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PubMed1982

Electrophysiology of the chemically sympathectomised dog.

The contribution of the sympathetic nervous system in the definition of various electrophysiological variables was studied in chemically sympathectomised dogs. Chemical sympathectomy was obtained following intravenous injection of 50 mg X kg-1 of 6-hydroxydopamine. Sympathectomised dogs presented significant increases in: basic sinus period, sino-atrial conduction time (SACT), AH and HV intervals of the His bundle electrogram, atrial functional (AFRP) and effective (AERP) refractory periods, atrio-ventricular node functional (AVNFRP) and effective (AVNERP) refractory periods, ventricular functional (VFRP) and effective (EVRP) refractory periods and atrial (AMAP) and ventricular (VMAP) monophasic action potential durations. Corrected sinus recovery time (CSRT) was not affected by chemical sympathectomy. Neither was the atrial ERP/MAP duration ratio. This new form of sympathectomy affects all the levels of the cardiac conduction system. Such results are in accordance with those obtained with surgical sympathectomy or the use of beta-blocking agents.

Animals↗
PubMed1983

Atrial flutter secondary to hypokalemia.

Electrophysiologic studies support significant hypokalemia as a cause of atrial flutter in a patient without manifest heart disease. Atrial flutter, reproducibly initiated and terminated by rapid atrial pacing during hypokalemia, was not inducible after potassium correction. In an individual with existing atrial conduction disease, hypokalemia may generate both non-uniform atrial refractoriness and atrial premature beats, and it may facilitate the development of atrial flutter as a re-entrant arrhythmia.

Aged↗
PubMed2000

Simultaneous occurrence of atrial fibrillation and atrial flutter.

INTRODUCTION: Early reports suggested that some patients with "atrial fibrillation/flutter" might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. METHODS AND RESULTS: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12-lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra-atrial conduction block during sinus rhythm, suggesting functional intra-atrial block as a mechanism for simultaneous atrial fibrillation/flutter. CONCLUSION: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.

Animals↗
PubMed1976

[Pathophysiology and diagnosis of bradyarrhythmias in sick sinus syndrome].

The sick sinus syndrome (SSS) is a complex cardiac disturbance involving impulse formation and conduction. Anatomy and physiology of the sinus node and atrial conduction are reviewed and the pathophysiology of bradycardia and tachycardia in the SSS is discussed. Finally, a practical approach to diagnosis is outlined.

Action Potentials↗
PubMed1992

[Two-stage Jatene procedure after Mustard or Senning operation].

We have successfully performed a two-stage Jatene procedure in four patients who showed severe anatomical right ventricular dysfunction after atrial switch (Mustard or Senning) operation for transposition of the great arteries. All four patients developed an adequate left ventricular pressure for the arterial switch operation by one or two-stage pulmonary artery banding. Left ventricular posterior wall thickness increased sufficiently enough after the banding although left ventricular ejection fraction showed significant decrease. After Jatene procedure left ventricular ejection fraction recovered, and RV end-diastolic volume which had been prominently enlarged preoperatively was dramatically normalized. Cardiac index increased from 3.6 +/- 1.6 l/min/m2 preoperatively to 5.3 +/- 6.1 l/min/m2 postoperatively with the decrease in left atrial pressure. Postoperative electrophysiological study revealed the recovery of sinus node function and atrial conduction by means of the take-down of atrial switch operation previously performed. We conclude that the Jatene procedure should be an ideal alternative in patients with right ventricular dysfunction after atrial switch operation. The left ventricle could be prepared by an effective pulmonary artery banding in most instances.

Cardiac Surgical Procedures↗
PubMedDate not supplied

Three patients with branch to branch reentrant ventricular tachycardia. Diagnostic and therapeutic considerations.

Three patients with repetitive episodes of relatively slow rate (170 beats per minute) ventricular tachycardia, with right bundle branch block (RBBB) QRS morphology during arrhythmia are presented. The clinical and electrophysiological characteristics and the therapeutic problems raised are analysed. The branch to branch reentry mechanism was considered as the underlying mechanism. The peculiar characteristics found in our cases are: almost normal heart, except right bundle branch block in two and left anterior hemiblock in one patient; relatively slow ventricular rate during tachycardia; delayed retrograde ventriculo-atrial conduction during tachycardia; the onset of tachycardia related to atrial or ventricular premature beats; the possibility to stop the tachycardia through ventricular pacing; therapeutical point of view, DC shock, ventricular pacing and iv mexiletin HCl were highly effective, but not iv lidocaine.

Bundle-Branch Block↗
PubMed1990

[Physiopathology of the sinus node and sinoatrial conduction].

New information about the pathophysiology of the sinus node and sino-atrial conduction has been published in the last few years. The sinus node consists of cells separated by a network of collagen fibres. This anatomical disparity explains the different electrophysiological characteristics of the node; the morphology of cellular action potentials depends on the site of recording. The dominant and most automatic pacemaker cells are situated in the cephalic region and the latent pacemaker cells in the caudal region. However, synchronisation of these different cellular activities is possible and results in a coherent signal. This complex synchronisation has been the object of several recent papers. The phenomenon of intrasinusal pacemaker shift and the stimuli which induce it have been studied in depth. In general, positive chronotropic stimuli tend to shift the dominant pacemaker towards the cephalic part and negative chronotropic stimuli towards the caudal part of the node. It is possible to assess pacemaker shift clinically and this phenomenon must be taken into consideration when studying sinus node function. Intercellular conduction and especially electrotonic conduction does not play a role in the genesis of the flux, which represents spontaneous cellular automatism, but in its mode of expression, that is to say the sinus rhythm. The pathophysiology of sinoatrial block is complex because it may be situated within and/or around the sinus node. The extrinsic or intrinsic mechanisms of these blocks may be interrelated. Variations in sinus rhythm must be taken into account in the genesis of sinoatrial block; an acceleration in rhythm may block conduction in the perisinusal region. Finally, our knowledge of the ionic fluxes underlying sinus automatism has also improved with individualization of the pacemaker current (if).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1981

His bundle interruption for control of inappropriate ventricular responses to atrial arrhythmias.

Forty-two patients with life-threatening or disabling atrial arrhythmias are discussed. Fifteen had Kent bundles as the basis for the reentry tachycardia, while 27 had arrhythmias that originated in or above the atrioventricular (AV) node. Nineteen of the latter had an AV node that conducted atrial impulses rapidly to the ventricle. These patients were classified as having enhanced conduction through the AV node, a diagnosis based on clinical and electrophysiological studies. Initially, the technique employed for His bundle interruption was, either separate or in combination, blind suture, electrocauterization, and incision of the septal portion of the right atrium. The technique later adopted was sharp division of the atrial septum at its attachment to the right fibrous trigone. Cryothermia was used in 31 patients. There were four failures. In the group in whom sharp division was used. there were two failures among 11 patients. Two patients, however, had to have a second operation. Following AV node-His bundle interruption, a junctional rhythm resulted and a pacemaker was always installed. Our studies indicate that interruption of atrial to ventricular conduction is a satisfactory operation for atrial arrhythmias that are disabling or life threatening and that are refractory to vigorous medical therapy. Cryothermic ablation is the preferable technique. However, if this is not successful, then division is required of the AV nod-His bundle junction by interruption of the insertion of the atrial septum into the right fibrous trigone.

Adolescent↗
PubMed1982

Electrophysiological studies with prenalterol.

Electrophysiological studies with prenalterol in 19 patients (6 women, 13 men, 5 with sinus node disease, 4 with AV node disease, 7 with double node disease, 2 with conduction disturbance below His bundle, 1 normal) showed that sinus node function (heart rate, sinus node recovery time) is uniformly improved by this beta-stimulator. Also AV conduction is significantly and uniformly improved (shortening of AH interval and of the functional refractory period of AV conduction). There is no or little influence on intra-atrial conduction and on conduction below the His bundle. However, spontaneous depolarisation in His-Purkinje fibers--as tested in patients with complete AV block and ventricular demand pacemaker--is increased through beta-stimulation with prenalterol as reflected by shorter escape intervals and higher frequency escape rhythm. Prenalterol may be of clinical use in patients with cardiomyopathies who developed bradycardia under digitalisation or patients with severe bradyarrhythmia either with or without digitalis. It might also be useful in rare emergency situations, when complete pacemaker failure develops.

Adrenergic beta-Agonists↗
PubMed2000

Complete sequence and characterization of chick ventricular myosin heavy chain in the developing atria.

We isolated five complementary DNA (cDNA) clones, encoding the chick ventricular myosin heavy chain (MyHC) by reverse transcription polymerase chain reaction (RT-PCR). The entire cDNA consists of 5995 nucleotides with the 52 bp 5'-untranslated region and the 129 bp 3'-untranslated region. The complete cDNA encodes 1937 amino acids. Expression of the chick ventricular MyHC gene was also studied by Northern blot analysis. This gene continued to be strongly expressed in the ventricle during cardiac development. On the other hand, its expression was moderate in the early embryonic atria, and was down-regulated during development. In the adult atria, this gene was expressed at very low levels. To determine the localization of the ventricular MyHC protein, an immunohistochemical study was performed. The ventricular MyHC was present in early embryonic atrial myocytes. During development, the expression of this protein in the atrial myocytes was down-regulated, but continued to be present in the atrial conduction system. Our results indicate that the ventricular MyHC appears in the primary atrial myocardium and is then localized in the conduction cells of the atria.

Animals↗
PubMed1983

Atrial pacing: intracardiac conduction assessed by his bundle electrograms acquired from the permanent atrial electrode at implantation.

His bundle electrograms were recorded from conventional J-shaped atrial electrodes at implantation in twelve consecutive patients who had sinus node disorder. Five patients with impairment of atrioventricular conduction, received atrioventricular (DVI) pacemakers. His bundle recording by this method is simple and reliable, avoids the discomfort of the conventional technique, and represents a new application for the well established atrial "J" electrode.

Adult↗
PubMed1986

[Features of the heart conduction system in alcoholic lesions of the myocardium].

An electrophysiologic functional study of the atrial conductive structure, the atrioventricular junction, the His-Purkinje system in 33 patients with second-stage chronic alcoholism showed impaired cardiac conduction through the atrioventricular node and, less commonly, the His-Purkinje system, to be the principal manifestation of alcoholic heart damage.

Adult↗
PubMed1989

Idiopathic familial atrial cardiomyopathy with diffuse conduction block.

Isolated atrial cardiomyopathy is rare and familial idiopathic atrial cardiomyopathy has only been described once. We describe a case characterized by severely reduced atrial contractile function, intermittent atrial electrical standstill, diffuse interatrial, intraventricular and atrioventricular block, complicated by systemic embolism. Whilst this condition is undoubtedly rare, other cases may be being mistaken for simple sinoatrial disease.

Adult↗
PubMed1992

Atrial fibrillation and flutter after coronary artery bypass surgery: epidemiology, risk factors and preventive trials.

Atrial fibrillation and atrial flutter are common arrhythmias after coronary artery bypass grafting. Although the consequences of the arrhythmia are generally not life-threatening, it constitutes a major clinical problem often requiring conversion to sinus rhythm. Atrial fibrillation or flutter can result in hypotension, heart failure, pneumonia, and stroke. This article reviews the literature on epidemiology, electrophysiology, risk factors, and preventive trials. The major conclusions are: (1) In patients undergoing coronary artery bypass surgery, the incidence of postoperative atrial fibrillation or flutter is 20-30%, the peak incidence being on the second or third postoperative day. (2) The strongest independent preoperative predictor for atrial fibrillation or flutter is the patients' age. (3) Intra-atrial conduction delay recorded pre and peroperatively may predict development of atrial fibrillation. (4) Peroperative inducibility of atrial fibrillation by pacing the right atrium may identify patients at risk for postoperative atrial fibrillation. (5) Development of postoperative atrial fibrillation or flutter has not been associated with peroperative or postoperative events. (6) The specificity and sensitivity of age and other possible relevant factors for prediction of atrial fibrillation or flutter after coronary artery bypass grafting is low. (7) No effective prophylactic regimen has yet been established.

Adrenergic beta-Antagonists↗
PubMed1985

[Changes in the indices of the atrial complex on a differentially amplified ECG in atrial infarct].

The atrial complex of differentially amplified ECG was examined in 19 patients with atrial infarction. The diagnosis of atrial infarction was based on the electrocardiographic features, and in 7 cases it was confirmed by postmortem examination. The electrocardiographic pattern was characterized by P-Q segment shift. Atrial infarction resulted in a decrease in the amplitude, the prolongation of atrial conduction time and the appearance of additional fragments in the atrial complex of differentially amplified ECG.

Adult↗
PubMed2001

Prospective evaluation of a simplified approach for common atrial flutter radio frequency ablation with only two catheters.

UNLABELLED: Intra-atrial conduction block within the inferior vena cava-tricuspid annulus isthmus (IVCT) has been shown to predict successful common atrial flutter ablation. However, its demonstration requires the use of several electrode catheters and mapping of the line of block. The aim of this study was prospectively to test the feasibility of a simplified ablation procedure using only two catheters. METHODS: Radio frequency (RF) ablation of common atrial flutter was performed in 30 patients with the sole use of a catheter for atrial pacing and a RF catheter. RF ablation lesions were created in the IVCT. Surface ECG criteria were used to monitor the conduction within the IVCT. The end point during low lateral atrial pacing was an increment in the interval between the pacing artefact and the peak of the R wave in surface lead II >50 ms and clockwise rotation of the P wave axis beyond -30 degrees and inferiorly. Then, the line of lesions was mapped during atrial pacing with the RF catheter. Additional RF lesions were applied if mapping disclosed a zone of residual conduction. Otherwise the procedure was stopped if mapping showed parallel double potentials all along the line. Finally, the block was reassessed with a 'Halo' catheter. RESULTS: Surface ECG criteria were met in 26 patients. Mapping the line of lesions showed a complete corridor of parallel double potentials in these 26 cases and in 3 of the 4 patients in whom ECG criteria were not met. Conduction evaluated with the Halo catheter showed bi-directional complete block in these 29 patients. After a follow-up of 16 +/- 4 months there was no recurrence of atrial flutter. CONCLUSION: Surface ECG criteria combined with mapping of the line of block demonstrate evidence of bi-directional IVCT block. This simplified RF ablation of common atrial flutter is feasible with a low recurrence rate.

Aged↗
PubMed1976

The significance of fetal electrocardiography in the diagnosis of intrauterine bradyarrhythmia.

From 11 cases of fetal bradycardia diagnosed by monitoring of 130 fetal electrocardiograms (ECG's) in high-risk pregnancies we have presented our experience in three selected cases of fetal bradyarrthythmia. Case 1 revealed on ECG blocked atrial premature beats simulating an extreme sinus bradycardia sequentially followed by conducted atrial premature beats. In case 2 we diagnosed ventricular premature beats in the form of persistent bigeminy which was controlled by intravenous propranolol. The last case illustrated the phenomenon of aberrant ventricular conduction known to occur in adult cardiology. The electrophysiologic basis of the variable arrhythmias was discussed. Detailed analysis of repeated direct fetal ECG's provided us with the diagnosis and understanding of the electrophysiologic mechanisms underlying the rhythm disturbances. This consequently determined the pharmacologic therapy and the obstetric approach relevant to each case. We have shown that by direct fetal electrocardiography it is possible to analyze accurately the rhythm disturbances. Persistent fetal bradycardia does not always signify fetal distress. We hope that this will lead to closer teamwork between the obstetrician and the cardiologist which will give an impetus to the future development of "fetal cardiology," thereby enhancing our understanding of the electrophysiology of the fetal heart.

Adult↗
PubMed1978

Exposure of concealed right bundle branch block in Wolff-Parkinson-White type B by pacing from the vicinity of the A-V node.

In two infants with Wolff-Parkinson-White type B, right bundle branch block was concealed during sinus rhythm and pacing from close to the atrial entrance of the right-sided accessory pathway. However, pacing from the vicinity of the A-V node, the A-V node itself, and the His bundle exposed the right bundle branch block by producing exclusive ventricular activation through the normal, A-V nodal His-Purkinje pathway. In addition, pacing from close to the A-V node also resulted in fusion beats characterized by absence of delta waves with (pseudo) normal QRS complexes and short H-V intervals. False patterns of tachycardia-dependent and bradycardia-dependent block in the accessory pathway also occurred. These dynamic phenomena were attributed to the (peri-A-V nodal) pacing-related, relatively early arrival of excitation at the ventricles through the normal pathways coexisting with delayed arrival of excitation via the accessory pathway. The latter in turn was due to the longer intra-atrial conduction time from paced (peri-A-V nodal) site to atrial entrance of the accessory pathway.

Atrioventricular Node↗