Enhanced atrioventricular conduction atrial fibrillation after lidocaine administration.
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We describe a patient, in whom electrophysiologic study revealed a "negative" P-A interval in the His bundle electrogram, a prolonged intraatrial conduction time and a prolonged spike to the P wave interval during atrial pacing. The abnormalities were due to extensive sinuatrial disease.
In this work we have searched for experimental evidence that would corroborate the idea that nodal threshold (NT) is the minimum electric field strength able to promote direct sinus node reset that, in turn, can be verified by a decrease in corrected sinus node recovery time (CSNRT). We have performed direct measurements of sinus node conduction time (SACT) and estimation of atrium sinus conduction time (ASCT). Stimulating pulses (pulse and train methods) generated a uniform electric field, with strength ranging from 1.5-fold to 5-fold the atrial threshold (AT), in the center of the perfusion chamber where isolated right atria were placed. The AT and NT were 67.4 and 192.7 mV cm(-1), respectively. The CSNRT values, obtained with stimulation strength below or above NT, were, respectively (ms; mean +/- standard error of mean) 38.1 +/- 0.42 and 25.2 +/- 0.30. In addition, we verified that NT corresponds to approximately 3-fold the AT; SACT was 1.34-fold ASCT and the overdrive suppression decreases with the increment of stimulation pulse strength. Therefore, by using a new and accurate approach for SNRT determination, we have provided additional experimental evidence for the development of alternative sinus node evaluation methods.
1/1 atrial flutter is a regularly described complication of class I anti-arrhythmics. It is, however, very rarely encountered with class III anti-arrhythmics because prolongation of the atrio-ventricular node refractory period prevents 1/1 nodo-ventricular conduction. There have only been seven cases of 1/1 atrial flutter with amiodarone reported in the literature. Here we describe a new case of 1/1 atrial flutter with amiodarone. Our case clearly illustrates not only the different pro-arrhythmic effects of amiodarone (prolongation of the flutter cycle, and infra-Hissian block) but also the pathophysiological mechanisms possible with 1/1 conduction (prolongation of the flutter cycle, considerable permeability of the AV node). It demonstrates the difficulties of diagnosing such a rhythm disturbance, and that it is sometimes poorly tolerated, as well as underlining the importance of early diagnosis (in this case by oesophageal recording). Preventive treatment of 1/1 flutter can include amiodarone, digitalis, a betablocker or a bradycardic calcium inhibitor.
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A 57 year old man developed recurrent tachycardia with QRS complexes of 0.13 second in duration at a rate of 140 beats per minute. Inverted P waves appeared to follow each QRS complex in the electrocardiographic leads II, III and aVF. The differentiation between ventricular tachycardia with1 : 1 V-A conduction and supraventricular tachycardia with aberrant ventricular conduction was difficult to make from the surface electrocardiogram. This differentiation is important for selection of appropriate therapy. The diagnosis of ventricular tachycardia with 1 : 1 V-A conduction was clearly established in this case on simultaneous recording of surface electrocardiogram, His bundle electrogram and high right atrial electrogram.
In 10 patients with the Kent's bundle W.P.W. syndrome, the action of amiodarone (5 mg/kg i.v.) on conduction along the normal and anomalous pathways was studied. The drug actions were: 1) constant increase of the anomalous pathway E.R.P., in one case with antegrade functional block; 2) constant reduction of antegrade conduction velocity along the anomalous pathway, in one case with antegrade functional block; 3) reduction of retrograde conduction velocity along the anomalous pathway in 6 cases out of 8, including one with retrograde functional block; 4) constant increase of the A-V node E.R.P.; 5) reduction of sub Hisian A-V conduction velocity in 3 cases out of 7. Episodes of reciprocating tachycardia could be initiated by atrial electrostimulation in 5 patients before administration and in 3 following administration of the drug. In connection with the electrophysiological properties of the two atrio-ventricular pathways and on the mechanism of tachycardia, the use of this drug in prevention of the circus movement tachycardia in patients with the W.P.W. syndrome is discussed.
The relationship between anatomy and function has long been recognised. Understanding the gross structure, and the myoarchitecture, of the atriums is fundamental to investigations into the substrates and therapy of atrial fibrillation. Based primarily on our experience with normal human hearts, this review provides, firstly, a basis of comparison of gross structures as seen in the clinical situation, and in animals commonly used in experimental studies. Secondly, we discuss the general arrangement of myocardial fibres with respect to gross topography in the normal human heart. The right atrium is dominated by an extensive array of pectinate muscles within the extensive appendage, whereas the left atrium is relatively smooth-walled, with a much smaller tubular appendage. Myoarchitecture displays parallel alignment of fibres along distinct muscle bundles, such as the terminal crest and Bachmann's bundle. Within the smooth wall of the left atrium, there is a marked transmural change in the orientation of the muscular fibres. Abrupt changes in orientation, and mixed arrangements, are common between bundles. Other than Bachmann's bundle, the muscular bridges which provide interatrial connections, and connections between the left atrium and the coronary sinus and inferior caval vein, are highly variable. Inhomogeneities both in gross structure and myoarchitecture are common in the normal heart. These should be taken into account when investigating hearts from patients known to have had a history of arrhythmias, in devising computer models, or when refining diagnostic and therapeutic strategies.
Direct recording of the sinus node potential in the bipolar mode using two electrodes of a quadripolar recording catheter positioned in the region of the sinus node at the junction of the superior vena cava to the right atrium was performed in 24 patients. Asynchronous overdrive atrial pacing was carried out using Strauss 'technique. Pharmacological denervation was carried out using intravenous propranolol (0,02 mg/kg) and atropine (0,04 mg/kg) using Jose's technique. An intravenous injection of a bolus of 20 mg of ATP was given in 3 cases. The sinus potential was identified by morphological criteria and confirmed after carotid sinus compression and atrial extrastimuli to exclude artefacts, especially the end of ventricular repolarisation of the preceding complex. The sinoatrial conduction time measured directly under basal conditions was considered normal when within 80 to 150 ms. Direct measurement of the sinus potential in the diagnosis of sinus node dysfunction seems to be less useful than the indirect techniques. On the other hand, it does confirm the diagnosis of sinoatrial block: five cases of special interest are described; in four cases the degree of sinoatrial block was variable: a significant increase of sinoatrial conduction time under basal conditions in 1 case; paroxysmal 3rd degree sinoatrial block revealed by programmed atrial stimulation in 2 cases; 2nd degree 2/1 sinoatrial block after injection of ATP in which the direct sinoatrial conduction time and sinus node function had been considered to be normal (1 case).(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of verapamil, a slow channel blocker and a potent antiarrhythmic drug, on retrograde V-A conduction were investigated following diagnostic cardiac catheterization in 12 children premedicated with lytic cocktail. Surface EKG, intra-atrial and His bundle electrograms, as well as right ventricular pacing with use of extra stimulus technique were obtained before and after a single intravenous dose of verapamil (0.15 mg/Kg, max 5 mg). Verapamil prolonged the AH interval in 9/12 and abolished or prolonged the retrograde V-A conduction whenever present (abolition in 5/12 and prolongation in 1/12). The duration of retrograde V-A conduction exceeded the antegrade conduction time in all. It is concluded that verapamil abolishes retrograde V-A conduction whenever present and this phenomenon may further explain the antiarrhythmic effects of the drug on retrograde conduction dependent (reentrant) arrhythmias.
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Rotigaptide (ZP123) increases gap junction intercellular communication (GJIC) and prevents stress-induced cardiac conduction velocity (CV) slowing. However, the effect of rotigaptide on established cardiac conduction slowing and the duration of effect on rotigaptide during washout is unknown. Metabolic stress (induced by superfusion with nonoxygenated glucose-free Tyrodes buffer) was associated with a 30% decrease in atrial CV in vehicle-treated rat atria. Rotigaptide treatment initiated after a period of 30 minutes of metabolic stress produced a rapid and significant increase in CV compared to vehicle-treated time controls. During washout of rotigaptide for 30 min (while subjected to metabolic stress), there was a minor decrease in atrial CV; however, this was not significantly different from atrial CV in a rotigaptide-treated time control group. Rotigaptide treatment rapidly normalizes established conduction slowing in atria subjected to metabolic stress. However, the cessation of effect was considerably slower than the onset of action.
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We report a 78-year-old man as the first documented case of double P waves separated by 400 msec on 12-lead ECG. These P waves had different polarities on lead V1. The first P wave represented activation of the lateral wall of the right atrium, and the latter P wave represented activation of the medial right atrium and the left atrium. Widely spaced double potentials were recorded craniocaudally along the line, presumably corresponding to the crista terminalis during sinus rhythm. For this to occur, conduction disturbance has to be present both in the upper and lower right atrium. Conduction disturbance in the upper right atrium would interrupt excitation from the sinus node to the medial wall, and conduction disturbance in the lower right atrium would interrupt excitation spreading from the lower lateral right atrium to the isthmus area where fragmented potentials were recorded. These multiple discrete lesions appear to constitute a unique electrical atriopathy in this patient.
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