Paradoxical delay in accessory pathway conduction during long R-P' tachycardia after interpolated ventricular premature complexes.
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Biomedical subjects
Publications and source records attributed to G H Bardy.
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In a series of 12 dogs, the electrophysiologic and histologic effects of a single damped sine-wave shock delivered via standard electrocatheters to the region of the coronary sinus orifice were investigated. Six dogs received 200 J and six received 360 J of stored energy. The shock was delivered to two consecutive proximal poles of a standard quadripolar catheter positioned at the coronary sinus orifice and connected to the positive output (anode) of a defibrillator. A disc electrode positioned on the anterior chest wall served as the cathode (negative pole). During the shock, voltage and current were recorded. Electrophysiologic testing was done before and 4 weeks after the shock. At 4 weeks, animals were killed and serial sections of the atrioventricular groove and conduction system were performed. No significant long-term change in atrioventricular conduction, spontaneous or induced atrial or ventricular arrhythmias was observed. However, transient atrioventricular block was seen in five and idioventricular rhythms in six animals in the short term. No persistent electrocardiographic changes were observed, and no sudden deaths occurred. Microscopically, transmural injury at the anulus proper or basilar ventricular epicardium was inconstant and infrequent. However, transmural atrial injury at the level of the coronary sinus was produced over a 10 +/- 5 mm length with the 200 J shock and a 21 +/- 6 mm length with the 360 J shock. Neither coronary artery injury nor damage to the conduction system was seen and cardiac tamponade did not occur. However, localized intramural atrial rupture of the coronary sinus wall (on the endocardial aspect only) was observed in each dog, consistent with barotrauma. With the present technique, atrial injury potentially capable of blocking the effects of accessory pathway conduction could be produced without other electrophysiologic alterations or complications. Injury to the anulus proper (and therefore to any accessory pathway per se) is probably unlikely. Barotrauma may play a significant role in the type of injury observed in this study.
Nonischemic ventricular tachycardia most commonly arises in the right ventricular free wall and is frequently refractory to medical therapy. Many different types of surgical procedures have been employed to treat medically refractory nonischemic ventricular tachycardia arising in the right ventricle, but the results of these procedures have been less than optimal. The majority of these surgical procedures have been directed toward ablation of the site (or sites) of origin of the tachyarrhythmia and have failed because of the frequent occurrence of multifocal or polymorphic ventricular tachycardia in these patients. We first employed localized surgical isolation procedures to control nonischemic ventricular tachycardia arising in the right ventricular free wall in 1979. These localized procedures evolved into the development of a technique for isolating the entire right ventricular free wall from the remainder of the heart to control ventricular tachyarrhythmias arising from multiple sites in the right ventricle. Case histories are reported of two patients who underwent localized isolation procedures in 1979 as well as two patients who underwent total disconnection of the right ventricle in 1982. The follow-up period in these four patients ranges from 2 to 5 years and the control of their tachyarrhythmias has been uniformly successful. However, surgical isolation of the entire right ventricular free wall has resulted in progressive dilatation of the right ventricle as documented by serial echocardiography. The pathophysiology of the progressive right ventricular dilatation postoperatively is discussed in terms of etiology and prevention, and the indications for application of localized and total isolation procedures for nonischemic right ventricular tachycardia are outlined.
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Epicardial mapping was used as a standard to investigate how well the limb leads, both alone and in conjunction with 5 select epicardial electrodes, can verify reproducibility in a common, open-chest canine model of ventricular tachycardia (VT). Reproducible VT was defined as 2 or more episodes of monomorphic VT with similar rates, limb lead tracings and epicardial maps. In this study, 21 dogs underwent 2-hour occlusion of the left anterior descending coronary artery followed by reperfusion. Three days later, programmed stimulation was used to induce VT that was analyzed with limb leads I, II and III and 27 simultaneously recorded, bipolar epicardial electrodes. Thirteen dogs had VT of which 11 had polymorphic VT (varying QRS morphology). Twelve dogs yielded at least 1 form of monomorphic VT. Eight had 2 or more distinct forms of monomorphic VT (pleomorphism). Four of these 8 dogs had pleomorphic VT that was not apparent from the limb lead tracings, but was recognized from the epicardial activation maps constructed from the 27 epicardial recordings. To provide a method of distinguishing various VTs without the need of full epicardial mapping, 5 of the 27 epicardial electrodes were selected. These were positioned over the midanterior and midposterior right and left ventricles, and the left ventricular apex. By analyzing electrogram morphology and activation time, VT reproducibility could be as accurately identified with these 5 electrodes as with epicardial mapping derived from 27 electrodes. In conclusion, multiple VT morphologies are common in this open-chest canine model. Limb lead recordings alone are inadequate for analysis of VT reproducibility.(ABSTRACT TRUNCATED AT 250 WORDS)
Standard electrocardiograms from 87 consecutive patients with tachycardia of left bundle branch block configuration were analyzed retrospectively for features that might be characteristic of tachycardia utilizing a nodofascicular Mahaim fiber. The study group consisted of 13 patients with nodofascicular tachycardia, 34 with supraventricular tachycardia and aberrant conduction over the His-Purkinje system, 22 with ventricular tachycardia and 18 with antidromic tachycardia utilizing a right-sided accessory atrioventricular pathway. Six variables present during tachycardia of left bundle branch block configuration were predictive of a nodofascicular fiber: cycle length between 220 and 450 ms, QRS axis of 0 to -75 degrees, QRS duration 0.15 second or less, R wave in lead I, rS wave in precordial lead V1 and a precordial transition from a negative to a positive QRS complex after lead V4. All six criteria were present in 16 of the 87 patients. No patient with ventricular tachycardia satisfied these criteria, whereas 3 of 34 with supraventricular tachycardia, 1 of 18 with antidromic tachycardia and 12 of 13 with tachycardia using a nodofascicular fiber did. It is concluded that analysis of the surface electrocardiogram during tachycardia may suggest the presence of a nodofascicular fiber.
The demonstrable value of EP studies for any given diagnostic or therapeutic category, in the last analysis, is largely a function of the subjects studied. Extrapolations from published data (that generally reflect a highly select patient population) to an individual patient can be fraught with error. Considerations of sensitivity and specificity must be balanced against the important need for information in patients at risk from life-threatening arrhythmias. We must never forget, however, that the EP substrate for any arrhythmia is not, as one might wish, a "black box" that should be expected to respond in a reproducible fashion to stimulation. The substrate is dynamic and subject to modification by change in autonomic tone, stretch, blood flow, basal rate, pH, electrolytes, oxygenation, and exposure to perhaps as yet undiscovered humoral mediators. The challenge to the clinical electrophysiologist is therefore not to exaggerate his efforts in one direction (i.e. programmed stimulation) while disregarding the other variables mentioned. Nor should we be disappointed and discard this approach because our expectations of an oversimplified model of arrhythmia testing are not fulfilled. Thus, in addition to careful stratification of patients, baseline studies should perhaps be carried out with more deliberate consideration of autonomic tone (exercise, isoproterenol), stretch (volume, handgrip, afterload), stress (physical and psychological), local anesthetic used, and body position. Only in this way will the scientific basis for acute and chronic EP testing be firmly established.
During the electrophysiologic study of 435 patients referred for evaluation of Wolff-Parkinson-White syndrome, 42 (10%) had preexcited reciprocating tachycardia (defined as a macro-reentrant tachycardia that used an accessory atrioventricular [AV] pathway for antegrade conduction). The ages of the patients ranged from 9 to 67 years (27 +/- 14). Thirty-three were male patients, nine female, and eight had Ebstein's anomaly. Preexcited reciprocating tachycardia cycle length was 220 to 430 msec (294 +/- 42). Significant hemodynamic compromise in the laboratory directly related to preexcitated reciprocating tachycardia occurred in only one patient. However, in 10 patients a transformation to atrial fibrillation was seen after a spontaneously occurring premature atrial contraction. Only 17 of the 42 patients with preexcited reciprocating tachycardia during electrophysiologic study had the same tachycardia documented clinically. These 17 patients were more often younger with multiple accessory pathways and with no history of orthodromic reciprocating tachycardia when compared with 25 patients in whom preexcited reciprocating tachycardia could be induced only in the laboratory. Preexcited reciprocating tachycardia was induced in the laboratory in 22 of 374 (6%) patients with single accessory pathways and in 20 of 61 (33%) of those with multiple accessory pathways. In the 20 patients with multiple accessory pathways, the spectrum of reentrant circuits included fusion over two or more accessory pathways or fusion over both an accessory pathway and the AV node. In the 22 patients with a single accessory pathway and true antidromic reciprocating tachycardia, all but two episodes were at least 4 cm from the AV node. No patient with true antidromic reciprocating tachycardia had a posterior septal accessory AV pathway. Only in patients with multiple accessory pathways was the posterior septal accessory AV pathway used as the antegrade limb.
Ten patients with an unusual form of ventricular tachycardia (VT) are described. All were young (mean age 21 years) at the onset of VT, symptoms were of long duration (mean 7 years), none had symptomatic organic heart disease, VT was induced by atrial and ventricular stimulation, VT had a characteristic QRS morphologic picture resembling right bundle branch block with left-axis deviation and 9 had early retrograde His deflections during VT. Supraventricular tachycardia (SVT) was excluded in every patient by electrophysiologic study, although QRS morphologic characteristics and clinical stability of these patients during tachycardia frequently led to the diagnosis of SVT before referral. Four patients received verapamil during electrophysiologic testing. Verapamil slowed and terminated VT in all. Three patients are being treated chronically with oral verapamil, 3 patients with conventional antiarrhythmic agents and 1 with a radiofrequency ventricular pacemaker.
The correlation of histologic and electrophysiologic findings in dogs undergoing transvenous ablation of atrioventricular (AV) conduction has not been described. The creation of complete AV block in 10 dogs was attempted by delivering a direct-current shock transvenously through a standard tripolar electrode catheter. The catheter was positioned to record the largest unipolar atrial and His bundle electrograms. A 280 J shock was delivered to the recording electrode by a standard cardioversion unit. After 1 shock, all dogs were in complete AV block refractory to isoproterenol (1 to 4 micrograms/min) and atropine (0.5 to 2.0 mg). Four weeks later, 5 dogs remained in complete AV block, 1 had first-degree block, and 4 had resumed normal AV conduction. Each dog with complete heart block had histologic evidence of severe damage to the AV node, His bundle, or both. On gross examination, these dogs were found to have discrete scars at the base of the septal leaflet of the tricuspid valve. Of the 5 dogs that had resumption of AV conduction, only 1 had histologic evidence of significant damage to the AV conduction system. That animal manifested a marked increase in the P-R interval (100 to 210 ms). Although temporary heart block occurred in each animal, chronic interruption of AV conduction was more difficult. Catheter location, atrial and His bundle electrogram relations, and the electrode used for delivery of energy were factors determining the effectiveness of this technique.
To examine whether different septal pacing sites could be distinguished by their epicardial activation patterns, six to eight stimulating electrodes were placed throughout the septum in seven open chest dogs. Unipolar electrograms were obtained from 52 epicardial electrodes during pacing from each stimulating electrode and isochronous epicardial maps were constructed. The location of each stimulating electrode was found by dissection, and its distance from the overlying epicardium was measured. To allow comparison among epicardial maps, the septum was conceptually subdivided into nine regions to which stimulating electrodes were assigned. Epicardial activation patterns from the same region were similar and these patterns allowed the region containing a stimulating electrode to be identified in many cases. Three other variables were found to have additional localizing value. There were: 1) the time from the stimulus to epicardial breakthrough, 2) the duration of epicardial activation, and 3) the area of epicardium activated in the first 5 ms after epicardial breakthrough. For those stimulating electrodes that could not be localized by their epicardial activation patterns, the distance of the stimulating electrode beneath the epicardium was well fit from these three variables by multiple regression (correlation coefficient [r] = 0.97). Thus, using all the previous factors, localization of septal pacing sites was possible in the noninfarcted dog heart by epicardial mapping.
Pseudomonas alcaligenes is a common soil and water inhabitant that has rarely been proven a human pathogen. We describe a fatal case of Pseudomonas alcaligenes endocarditis. The need for accurate identification of unusual organisms isolated in a clinical setting are discussed.
Late fractionated potentials, recorded during cardiac mapping to find the source of a ventricular arrhythmia, have been ascribed particular localizing value. Re-entry is assumed when these highly amplified and filtered recordings span diastole during tachycardia. The purpose of this study was to see if such potentials can occur artifactually. A saline soaked 7 X 2 X 3 cm sponge was sewn to the epicardium of the right ventricle in five non-infarcted, open-chest dogs. Two bipolar button electrodes, one with 1 mm and one with 1 cm interelectrode spacing, were attached to the outer surface of the sponge and a bipolar wire hook electrode was placed just under the outer surface of the sponge. Thus all three electrodes were 3 cm from the nearest myocardium yet still subjected to cardiac motion. The electrodes were recorded at gains of 4,000-40,000 and filtered to pass 50-300 hertz. One to three rapid deflections were recorded during the QRS from all electrodes. In seven of the the 15 electrode recordings, two or three additional deflections, 1100-200 microV in amplitude, occurred after the QRS. These late potentials were fractionated and recurred reproducibly from cycle to cycle. In two cases, these late fractionated potentials could be made to span diastole by rapid pacing to simulate tachycardia. Clamping the sponge to sliminate motion between the sponge and electrode caused this late activity to disappear. Thus, in highly amplified and filtered recordings, electrode motion can cause artifacts resembling late fractionated potentials and continuous electrode activity.
A dog model of torsades de pointes (TdP) was developed. Twenty 18-30-kg dogs had cardiopulmonary bypass instituted to maintain stable temperature, perfusion pressure and oxygenation. Quinidine, 30 mg/kg, was then administered and burst ventricular pacing was used to induce arrhythmias. The left anterior descending coronary artery was occluded for 15 minutes and repeat pacing studies were performed. Maps of epicardial activation were made from 27 simultaneously recorded electrograms obtained from 1-mm bipolar electrodes secured to the epicardium with a nylon mesh sock. Arrhythmias in five dogs met criteria for the diagnosis of TdP: All had the characteristic undulating QRS morphology typically associated with TdP, all occurred in the setting of QT prolongation and all ended spontaneously. The epicardial maps demonstrated that each change in QRS morphology was associated with a change in the site of epicardial breakthrough. Those QRS complexes during the transition from one morphology to the next were associated with fusion cycles in which both the old and new sites of epicardial breakthrough were present. In essence, two or more competing activation sequences were vying for control of epicardial depolarization. This conclusion was strengthened by our ability to simulate TdP in the surface ECG and in epicardial maps by simultaneously pacing from two widely separated ventricular sites at slightly different, varying rates.
An increasing number of people who have undergone surgical repair of tetralogy of Fallot are living long lives. Several late sequelae of corrected tetralogy of Fallot have been found, including residual ventricular septal defect, restenosis of the pulmonary outflow tract, ventricular tachycardia, and right ventricular failure from pulmonary insufficiency. A long-term survivor of corrected tetralogy of Fallot is reported with acquired coronary artery disease unrelated to the congenital anomaly or its correction as an additional cause of late morbidity in this select but growing population of patients.
This report describes a catheter technique for ablating the His bundle and its application in nine patients with recurrent supraventricular tachycardia that was unresponsive to medical management. A tripolar electrode catheter was positioned in the region of the His bundle, and the electrode recording a large unipolar His-bundle potential was identified. In the first patient, two shocks of 25 and 50 J, respectively, were delivered by a standard cardioversion unit to the catheter electrode, resulting in an intra-His-bundle conduction defect. Subsequent delivery of 300 J resulted in complete heart block. In the next eight patients, an initial shock of 200 J was used. The His bundle was ablated by this single shock in six of these patients and by an additional shock of 300 J in one. In the remaining patient, conduction in the atrioventricular node was modified, resulting in alternating first and second-degree atrioventricular block. A stable escape rhythm was preserved in all patients. The procedure was well tolerated, without complications, and all patients have remained free of arrhythmia, without medication, for follow-up periods of two to six months.