Antegrade Direction Research Articles

Optimal Programming of Antitachycardia Pacing Functions

The majority of ventricular tachyarrhythmias for which implantable cardioverter de~brillators are implanted is due to reentry. In order for paced beats to entrain or terminate a tachycardia, the arrhythmia must have an excitable gap, i.e., tissue in the circuit between the activation wavefront and the tail of refractoriness that can be depolarized by an electrical impulse entering the tachycardia circuit. When reentry is the mechanism, ventricular tachycardia can often be entrained and/or terminated by pacing [1]. Entrainment occurs when impulses enter the circuit and propagate in the antegrade direction but collide with the previous impulse in the retrograde direction. Antitachycardia pacing algorithms in implantable cardioverter de~brillators are based on the principles of entrainment [2]. The tachycardia terminates when an impulse collides in the retrograde direction and blocks in the antegrade direction. Antitachycardia pacing has several advantages over shock therapy for ventricular tachycardia. First, because it does not require that capacitors be charged, antitachycardia pacing can be delivered more quickly. This decreases the likelihood that the patient will develop hypotension or myocardial ischemia from the arrhythmia. Second, antitachycardia pacing is better tolerated than shock therapy. Direct current countershocks are often associated with pain, and, when they occur frequently, can cause signi~cant patient anxiety. In contrast, antitachycardia pacing may be associated with brief palpitation or dizziness, but is rarely associated with discomfort. Many patients are not aware of antitachycardia pacing events at all. Because it is so well tolerated, antitachycardia pacing may, in selected patients, obviate the need for antiarrhythmic drugs which are sometimes necessary to decrease the frequency of ventricular tachycardia and the attendant shocks. Third, antitachycardia pacing, when successful, uses far less energy than a direct current counter shock. In some patients this may promote longer implantable cardioverter de~brillator battery life. For all of its potential bene~ts, antitachycardia pacing is not without risk. The major risk associated with antitachycardia pacing is that of proarrhythmia. Antitachycardia pacing has the potential to accelerate an hemodynamically well tolerated ventricular tachycardia into one that is associated with hemodynamic collapse or one that is more dif~cult to terminate, even with a shock [3]. Studies suggest that this may occur in 2 to 21% of cases [4]. Proarrhymia may also occur if an implantable cardioverter de~brillator misclassi~es a supraventricular tachyarrhythmia as ventricular tachycardia [3]. In such a case, antitachycardia pacing may induce ventricular tachycardia. This is most likely to occur in patients with slow ventricular tachycardia, the rate of which overlaps with that of sinus tachycardia or other atrial arrhythmias. Finally, antitachycardia pacing, if it is unsuccessful, may delay the delivery of de~nitive shock therapy for an arrhythmia. This has the potential to subject a patient to myocardial ischemia and may limit the ef~cacy of the countershock.

Difficult Femoral Arteriovenous Fistula in a Child

Difficult Femoral Arteriovenous Fistula in a Child

Involvement of the Calcium Inward Current in Cardiac Impulse Propagation: Induction of Unidirectional Conduction Block by Nifedipine and Reversal by Bay K 8644

In general, the fast sodium inward current (INa) is regarded as the main inward current ensuring fast and safe excitation of the normally polarized working myocardium. However, under conditions of locally delayed excitation in the millisecond range, the slow inward current (ICa) might additionally contribute to the success of impulse propagation. This hypothesis was tested in patterned growth cultures of neonatal rat ventricular myocytes, which consisted of narrow cell strands connected to large rectangular cell monolayers, where INa or ICa could be modified in the narrow cell strand adjacent to the expansion by a microsuperfusion system. As assessed during antegrade (strand-->expansion) propagation under control conditions using a system for multiple site optical recording of transmembrane voltage (MSORTV), this cell pattern gave either rise to local activation delays at the expansion ranging from 0.5 to 4 ms (dcontrol), or it induced undirectional conduction blocks (UCBs) in the antegrade direction. Irrespective of the size of dcontrol, suppression of the sodium current with tetrodotoxin confined to the cell strand adjacent to the expansion invariably induced UCB in the antegrade direction. If dcontrol was > 1 ms, UCB could also be elicited by suppression of ICa alone with nifedipine. Conversely, if UCB was present under control conditions, the inclusion of Bay K 8644 in the microsuperfusion established successful bidirectional conduction. These results suggest that ICa can be critically important for the success of impulse propagation across abrupt expansions of excitable tissue even if INa is not concurrently depressed.

Accessory atrioventricular pathways with only antegrade conduction in patients with symptomatic Wolff-Parkinson-White syndrome. Clinical features, electrophysiological characteristics and response to radiofrequency catheter ablation.

Information about accessory pathways conducting only in the antegrade direction is limited. The purposes of the present study were to prospectively investigate the clinical features, electrophysiological characteristics, effects of radiofrequency catheter ablation and recurrent atrial fibrillation after successful ablation in patients with accessory pathways conducting only in the antegrade direction, and to compare them with those who had pathways capable of bidirectional conduction in a consecutive series of 759 patients. Electrophysiological studies and radiofrequency catheter ablation were performed in 33 study patients with antegrade-only accessory pathways and in 377 patients with bidirectional accessory pathways for comparison. The patients with accessory pathways conducting only in the antegrade direction were older (47 +/- 16 vs 40 +/- 16 years, P = 0.037) and had a higher incidence of atrial fibrillation (100% vs 27.1%, P < 0.001) as well as related syncope (33.3% vs 10.1%, P = 0.001). The study patients also had more accessory pathways located in the posterior septum and a higher incidence of retrograde atrioventricular nodal conduction. The biophysical variables, success and complication rates of radiofrequency ablation were similar in both groups. During the follow-up period of 32 +/- 12 months, symptomatic atrial fibrillation after successful ablation did not recur in 79% and 81% of patients with unidirectional and bidirectional accessory pathways, respectively. Furthermore, old age and cardiovascular diseases were independent predictors of recurrent atrial fibrillation after radiofrequency ablation. In conclusion, this study showed that atrial fibrillation with preexcitation was the usual presentation in patients who had symptomatic Wolff-Parkinson White syndrome with an antegrade-only accessory pathway, and might be related to antegrade conduction of the accessory pathway. Therefore elimination of antegrade-only and bidirectional pathways by radiofrequency ablation could prevent the recurrence of symptomatic atrial fibrillation in younger patients without cardiac disease.

Morphological and functional aspects of the human spermatic cord veins.

It is well known that varicocele of the testis may lead to a damage of testicular tissue and therefore is one etiologic factor for male infertility. Successful varicocele treatment may result in preserving or restoring fertility. Antegrade sclerotherapy has proved to be safe, economical and effective (Bruns et al., 1996). The major component of this procedure is the preparation of the pampiniform plexus. After insertion of a canula into a selected vein of the plexus and fluoroscopic control showing drainage by the internal spermatic vein, a sclerosing agent (AthoxysklerolR) is injected in an antegrade direction. By analysis of the vascular organization of the pampiniform plexus (Ergun et al., 1994) it could be demonstrated that the testicular veins are organized in two main groups and form two vein plexus. One of these vein groups forms a tight plexus around the testicular artery, the other vein group is embedded in a large macroscopically visible section of fatty tissue. To save the testicular artery from injury during dissection, the vein group in this lateroventral compartment should be dissected for antegrade sclerotherapy.

Rate-dependent functional properties of retrograde atrioventricular nodal conduction in experimental animals.

While rate-dependent atrioventricular (AV) nodal functional properties play a major role in determining antegrade AV nodal conduction, their existence and characteristics have not been assessed during retrograde AV nodal impulse propagation. Pacing protocols were used to study selectively AV nodal recovery, facilitation, and fatigue in 6 isolated, superfused rabbit AV nodal preparations and in 11 morphine-chloralose anesthetized dogs. All three properties were identifiable during retrograde AV nodal activation in rabbits. Retrograde recovery and fatigue were clearly demonstrated in dogs, but facilitation could not be evaluated because of echo beats during retrograde premature stimulation. Functional properties were qualitatively similar during retrograde and antegrade propagation; however, important quantitative differences were noted. The time constant for recovery from activation was significantly greater in the retrograde [rabbits, 69 +/- 8 (SE) ms; dogs, 93 +/- 11 ms] compared with the antegrade direction (rabbits, 50 +/- 5 ms; dogs, 58 +/- 4 ms; P < 0.05 vs. retrograde for each species). The magnitude of fatigue resulting from sustained increases in rate was also substantially greater in the retrograde direction in both rabbits (17 +/- 2 vs. 10 +/- 1 ms antegrade, P = 0.01) and dogs (20 +/- 4 vs. 6 +/- 1 ms antegrade, P < 0.01). Conduction time and refractory period were both greater in the retrograde compared with antegrade direction, and directional differences in conduction properties were magnified as activation rate increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Reappraisals of atrioventricular node reentrant tachycardia: lessons learned from surgical treatment

The exact site of reentrant circuit involved in the atrioventricular node reentrant tachycardia was questioned. Seven patients (6 females and 1 male), aged 21 to 64 years (mean = 40 ± 17 years), with refractory nodal reentry, underwent surgical treatment. The associated cardiac diseases included rheumatic valvar disease in two and an atrial septal defect. Electrophysiologic studies before surgery showed dual nodal pathways in 4 patients. Right atrial endocardial mapping was performed and the earliest retrograde atrial activation during tachycardia was mapped to the apex of the triangle of Koch in 6 patients and near the orifice of coronary sinus in one. Perinodal dissection was performed according to the location of earliest retrograde atrial activity. Care was taken to preserve as much of the atrioventricular node and its arterial supply as was possible. Immediately after surgery, conduction in an antegrade direction recovered and the tachycardia could no longer be reproduced. There was no surgical mortality or morbidity. At 10 to 26 months of follow-up, all patients remain free of tachycardia without antiarrhythmic drrgs. Four patients underwent repeated electrophysiologic studies at 2 weeks to 6 months after surgery. Dual nodal pathways were no longer demonstrated. It is concluded that the perinodal atrial tissue plays a part in the atrioventricular nodal reentry, and that surgical dissection is a simple and effective treatment for patients with refractory atrioventricular node reentrant tachycardia.

Diprafenone for treatment of Wolff-Parkinson-White syndrome

The effect of intravenous (1.5 to 2.0 mg/kg body weight) and oral (300 to 375 mg/d) diprafenone was studied in 15 patients with the Wolff-Parkinson-White syndrome and symptomatic supraventricular tachycardia. Intravenous application of diprafenone significantly increased atrioventricular nodal conduction time as well as the effective refractory periods of the right ventricle and the accessory pathway in both the antegrade and retrograde directions. Antegrade conduction block in the accessory pathway occurred in two patients after the dose was increased to 2.0 mg/kg body weight. Intravenous diprafenone suppressed the inducibility of supraventricular tachycardia in two patients, but the tachycardia cycle length was significantly increased in all other patients. Fourteen patients were treated with oral diprafenone, and 11 were asymptomatic during a 17-month follow-up, two of these after the dose had been increased to 375 mg/d. Oral therapy had to be withdrawn in two patients because of adverse gastrointestinal side effects and in one because of recurring bronchospasm.

Heterogeneous acinar localization of the asialoglycoprotein internalization system in rat hepatocytes.

Desialylated glycoprotein is rapidly cleared from plasma by a receptor-mediated endocytic mechanism located on hepatocytes. We studied the hepatic acinar distribution of this asialoglycoprotein transport system with the ligand 125I-asialoorosomucoid using rat liver perfused in either antegrade or retrograde direction in combination with quantitative light microscopic autoradiography. Grain distribution along the acinus appeared dependent on the perfusion direction. A rather shallow zone 1 to zone 3 gradient was observed if livers were perfused in the normal direction. However, a statistically significantly steeper zone 3 to zone 1 gradient was detected in retrograde perfusions. Kinetic analysis of perfusate clearance profiles yielded a hepatic clearance of 21.6 +/- 1.3 ml per min in antegradely perfused liver. Hepatic extraction was calculated to be 60.1 +/- 7.4%. Biliary secretion of radioactivity amounted to 1.89 +/- 0.18% of the dose within 1 hr after injection and consisted of intact material (1.39 +/- 0.25%) and radioactive low-molecular-weight degradation products (0.52 +/- 0.08%), of which more than 90% could be accounted for by 125I-. Apart from a minor difference regarding biliary secretion of an unidentified glycopeptide (less than 0.1% of the injected dose), transport data for the retrogradely perfused livers were identical to those obtained with livers perfused in antegrade direction, emphasizing the functional equivalence of both groups of livers. The autoradiographic data indicate that zone 3 hepatocytes take up 125I-asialoorosomucoid more avidly than zone 1 cells. The kinetic and biochemical data indicate that further processing in the hepatocytes is virtually similar in the two zones.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatocyte heterogeneity in response to icosanoids

1. The metabolic and hemodynamic effects of prostaglandin F2 alpha, leukotriene C4 and the thromboxane A2 analogue U-46619 were studied during physiologically antegrade (portal to hepatic vein) and retrograde (hepatic to portal vein) perfusion and in a system of two rat livers perfused in sequence. 2. The stimulatory effects of prostaglandin F2 alpha (3 microM) on hepatic glucose release, perfusion pressure and net Ca2+ release were diminished by 77%, 95% and 64%, respectively, during retrograde perfusion when compared to the antegrade direction, whereas the stimulation of 14CO2 production from [1-14C]glutamate by prostaglandin F2 alpha (which largely reflects the metabolism of perivenous hepatocytes) was lowered by only 20%. Ca2+ mobilization and glucose release from the liver comparable to that seen during antegrade perfusion could also be observed in retrograde perfusions; however, higher concentrations of the prostaglandin were required. 3. The glucose, Ca2+ and pressure response to leukotriene C4 (20 nM) or the thromboxane A2 analogue U-46619 (200 nM) of livers perfused in the antegrade direction were diminished by about 90% during retrograde perfusion. Sodium nitroprusside (20 microM) decreased the pressure response to leukotriene C4 (20 nM) and U-46619 (200 nM) by about 40% and 20% in antegrade perfusions, respectively, but did not affect the maximal increase of glucose output. 4. When two livers were perfused antegradely in series, such that the perfusate leaving the first liver (liver I) entered a second liver (liver II), infusion of U-46619 at concentrations below 200 nM to the influent perfusate of liver I increased the portal pressure of liver I, but not of liver II. At higher concentrations of U-46619 there was also an increase of the portal pressure of liver II and with concentrations above 800 nM the pressure responses of both livers were near-maximal [19.6 +/- 0.8 (n = 7) cm H2O and 16.5 +/- 1.1 (n = 8) cm H2O for livers I and II, respectively]. There was a similar behaviour of glucose release from livers I and II in response to U-46619 infusion. When liver I was perfused in the retrograde direction, a significant pressure or glucose response of liver II (antegrade perfusion) could not be observed even with U-46619 concentrations up to 1000 nM. 5. Similarly, the perfusion pressure increase and glucose release induced by leukotriene C4 (10 nM) observed with liver II was only about 20% of that seen with liver I.(ABSTRACT TRUNCATED AT 250 WORDS)

Reassessment of AV and VA Conduction and AV Junctional Reentry in the Normal Dog Heart: The Role of Altered Autonomic Tone

The effects of isoproterenol, atropine, and metoprolol on atrioventricular (AV) and ventriculoatrial (VA) conduction were studied in 30 normal dogs under pentobarbital anesthesia using percutaneously introduced catheters. The inducibility of AV junctional reentry was also assessed before and after drug administration. Resting AV conduction was normal in all dogs, but VA conduction was present in only 57%. Isoproterenol facilitated both antegrade and retrograde conduction, with a preferential effect on retrograde conduction. VA conduction was demonstrated after isoproterenol in 91% of dogs. After testing all drugs, VA conduction was demonstrable in at least one study in 97% of dogs. Atropine had less effect than isoproterenol, suggesting that basal vagal tone was not high in this model. Dual AV nodal pathways were detectable in the antegrade direction in four (13%) dogs, and in the retrograde direction in an additional four (13%) dogs. Single AV junctional echoes were inducible with atrial stimulation in one dog with dual antegrade pathways, but were inducible with ventricular stimulation in at least one study in 83% of dogs with intact retrograde conduction. Sustained AV junctional reentry was never induced before or after drug administration. In conclusion, VA electrical continuity is almost always intact in the normal dog, but its demonstration is significantly modified by the autonomic nervous system. Isoproterenol has preferential effects on retrograde conduction and may have selective influence on distal AV nodal conduction. Twenty-six percent of normal dogs have evidence of dual AV nodal pathways. Single AV junctional echoes are inducible with ventricular stimulation in the majority of dogs and are a normal finding. Sustained AV junctional reentry is not inducible in the normal intact dog heart.

Differential vagal effects on antegrade vs. retrograde atrioventricular conduction.

The influence of postganglionic vagal stimulation (PGVS) on antegrade and retrograde atrioventricular nodal conduction was studied in 17 isolated rabbit heart tissue preparations by pacing at the crista terminalis or His bundle, respectively. The effect of short bursts of PGVS on prolongation of atrioventricular conduction was phase dependent with respect to the cardiac cycle. This phasic dependency was more pronounced during antegrade atrioventricular conduction. Although the control retrograde atrioventricular conduction time was longer than the antegrade (P less than 0.05) at or near the time in the cycle during which vagal stimulation caused maximal prolongation of conduction time (optimal phase), PGVS-induced maximal prolongation of the antegrade atrioventricular conduction time was significantly greater than that of the retrograde (P less than 0.02). Moreover, when PGVS was introduced at a fixed phase in the cycle, but with increasing amplitude, antegrade atrioventricular conduction time was progressively prolonged, and block was observed first in the antegrade direction, whereas retrograde atrioventricular conduction continued. Microelectrode recordings during these experiments showed consistently that PGVS-induced hyperpolarization in the N region of the atrioventricular node was greater during antegrade atrioventricular conduction. This suggests that vagal effects depended not only on the intensity and phase of stimulation, but also on electronic influences which apparently are different during antegrade and retrograde conduction.

Triple antegrade nodal pathway in a patient with supraventricular paroxysmal tachycardia

A 69-year-old patient is described in whom programmed atrial extrastimulus testing revealed dual discontinuity of atrioventricular nodal conduction suggesting a triple antegrade nodal pathway. In this patient, programmed right ventricular pacing initiated two types of tachycardia due to intranodal reciprocating rhythms. In both cases, antegrade conduction occurred via the slow nodal pathway, and retrograde conduction by the fast and intermediate pathways, respectively. During ventricular extrastimulus testing, a single echo beat was elicited via a third circuit: the intermediate nodal pathway in a retrograde direction, and the fast pathway in an antegrade direction.

Percutaneous transluminal laser angioplasty for treatment of peripheral vascular disease. Clinical experience with 16 patients.

Percutaneous transluminal laser angioplasty of the peripheral arteries was performed in 16 patients with pain at rest, objective evidence of severe peripheral ischemia, conditions requiring amputation, and/or medical contraindications to surgery. In 14 patients the ipsilateral femoral artery was entered in an antegrade direction using the Seldinger technique, base-line angiograms taken, and laser angioplasty performed using argon ions transported to the target site by a 400-mu quartz fiber. Patency was established in 50% of cases and correlated directly with both total energy delivered and time and power per exposure: the lower the energy, the higher the patency rate. Complications included spasm, pain, and mechanical or laser perforation. The authors conclude that while percutaneous transluminal laser angioplasty of peripheral arteries using argon radiation is possible in man, its clinical value has not been established.

Functional His-Purkinje system behavior during sudden ventricular rate acceleration in man.

During sudden rate acceleration the assessment of human His-Purkinje system (HPS) behavior in the antegrade direction is generally limited by the maximal attainable input frequency due to atrioventricular nodal (AVN) refractoriness. With incremental ventricular pacing, however, faster rates of input into the HPS are achievable. In seven patients with normal HPS function, the HPS response to an abrupt increase in ventricular rate was systematically evaluated with a pacing protocol in which rapid ventricular pacing at any constant cycle length (CL; range 280 to 400 msec) could be initiated at a programmed interval after the last beat of a paced ventricular or atrial basic drive. The following four patterns of HPS behavior accompanying sudden ventricular rate acceleration were observed: (I) 1:1 response without conduction delay, (II) 1:1 response with initial conduction delay but subsequent accommodation, (III) occurrence initially of 2:1 or 3:2 Wenckebach block followed by either subsequent accommodation or repetitive block, and (IV) sustained conduction delay with persistent appearance of the His deflection beyond the ventricular electrogram. The three latter patterns were found to be functional in nature, i.e., dependent on the CL just before rate acceleration, with improved conduction and ability to accommodate facilitated at shorter preceding CLs. Furthermore, with the availability of additional recordings from the right bundle branch, it could be postulated that pattern IV represented retrograde right bundle branch block that was sustained because of repetitive antegrade concealment by impulses conducted retrogradely via the left bundle branch (“linking” phenomenon). We conclude that functional delay and/or block in the HPS is relatively common during constant CL ventricular pacing at rapid rates (i.e., greater than 160/min) and recognition of this fact is important for accurate interpretation of electrophysiologic phenomena.

Mechanisms for the success and failure of pacing for termination of ventricular tachycardia: clinical and hypothetical considerations.

The effectiveness of pacing techniques for termination of ventricular tachycardia is well established, and of great value in the electrophysiologic laboratory, and, to a more limited degree, for chronic therapy using implanted anti-tachycardia devices. Although it appears that most clinical ventricular tachycardias are due to reentrant mechanisms, responses to antitachycardia pacing have often been difficult to understand. In this paper, clinical observations are correlated with hypothetical constructs and considerations, in an attempt to derive some general principles related to the success and failure of pacing for ventricular tachycardia. In these analyses, it appears that properties of conductivity and refractoriness in the myocardium are as important as the properties of the tachycardia circuit. Programmed extrastimuli or rapid pacing result in shortening of the effective refractory period of the myocardium, together with depressed conduction velocity of the stimulated wavefront. However, the changes in wavefront conductivity do not occur in step with changes in the effective refractory period; as a result, the stimulated wavefront arrives at the tachycardia circuit in a pattern which differs from the stimulation pattern. In general, it appears that termination of the tachycardia is favored when the stimulated wavefront arrives at the tachycardia circuit at a point when it cannot enter the circuit in an antegrade direction. These conditions are favored by a refractory period in the circuit which is moderately long compared to that of the myocardium. Constructions explaining the observation of a tachycardia termination zone are presented, together with explanations for failure to achieve termination, and for various patterns of acceleration.

Qualitative Evaluation of Antegrade Percutaneous Transluminal Angioplasty by Pressure Waveform Parameters

When percutaneous transluminal angioplasty (PTA) is performed in an antegrade ("downstream") direction, intraluminal gradient measurements across the stenotic segment are not possible. Pressures recorded proximal to the lesion were evaluated for possible hemodynamic clues of changes in flow in ten consecutive patients before and after PTA. In all patients in whom the procedure was successful, the systolic pressure decreased by an average of 35 mm Hg. This decrease was not evident in the failed procedures. It is concluded that proximally recorded pressure changes can be used as an objective criterion to assess the success of PTA performed in arteries.

Accessory atrioventricular pathways that conduct only in the antegrade direction.

Patients with accessory atrioventricular pathways that conduct only in the antegrade direction represent an unusual variant of the Wolff-Parkinson-White syndrome. This report describes such patients and compares them with patients with accessory pathways that demonstrate bidirectional conduction. Of 143 patients with single accessory pathways, seven demonstrated exclusive antegrade conduction (study group), 111 demonstrated bidirectional conduction (control group), and 25 demonstrated exclusive retrograde conduction. Study group patients were significantly older than patients in the control group (42 +/- 9.8 years and 31.4 +/- 13.9 years, respectively, p < 0.0001). Refractoriness and conduction characteristics of the accessory pathways in the antegrade direction in the study group were not different from those in the control group. Control group patients presented with atrioventricular reentrant tachycardia (58 of 111), atrial fibrillation (23 of 111), both of these arrhythmias (19 of 111), or no documented arrhythmia (11 of 111). Study group patients presented with only atrial fibrillation (six of seven). An accessory pathway with only antegrade conduction is a rare cause of symptoms in the Wolff-Parkinson-White syndrome. These patients are asymptomatic until atrial fibrillation develops as the patient ages. Despite the absence of retrograde conduction over the accessory pathway, its antegrade functional properties are similar to pathways that demonstrate bidirectional conduction.

Anatomic substrate of impaired antegrade conduction over an accessory atrioventricular pathway in the Wolff-Parkinson-White syndrome.

We present a patient with Wolff-Parkinson-White syndrome who died of a myocardial infarction 19 months after clinical electrophysiologic studies. These studies suggested the presence of a left atrioventricular accessory pathway that sustained conduction well in the retrograde direction but only intermittently in the antegrade direction. Postmortem examination of the heart revealed three accessory atrioventricular pathways in proximity to each other in the posterolateral atrioventricular region. One pathway showed complete fibrosis and two showed patchy fibrosis. The fibrosis suggests an anatomic basis for the impaired antegrade conduction observed in life.

Aprindine for treatment of supraventricular tachycardias: With particular application to Wolff-Parkinson-White syndrome

Ten patients with recurrent or continuous Supraventricular tachycardia difficult to control with conventional antiarrhythmic agents were treated with aprindine, a new antiarrhythmic drug. Nine patients had Wolff-Parkinson-White syndrome. An electrophysiologic study was performed before and during oral administration of aprindine. At the time of the first study, circus movement Supraventricular tachycardia was initiated in Patients 1 to 8. During administration of aprindine, circus movement Supraventricular tachycardia could no longer be initiated in Patients 1 to 4 but was initiated with difficulty in Patients 5 and 6 and with greater ease in Patients 7 and 8. In Patient 9, aprindine therapy slowed the ventricular response during atrial flutter from 1:1 conduction over the accessory pathway to 2:1 conduction over the normal pathway; in Patient 10, it slowed the ventricular rate during atrial fibrillation from 140–180 to 80–100 beats/min. Patients 1 to 6, 9 and 10 had an excellent clinical response, but treatment with aprindine was discontinued in Patients 7 and 8. Electrophysiologic evaluation revealed that aprindine produced complete block or increased refractoriness of the accessory pathway in an antegrade direction in all patients and in a retrograde direction in all but two (Patients 7 and 8) tested. Aprindine also slowed conduction in the accessory pathway and, when Supraventricular tachycardia could still be initiated, it occurred at a slower rate. Neurologic side effects occurred primarily during the initial administration and dose adjustment of aprindine.