, His--Purkinje system, and bundle branch refractory periods were unchanged. The clinical implications of these properties are discussed.

Adult↗
PubMed1999

Reduction of atrial fibrillation inducibility by radiofrequency ablation: an experimental study.

UNLABELLED: A study is made of the antifibrillatory effects of radiofrequency (RF)-induced atrial lesions using nine Langendorff-perfused rabbit hearts in which the atrial electrophysiological properties and atrial fibrillation (AF) inducibility were modified by atrial stretching. Using a multiple electrode consisting of 121 unipolar electrodes, determinations were made of the atrial refractory periods, conduction velocity, wavelength of the atrial activation process, and the inducibility of sustained AF episodes (duration over 30 s) by atrial burst pacing in four situations: (a) control; (b) following dilatation of the right atrium; (c) after adding an RF linear lesion at the cava-tricuspid annulus isthmus; and (d) after adding two RF linear lesions rounding the base of the right atrial appendage and extending from the inferior zone of the sulcus terminalis to the anterior wall of the appendage. Under control conditions, AF was not induced in any of the experiments. The wavelengths were 10.5 +/- 1.2 cm for basic cycles of 250 ms and 6.6 +/- 0.5 cm for cycles of 100 ms. Following dilatation, a significant decrease was recorded in the atrial refractory periods, conduction velocity, and wavelength, which reached values of 6.1 +/- 0.7 cm (250-ms cycle, P < 0.01), and 3.9 +/- 0.3 cm (100-ms cycle, P < 0.01); AF was induced in five cases (P < 0.05). After producing the lesion at the cava-tricuspid isthmus, the electrophysiological modifications induced by atrial dilatation persisted (wavelength = 6.2 +/- 0.6 cm (250-ms cycle) and 4.3 +/- 0.3 cm (100-ms cycle); P < 0.01 vs the control) and AF was triggered in eight cases (P < 0.0001). In turn, on adding the two lesions at the right atrial free wall and appendage, AF was induced only in one experiment (P = NS vs control), and the dilatation-induced decrease in refractoriness and wavelength was attenuated. Nevertheless, differences remained significant with respect to the controls, with the exception of the functional refractory periods determined at cycles of 100 ms. In this phase, the wavelength was 6.6 +/- 0.7 cm (250-ms cycle, P < 0.01 vs control) and 4.9 +/- 0.5 cm (100-ms cycle; P < 0.05). Atrial conduction between the zones separated by the lesions was blocked at any frequency, or selectively at rapid atrial activation frequencies. IN CONCLUSION: (a) the production of three linear lesions in the right atrium (cava-tricuspid isthmus, atrial appendage, and inferior free wall) reduces AF inducibility in the experimental model used; (b) conduction block (either absolute or frequency dependent) through the lesions, reduction in tissue mass caused by lesion creation, and possibly the attenuation of the shortening of atrial refractoriness and wavelength in the zones not separated by the lesions are implicated in the reduction of AF inducibility; and (c) the single lesion in the cava-tricuspid isthmus does not impede AF inducibility.

Animals↗
PubMed1985

Role of atrial fibrillation and atrioventricular conduction (including Wolff-Parkinson-White syndrome) in sudden death.

A short refractory period of the accessory pathway is considered a major threat for sudden death in patients with Wolff-Parkinson-White syndrome and atrial fibrillation. RR interval and QRS signal analysis together with signal analysis of a bipolar high right atrial electrogram were obtained in six patients with Wolff-Parkinson-White syndrome and either induced or spontaneous atrial fibrillation. A record of a sufficiently long episode of atrioventricular (AV) conduction by way of the bypass tract that could be used for satisfactory RR interval sequence and QRS analysis was obtained from only one patient. The results were compared with those of a representative patient with atrial fibrillation and normal AV nodal-His conduction. In a patient with Wolff-Parkinson-White syndrome, atrial fibrillation and AV conduction by way of the bypass tract may exhibit high ventricular rates (median RR intervals of about 300 ms) and long/short RR interval ratios of just over 1 (RR intervals not exceeding 400 ms). The right atrial electrogram showed a noiselike excitation pattern. This study suggests that rather than a short refractory period of the bypass tract, it is lack of concealed conduction, responsible for the presence of long RR intervals, that allows the ventricles to reach very high ventricular rates and at times to fibrillate. The normal AV nodal-His system seems to protect the heart against high ventricular rates and ventricular fibrillation during atrial fibrillation by its relatively long refractory period and capacity to induce long RR intervals by means of concealed conduction.

Atrial Fibrillation↗
PubMed1980

Effects of an interpolated premature ventricular contraction on the AV conduction of the subsequent premature atrial depolarization. An apparent facilitation.

Nodal conduction is usually studied by tracing the H1 H2 on function of A1 A2 curves. If one interpolates a PVC before A1, there is a decrease in H1 H2. This might be explained by an A1 H1 interval lengthening (delta A1 H1). This study was done on 14 consecutive patients in whom a PVC can be interpolated (blocked at the A-V junction). In the majority of these patients, there is a downward and a right hand shift in the curve after an interpolated PVC. On other hand, the curves representing the sum H1 H2 + delta A1 H1 on function of A1 A2 were shifted upward and to the right in 12 of the 14 patients. This indicates inhibition which manifests itself not only by an ERP increase but also by an A2 H2 increase.

Arrhythmias, Cardiac↗
PubMed1997

Clinical importance of intramural blood vessels in the sino-atrial segment of the conducting system of the heart.

We studied the morphology and histology of intramural vessels in the sino-atrial [S-A] segment of the cardiac conducting system because of the clinical relevance of the anatomy of the microvascular system for those performing cardiac surgery or coronary angiography, catheterization or arterialization. In 25 human and 25 canine hearts the vasculature was fixed by the Komahidze method, the anatomy was studied and sections were stained and studied by microscopy. Of clinical importance is a finding of considerable variation in the exact anatomy of the arterial supply. The sinonodal artery is a large artery originating from the right or left coronary arteries. In some cases the coronary arterial course could not be demonstrable by coronary angiography thus increasing the risk of coronary artery surgery at the site. Cross connections also permit the extra-cardiac circulation to supply the nodal tissue. The S-A node has a rich intramural network of anastomosing blood vessels which is of surgical importance in the case of damage and surgical procedures. The density of the capillary network in the node is greater than that in adjacent atrial tissue. The distribution and density of the smallest anastomotic blood vessels were different in various parts of the node, the capillary net was most dense in sections from dorsal parts of the S-A node. No marked differences were found when human and canine systems were compared. Canine preparations could be used for analysis of the S-A node vascularization because of their similarity to the human heart. These findings are clinically relevant to the S-A node dysfunction that may follow cardiac surgical procedures. Surgeons should be aware that there is considerable variation in the exact anatomy of the arterial supply of the S-A node which might be important for cardiological examination and treatment (cardiac surgery, coronary angiography, etc.).

Animals↗
PubMed2005

Differential pacing for distinguishing slow conduction from complete conduction block of the tricuspid-inferior vena cava isthmus after radiofrequency ablation for atrial flutter--role of transverse conduction through the crista terminalis.

BACKGROUND: Partial conduction block has been suggested a predictor of recurrence of atrial flutter (AFL). AIM: The aim of this study was to assess transverse conduction by the crista terminalis (CT) as a problem in evaluating isthmus block and the usefulness of differential pacing for distinguishing slow conduction (SC) and complete conduction block (CB) across the ablation line. METHODS: We assessed 14 patients who underwent radiofrequency catheter ablation of the eustachian valve/ridge-tricuspid valve isthmus for typical AFL. Activation patterns along the tricuspid annulus (TA) suggested incomplete CB across the isthmus. In these patients, atrial pacing was performed from the low posteroseptal (PS) and anteroseptal (AS) right atrium (RA) while the ablation catheter was placed at the ablation line where double potentials (DPs) could be recorded. The pattern of activation of the RA free wall was assessed by a 20-pole catheter positioned along the CT during pacing from the coronary sinus (CS) ostium (CSos) and low lateral RA (LLRA). RESULTS: Faster transverse conduction across the CT resulted in simultaneous or earlier activation of the distal halo electrodes than of the more proximal electrodes, suggesting incomplete conduction block across the isthmus. CB (13) and SC (1) were detected as changes in the activation times of the first and second components of DPs (DP1, DP2) during PS RA pacing and AS RA. Similar changes in the activation times DP1 and DP2 during AS RA pacing as compared to PS RA reflected SC through the isthmus, whereas increased DP1 activation time and decreased of DP2 activation time reflected complete conduction block across the isthmus. CONCLUSIONS: Transverse conduction across the CT influences the sequence of activation along the TA after isthmus ablation. Differential pacing can distinguish SC from complete conduction block across the ablation line in the isthmus.

Adult↗
PubMed1984

Effects of diltiazem on atrioventricular conduction and arterial blood pressure: correlation with plasma drug concentrations.

Atrial and atrioventricular conduction variables were studied at control and at the end of each of six consecutive 45-min diltiazem administration periods in eight closed chest-anesthetized dogs. Diltiazem was given as a bolus (50 micrograms/kg, i.v.) followed by an infusion (0.5 micrograms X kg-1 X min-1); doses were doubled in subsequent periods. The plasma concentrations, measured by gas-liquid chromatography, ranged from 8 to 1400 ng/mL and correlated strongly with the doses (r = 0.92; p less than 0.01). The Wenckebach cycle length, basic conduction time, and functional refractory period of the atrioventricular (AV) node increased proportionally with plasma concentration (respective r = 0.90, 0.89, 0.80; p less than 0.01). The minimum mean plasma concentrations affecting these variables significantly were 37, 83, and 175 ng/mL, respectively. Second or third degree AV blocks developed in all dogs for plasma concentrations between 379 and 1400 ng/mL. In four dogs which were given isoproterenol (0.2 micrograms X kg-1 X min-1), these blocks disappeared within 1 min. Atrial conduction time and functional refractory period were slightly but significantly shortened by diltiazem with mean plasma concentrations of 175 ng/mL and over. His-Purkinje intervals were not significantly changed by diltiazem. Systolic and diastolic arterial pressures were decreased by diltiazem (r = -0.64, r = -0.79; p less than 0.01) starting with a mean plasma concentration of 83 ng/mL. We conclude that AV nodal conduction variables are progressively prolonged with increasing plasma concentrations of diltiazem; plasma concentrations affecting blood pressure and AV nodal variables overlap; and the AV blocks produced by toxic concentrations of diltiazem can be corrected by isoproterenol.

Animals↗
PubMed1988

Ventricular response to atrial fibrillation: role of atrioventricular conduction pathways.

Irregularity of the ventricular rhythm is a hallmark of patients with atrial fibrillation, yet the genesis of the irregularity is not yet fully understood. The role of the atrioventricular (AV) node in determining the irregularity of the ventricular response to atrial fibrillation was investigated by comparing the frequency distributions of the atrial (AA) and the ventricular (RR) intervals. Atrial electrograms and surface electrocardiographic leads were recorded during sustained atrial fibrillation in 12 patients with conduction over the AV node. The scaling factor (mean RR interval/mean AA interval) quantified the ability of the conduction pathway to scale the atrial input to a slower ventricular response and ranged from 2.55 to 5.92 (mean +/- SD 3.77 +/- 0.92). The coefficient of variation (SD/mean) measured the relative variability of the AA and RR interval distributions. The atrial and ventricular coefficients of variation were not significantly different (0.20 +/- 0.04 versus 0.21 +/- 0.03, p greater than 0.27). Similar recordings were analyzed in six patients with conduction over a accessory AV pathway. The scaling factor ranged from 1.54 to 2.46 (2.02 +/- 0.39) and, as was the case for patients with conduction over the AV node, the atrial and ventricular coefficients of variation did not significantly differ (0.24 +/- 0.08 versus 0.27 +/- 0.10, p greater than 0.6). For both groups of patients, ventricular variability and the maximal RR intervals were predicted by the product of the scaling factor and either atrial variability or maximal AA intervals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Accessory pathway potential recording in a case of permanent junctional reciprocating tachycardia with decremental conduction localized on the atrial site.

Permanent junctional reciprocating tachycardia (PJRT) is an uncommon form of atrioventricular reentrant tachycardia due to the presence of an accessory pathway characterized by slow and decremental retrograde conduction. We report a case of PJRT where we demonstrated the possibility of recording a distinct accessory pathway potential. Decremental retrograde conduction was evident using ventricular extrastimuli and it was also adenosine-sensitive. Delivering ventricular extrastimuli a prolongation of the accessory pathway potential-atrium interval was seen demonstrating that decremental conduction was located at the atrial insertion of the pathway. The accessory pathway was successfully ablated using the potential as the target of radiofrequency delivery. These electrophysiological findings seem to support the hypothesis that a nodal-like structure may be responsible for this arrhythmia.

Catheter Ablation↗
PubMed1986

Effect of pharmacologic autonomic blockade on ventriculoatrial conduction.

To determine the influence of autonomic tone on retrograde ventriculoatrial (VA) conduction, incremental atrial and ventricular pacing was performed before and after pharmacologic autonomic blockade in 28 patients. VA conduction during ventricular pacing was demonstrated, with highest frequency in patients capable of 1:1 atrioventricular (AV) conduction at atrial paced cycle lengths of 300 ms or less (7 of 7, 100%). In subjects with 1:1 AV conduction at minimum cycle lengths of 300 to 500 ms, 14 of 21 (67%) demonstrated VA conduction in the control state; however, only 12 of 21 (57%) did so after autonomic blockade. The lowest frequency was observed in those capable of 1:1 AV conduction at minimum cycle lengths of 505 ms or more before and after autonomic blockade (2 of 7, [29%], p less than or equal to 0.02 compared with values in the first group). No change in the mean minimum ventricular paced cycle length at which 1:1 VA conduction could be maintained was demonstrated after autonomic blockade. In individual subjects, incremental change in this cycle length after autonomic blockade correlated positively with the corresponding change in minimum atrial cycle length at which 1:1 AV conduction could be maintained (r = 0.62, p less than 0.005), and was concordant in direction in 18 of 21. In conclusion, the sympathetic and parasympathetic modulation of VA conduction is balanced and concordant in direction to the effect on AV nodal conduction.

Adolescent↗
PubMed2003

Directions of atrial excitation wavefront influenced antegrade conduction of manifest accessory atrioventricular pathway: a case report.

We report a case of left accessory atrioventricular pathway (AP) which antegrade conduction was manifest during pacing from the anterior site of the atrial insertion, but absent during pacing from the posterior site. Infusion of adenosine triphosphate during pacing from the posterior site induced a conduction block of atrioventricular node without affecting the persistent antegrade conduction block of the AP. These findings suggested that the different response of the AP according to the directional change of atrial conduction was not due to a "linking" phenomenon, but may relate to the impedance mismatch because of an oblique fashion of the pathway.

Cardiac Pacing, Artificial↗
PubMed1985

Ventriculoatrial conduction: a cause of atrial malpacing in AV universal pacemakers. A report of two cases.

Retrograde atrial activation during ventricular pacing has often been a cause of intermittent or persistent arrhythmias (pacemaker-mediated tachycardia) in AV universal pacemakers. We recently encountered two cases in which VA conduction was responsible for atrial malpacing in patients with an implanted AV universal pacemaker, one programmed in DDD and one in DVI mode. Atrial malpacing was induced by the atrial refractoriness due to retrograde activation. In the first patient, it was observed when the pacemaker was programmed to a rate of 110 ppm (lower rate) and an AV interval of 200 ms in order to check crosstalk. In the second patient, it was observed after ventricular premature contractions.

Aged↗
PubMed1993

Differentiation between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation using RR interval scattergram.

BACKGROUND: Differentiation between aberrant ventricular conduction and ventricular ectopy during atrial fibrillation (AF) is of etiologic, prognostic, and therapeutic importance. We developed a noninvasive technique to diagnose aberrant ventricular conduction and ventricular ectopy in AF. METHODS AND RESULTS: We studied the Holter ECGs of 34 patients with paroxysmal AF and 62 patients with chronic AF. In all the patients, frequent wide QRS complexes were observed, and 32 patients were shown by electrophysiological examination to have ventricular ectopies or aberrant ventricular conductions. We obtained the RR interval scattergrams by plotting sequential pairs of RR intervals. Each point has the (n)th RR interval as its x value and the (n + 1)th RR interval as its y value. The irregularity of the RR intervals in AF resulted in widely scattered points delineated by the envelope along the axes. The y value of the envelope along the x axis indicates the shortest coupling interval to the preceding RR interval. Therefore, this curve defines the functional refractory period of atrioventricular conduction. The scattergram of the RR interval pairs immediately preceding the aberrant conduction (coupling points of aberrant conduction) specifically distributed along the envelope. In contrast, the coupling points of ventricular ectopies showed different distributions that had no relation to the envelope. That is, it included three typical patterns, ie, linear distribution below the envelope, linear distribution partially overlapped in the area of normal AF conduction, and chaotic distribution in the AF area. None of the scattergrams of ventricular ectopies showed curvilinear distribution along the envelope as aberrant conduction did. The specific distribution of the aberrant conduction on the RR interval scattergram suggested that aberrant conduction in AF could result from the difference of refractory periods between the AV node and bundle branch block. CONCLUSIONS: We conclude that the RR interval scattergram makes it possible to differentiate between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation, and thus, it is a useful noninvasive clinical tool.

Atrial Fibrillation↗
PubMed1991

Depression of atrial rate, atrioventricular nodal conduction, and cardiac contraction by diltiazem and volatile anesthetics in isolated hearts.

The direct effects of isoflurane, halothane, and enflurane alone or combined with diltiazem were examined in 49 isolated perfused guinea pig hearts. Recording electrodes were placed in the right atrium and left ventricular septal wall to measure spontaneous atrial rate and atrioventricular conduction time (AVCT). The right atrium was paced at 3-7 Hz (n = 10) to examine rate-dependent effects on AVCT, Wenckebach's periodicity, and ventricular response rates with atrioventricular (AV) block. Isovolumetric left ventricular pressure (LVP) was measured with a saline-filled balloon placed through the mitral valve. Hearts were perfused with oxygenated Krebs-Ringer's solution at 55 mmHg equilibrated with low or high concentrations of isoflurane (0.7 and 1.5%), halothane (0.5 and 1%), or enflurane (1.1 and 2.2%). Hearts were also perfused with a low or high concentration of diltiazem (75 and 150 ng/ml) alone and during anesthetic exposure. Significant findings of combined exposure were as follows: 1) the low isoflurane, halothane, or enflurane concentration plus a low or high diltiazem concentration decreased LVP compared with control and diltiazem alone; low isoflurane plus the high diltiazem concentration decreased LVP more than isoflurane alone. The high isoflurane, halothane, or enflurane concentration plus the low or the high diltiazem concentration decreased LVP from control, anesthetics and diltiazem alone. Diltiazem plus halothane or enflurane decreased LVP more than diltiazem plus isoflurane. 2) Diltiazem plus low or high isoflurane, halothane, or enflurane concentrations decreased spontaneous atrial rate from control and the agents alone, except the high isoflurane concentration plus the low diltiazem concentration was not greater than that of isoflurane alone. Diltiazem plus halothane or enflurane decreased atrial rate more than diltiazem plus isoflurane. 3) Low and high diltiazem concentration plus low isoflurane, halothane, or enflurane concentrations did not prolong AVCT more than the individual agents alone, but low or high diltiazem plus high isoflurane, halothane, or enflurane concentrations increased AVCT more than each anesthetic alone. In nonpaced hearts, AV block occurred only with high diltiazem plus low enflurane (23%) concentrations and the high enflurane concentration (31%). 4) In hearts paced at 5 and 6 Hz, AVCT increased above controls during a low or high concentrations of diltiazem, during enflurane, and during the low or high concentration of diltiazem plus enflurane; AVCT increased more with the low concentration of diltiazem plus enflurane than with the low diltiazem concentration alone.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthetics↗
PubMed1998

Acute and long-term effects of consecutive radiofrequency applications on conduction properties of the subeustachian isthmus in type I atrial flutter.

INTRODUCTION: Bidirectional conduction block at the subeustachian isthmus predicts long-term efficacy of atrial flutter ablation. Limited data are available on the incidence and outcome of minor conduction changes such as unidirectional or incomplete block. This prospective study sought to systematically assess discrete acute and long-term alterations of bidirectional conduction prior to a complete conduction block. METHODS AND RESULTS: In 41 patients with type I atrial flutter, pulse propagation through the subeustachian isthmus during low lateral and proximal coronary sinus pacing was documented and analyzed following each consecutive radiofrequency (RF) application. In cases of altered conduction properties and noninducibility of atrial flutter, patients were followed-up for 12 months. Three sets of results were found. First, following RF application, 23 patients presented a progressive conduction delay prior to a complete conduction block. Second, RF application did not always affect counterclockwise and clockwise conduction simultaneously or to the same extent. In 13 patients, an initial alteration of counterclockwise conduction was present before an alteration of clockwise conduction; in 5 patients, clockwise conduction was primarily affected. Third, the recurrence rate of typical atrial flutter was 9% (2/22) in patients with a complete bidirectional conduction block, 54% (7/13) in patients with unidirectional conduction block, and 100% (6/6) in patients with sole bidirectional conduction delay. CONCLUSION: In 50% of the patients, consecutive RF applications resulted primarily in a progressive conduction delay rather than a sudden conduction block. Since counterclockwise and clockwise conduction were not always affected simultaneously or to the same extent, lateral as well as septal pacing is recommended for improvement of bidirectional conduction block. Normalization of primarily altered conduction and, therefore, recurrence of atrial flutter are high in all patients without bidirectional block.

Adult↗
PubMed1989

[Atrial flutter with 1:1 AV conduction during intravenous flecainide treatment].

Acute drug treatment of recent onset atrial flutter may reduce the ventricular rate by increasing block in the A-V node (digitalis/verapamil) or act by directly affecting the atria by reducing the atrial rate or converting flutter to sinus rhythm (1a and 1c antiarrthythmic drugs). Treatment that reduces the atrial rate may cause 1:1 A-V conduction. Quinidine and disopyramide are well known for increasing A-V conduction to 1:1 in some patients, because of their anticholinergic effect on the A-V node. Flecainide, a 1c antiarrhythmic drug, slows down atrial conduction, reducing flutter rate by 1/3. Clinical studies have shown flecainide to be effective in converting atrial fibrillation, atrial tachycardia, A-V reentry and A-V nodal reentry tachycardias to sinus rhythm. The effect on atrial flutter has been less impressive. Flecainide prolongs A-V conduction and increases Wenckebach cycle length. In spite of this, 1:1 A-V conduction may occur during treatment with intravenous flecainide for atrial flutter. We present a case where this is demonstrated and review the literature.

Aged↗
PubMed1996

Conduction barriers in human atrial flutter: correlation of electrophysiology and anatomy.

Animal models of atrial flutter and early mapping studies of human atrial flutter have suggested the importance of barriers in this reentrant arrhythmia. The consistency of rate and morphology of typical atrial flutter suggest a common anatomic substrate for this arrhythmia. The unique endocardial architecture of the right atrium provides anatomic barriers around which reentry occurs. In typical human atrial flutter, the crista terminalis, eustachian ridge, and tricuspid annulus have been identified as barriers to conduction. The importance of conduction barriers, methodology for defining barriers, the anatomic substrate for these barriers, and the role of these barriers in other atrial arrhythmias are discussed.

Animals↗