Efficacy and safety of out-of-hospital self-administered single-dose oral drug treatment in the management of infrequent, well-tolerated paroxysmal supraventricular tachycardia.

OBJECTIVES: We tested the efficacy of two drug treatments, flecainide (F) and the combination ofdiltiazem and propranolol (D/P), administered as a single oral dose for termination of the arrhythmic episodes. BACKGROUND: Both prophylactic drug therapy and catheter ablation are questionable as first-line treatments in patients with infrequent and well-tolerated episodes of paroxysmal supraventricular tachycardia (SVT). METHODS: Among 42 eligible patients (13% of all screened for SVT) with infrequent (< or =5/year), well-tolerated and long-lasting episodes, 37 were enrolled and 33 had SVT inducible during electrophysiological study. In the latter, three treatments (placebo, F, and D/P) were administered in a random order 5 min after SVT induction on three different days. RESULTS: Conversion to sinus rhythm occurred within 2 h in 52%, 61%, and 94% of patients on placebo, F and D/P, respectively (p < 0.001). The conversion time was shorter after D/P (32 +/- 22 min) than after placebo (77 +/- 42 min, p < 0.001) or F (74 +/- 37 min, p < 0.001). Four patients (1 placebo, 1 D/P, and 2 F) had hypotension and four (3 D/P and 1 F) a sinus rate <50 beats/min following SVT interruption. Patients were discharged on a single oral dose of the most effective drug treatment (F or D/P) at time of acute testing. Twenty-six patients were discharged on D/P and five on F. During 17 +/- 12 months follow-up, the treatment was successful in 81% of D/P patients and in 80% of F patients, as all the arrhythmic episodes were interrupted out-of-hospital within 2 h. In the remaining patients, a failure occurred during one or more episodes because of drug ineffectiveness or drug unavailability. One patient had syncope after D/P ingestion. During follow-up, the percentage of patients calling for emergency room assistance was significantly reduced as compared to the year before enrollment (9% vs. 100%, p < 0.0001). CONCLUSIONS: The episodic treatment with oral D/P and F, as assessed during acute testing, appears effective in the management of selected patients with SVT. This therapeutic strategy minimizes the need for emergency room admissions during tachycardia recurrences.

Significance of newly acquired negative T waves after interruption of paroxysmal reentrant supraventricular tachycardia with narrow QRS complex.

Sixty-three patients with paroxysmal supraventricular tachycardia were studied and 25 patients (39%) showed newly acquired negative T waves after tachycardia termination. Silent coronary artery disease could not be found in about 90% of these patients; moreover, age, sex, organic heart disease, and tachycardia duration and rate did not predict the appearance of negative T waves.

Atrioventricular nodal versus atrioventricular supraventricular reentrant tachycardias: characterization by an integrated Doppler electrophysiological hemodynamic study.

During reentrant supraventricular tachycardias involving the atrioventricular node (AVN-SVT) or an AV bypass tract (AV-SVT), atrial pressure increases. While in AVN-SVT this increase relates to atrial contraction during ventricular systole, the mechanism remains unclear in AV-SVT. This study sought to clarify this mechanism. During 11 AVN-SVTs and 9 AV-SVTs, anterograde flow through the AV valves and retrograde flow in the pulmonary and hepatic veins were studied by pulsed-wave (PW) Doppler measuring the time interval between the ECG-R wave and (1) the end of venous retrograde flows, and (2) the beginning of valvular anterograde flows. The positive or negative difference between these two time intervals guided recognizing the atrial contraction against open or closed AV valves. Intracavitary pressures and cardiac index were also measured. During AVN-SVTs, venous retrograde flows always ended before the anterograde valvular flows, indicating atrial contraction against closed AV valves. During AV-SVTs, pulmonary retrograde flow ended before the beginning of mitral anterograde flow in five cases, began before but ended during the anterograde flow in three cases, and overlapped to the anterograde flow in one case. A corresponding behavior was observed at the right side of the heart. In both SVTs, atrial pressures increased and end-diastolic ventricular pressure and cardiac index decreased similarly. During AVN-SVT, the atrial contraction always occurs against closed AV valves, and during AV-SVT it generally occurs against totally or partially closed AV valves, explaining similar atrial pressure and cardiac index changes in both SVTs.

Atrial and ventricular pressures in atrial flutter.

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 +/- 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Both the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 +/- 15 beats/min) or in those with variable conduction (heart rate 96 +/- 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.

Modification of antegrade slow pathway is not crucial for successful catheter ablation of common atrioventricular nodal reentrant tachycardia.

We tested the hypothesis that in some patients affected by typical AVNRT, successful catheter ablation treatment may be achieved independently of specific measurable electrophysiological modifications of antegrade AV node conducting properties. Standard electrophysiological parameters and comparable antegrade AV node function curves were obtained, before and after successful ablation, in 104 patients (mean age 52 +/- 16 years; 69 women and 35 men) affected by the common form of AVNRT. The end point of the ablation procedure was noninducibility of AVNRT and of no more than one echo beat. For the purpose of this study, AV node duality was defined as an increase of > or = 50 ms in the A2H2 interval in response to a 10 ms decrease of the A1A2 coupling interval. Before ablation, AV node duality was present in 65 patients (62%) and absent in 39 patients (37%). Ablation caused measurable modifications of electrophysiological properties of the AV node in most patients with elicited AV node duality, but not in most patients without demonstrable AV node duality. After ablation, AV node duality persisted in 20 patients who had it before, whereas a new duality that could not be elicited before appeared in 5 patients. During 19 +/- 6 months of follow-up, clinical AVNRT recurred in 1 of 45 patients who had disappearance of AV node duality after ablation, in 1 of 34 patients who did not show AV node duality before and after ablation, and in 1 of 20 patients who had persistence of AV node duality after ablation. In conclusion, modifications of antegrade conduction properties of the AV node are not crucial for the cure of AVNRT in many patients.

Prospective, randomized study of atrioventricular ablation and mode-switching, dual chamber pacemaker implantation versus medical therapy in drug-resistant paroxysmal atrial fibrillation. The PAF study. Paroxysmal Atrial Fibrillation.

We performed a prospective randomized 6-month evaluation of the clinical effects of atrioventricular junctional ablation together with placement of a DDDR mode-switching pacemaker vs pharmacological treatment in 43 patients with intolerable paroxysmal atrial fibrillation not controlled with antiarrhythmic drugs. Ablation and pacemaker treatment were highly effective and superior to drug therapy in controlling symptoms and improving quality of life. However, discontinuation of drug therapy exposed patients to further recurrences of paroxysmal atrial fibrillation and the risk of developing permanent atrial fibrillation.

The natural course of untreated sick sinus syndrome and identification of the variables predictive of unfavorable outcome.

We performed a prospective study in 35 untreated patients aged > or = 45 years, who had a mean sinus rate at rest of < or = 50 beats/min and/or intermittent sinoatrial block, and symptoms attributable to sinus node dysfunction. The patients were followed up for up to 4 years (mean 17 +/- 15 months). During follow-up, 20 patients (57%) had cardiovascular events that required treatment: 8 had syncope (23%); 6 had overt heart failure (17%); 4 patients had chronic atrial fibrillation (11%); and 2 patients had poorly tolerated episodes of paroxysmal tachyarrhythmias (6%). Actuarial rates of occurrence of all events were 35%, 49%, and 63%, respectively, after 1, 2, and 4 years. At univariate analysis, age > or = 65 years, end-systolic left ventricular diameter > or = 30 mm, end-diastolic left ventricular diameter > or = 52 mm, and ejection fraction < 55% were predictors of cardiovascular events. At multivariate analysis, age, end-diastolic diameter, and ejection fraction remained independent predictors of events. Actuarial rates of occurrence of syncope were 16%, 31%, and 31%, respectively, after 1, 2, and 4 years. Both univariate and multivariate predictors of syncope were history of syncope and corrected sinus node recovery > or = 800 ms. A favorable outcome was observed in the remaining 43% of patients. Thus, clinical cardiovascular events occur in most untreated sick sinus syndrome patients during long-term follow-up, even though a favorable course can be expected in 43% of patients. The outcome can be partly predicted on initial evaluation. In the patients with a favorable outcome, treatment can safely be delayed.

Short-term hemodynamic effects of DDD pacing from ventricular apex, right ventricular outflow tract and proximal septum.

Recently, short-term hemodynamic benefits of right ventricular outflow tract (RVOT) or proximal septum (His bundle area) pacing have been reported in comparison with traditional apical stimulation in preliminary investigations. The purpose of the present study was to compare the hemodynamics obtained during DDD pacing from ventricular apex, RVOT and proximal septum in patients with normal left ventricular function. A simultaneous hemodynamic and Doppler-echocardiographic study was performed in 21 patients (age 67 +/- 7 years) with sick-sinus syndrome (8 pts) or 2nd-3rd degree atrioventricular (AV) block (13 pts). The three stimulation sites were randomized and pacing was applied at an identical rate (84 +/- 5 beats/min) and at a constant AV delay (150 ms). Electrocardiographic, hemodynamic and Doppler-echocardiographic investigations were performed during stimulation from each site. The QRS duration did not show significant differences during DDD pacing from ventricular apex, RVOT and proximal septum. The hemodynamic measurements (systemic pressures, mean pulmonary wedge pressure, pulmonary pressures, right ventricular end-diastolic pressure, mean right atrial pressure, cardiac index, systemic vascular resistance and arteriovenous O2 difference) did not show significant differences during pacing from the three sites. Moreover, no significant differences were observed for the Doppler-echocardiographic measurements of systolic function (aortic stroke distance, left ventricular ejection fraction) and diastolic function (isovolumetric relaxion time, mitral E/A ratio, deceleration rate of the E wave). The results suggest that in patients with normal left ventricular function DDD pacing from RVOT or proximal septum does not improve cardiac function with regard to apical pacing.

Assessment of atrioventricular junction ablation and DDDR mode-switching pacemaker versus pharmacological treatment in patients with severely symptomatic paroxysmal atrial fibrillation: a randomized controlled study.

BACKGROUND: The purpose of the study was to evaluate the effect of AV junction ablation and pacemaker implantation on quality of life and specific symptoms in patients with paroxysmal atrial fibrillation (AF) not controlled by drugs. METHODS AND RESULTS: We performed a multicenter, randomized, 6-month evaluation of the clinical effects of AV junction ablation and DDDR mode-switching pacemaker (Abl+Pm) versus pharmacological treatment in 43 patients with intolerable, recurrent paroxysmal AF of three or more episodes in the previous 6 months not controlled with three or more antiarrhythmic drugs. Before completion of the study, 3 patients in the drug group withdrew because of the severity of their symptoms and 1 patient assigned to the Abl+Pm group in whom the ablation procedure failed. At the end of the 6 months, the 21 patients of the Abl+Pm group who completed the study showed, in comparison with the 18 of the drug group, lower scores in the Living with Heart Failure Questionnaire (-51%, P=.0006), palpitations (-71%, P=.0000), effort dyspnea (-36%, P=.04), exercise intolerance score (-46%, P=.001), and easy fatigue (-51%, P=.02). The scores for rest dyspnea, chest discomfort, and NYHA functional classification were also lower (-56%, -50%, and -17%, respectively) in the Abl+Pm group, although not significantly. At the end of the study, palpitations were no longer present in 81% of the Abl+Pm group and in 11% of the drug group (P=.0000). AF was documented in 31 of 122 visits (25%) in the Abl+Pm group and in 9 of 107 examinations (8%) in the drug group (P=.0005); chronic AF developed in 5 (24%) and 0 (0%) in the two groups, respectively (P=.04). CONCLUSIONS: In patients with paroxysmal AF not controlled by pharmacological therapy, Abl+Pm treatment is highly effective and superior to drug therapy in controlling symptoms and improving quality of life. The discontinuation of drug therapy exposes patients to further recurrences of paroxysmal AF and the risk of developing permanent AF.

Effects of permanent pacemaker and oral theophylline in sick sinus syndrome the THEOPACE study: a randomized controlled trial.

BACKGROUND: Pacemakers and theophylline are currently being used to relieve symptoms in patients with sick sinus syndrome (SSS). However, the impact of either therapy on the natural course of the disease is unknown. We conducted a randomized controlled trial to prospectively assess the effects of pacemakers and theophylline in patients with SSS. METHODS AND RESULTS: One hundred seven patients with symptomatic SSS (age, 73 +/- 11 years) were randomized to no treatment (control group, n = 35), oral theophylline (n = 36), or dual-chamber rate-responsive pacemaker therapy (n = 36). They were followed for up to 48 months (mean, 19 +/- 14 months). During follow-up, the occurrence of syncope was lower in the pacemaker group than in the control group (P = .02) and tended to be lower than in the theophylline group (P = .07). Heart failure occurred less often in patients assigned to pacemaker therapy and theophylline than in control patients (both, P = .05), whereas the incidence of sustained paroxysmal tachyarrhythmias, permanent atrial fibrillation, and thromboembolic events did not show any apparent difference among the three groups. Heart rate was higher in the theophylline group than in the control group. Both pacemaker therapy and theophylline improved symptom scores after 3 months of treatment; however, a similar improvement was observed in the control group. CONCLUSIONS: In patients with symptomatic SSS, therapy with theophylline or dual-chamber pacemaker is associated with a lower incidence of heart failure; pacemaker therapy is also associated with a lower incidence of syncope. The therapeutic benefits of pacemakers and theophylline on symptoms are partly a result of spontaneous improvement of the disease.

Multiple mechanisms of successful slow-pathway catheter ablation of common atrioventricular nodal re-entrant tachycardia.

BACKGROUND: In patients with atrioventricular nodal re-entrant tachycardia, modifications of the antegrade atrioventricular nodal function curve caused by catheter ablation of the so-called slow pathway are heterogeneous, but have not yet been systematically evaluated. AIM: To test the hypothesis that successful treatment is independent of specific electrophysiological modifications of atrioventricular nodal conducting properties. METHOD: Standard electrophysiological parameters and comparable antegrade atrioventricular nodal function curves were obtained, before and after successful ablation, in 104 patients (mean age 52 +/- 16 years: 69 women) affected by the common form of atrioventricular nodal re-entrant tachycardia. RESULTS: Three different major patterns of antegrade atrioventricular nodal function curve were caused by ablation: downward shift of the curve with disappearance of atrioventricular nodal duality, suggesting the elimination of the slow pathway in 54 (52%) patients (type 1): absence of clear modifications of the curve (and of slow pathway ablation) in 33 (32%) patients (type 2); upward shift of the curve, suggesting a further slowing of conduction velocity through the slow pathway in 17 (16%) patients (type 3). Type-1 pattern was more frequent in patients < or = 45 years, whereas type-2 pattern was more frequent in those > 45 years. CONCLUSION: Successful ablation of atrioventricular nodal re-entrant tachycardia is independent of specific modifications of antegrade atrioventricular conduction and probably depends on critical nodal and perinodal tissue damage at different sites on the re-entrant circuit. The effects of ablation are influenced by patient age.

Clinical usefulness of slow pathway ablation in patients with both paroxysmal atrioventricular nodal reentrant tachycardia and atrial fibrillation.

Some patients with atrioventricular (AV) node reentrant tachycardia (AVN RT) also presented with atrial fibrillation (AF). In this study we demonstrate that slow pathway ablation is able to suppress both AVN RT and AF in subjects without structural heart abnormalities, whereas in patients with structural heart abnormalities after ablation AF frequently recurs.

Effects of intravenous propranolol on cardiovascular hemodynamics during supraventricular tachycardia.

Hemodynamic variables were evaluated in 10 patients during supraventricular tachycardia before and after administration of intravenous propranolol. The drug markedly worsened the already compromised hemodynamic pattern of supraventricular tachycardia.

Hemodynamics of idiopathic paroxysmal atrial fibrillation.

The hemodynamics of induced atrial fibrillation (AF) was investigated in 15 patients (ages 58 +/- 11 years) with paroxysmal AF presenting without organic heart disease or hypertension. A hemodynamic study was performed both during sinus rhythm and after the induction of AF. The mean heart rate increased from 73 +/- 11 to 128 +/- 18 beats/min (P < 0.001) after AF. Systolic and mean aortic pressures did not significantly change, and diastolic aortic pressure increased (78 +/- 11 vs 89 +/- 12 mmHg, P < 0.01). Left ventricular end-diastolic pressure decreased during AF (9 +/- 3 vs 6 +/- 2.6 mmHg, P < 0.005), whereas mean pulmonary wedge pressure increased (8 +/- 2 vs 12 +/- 4 mmHg, P < 0.001). Systolic pulmonary arterial pressure did not show significant variations, and there was a slight but statistically significant increase in the diastolic and mean pulmonary arterial pressures (P < 0.01). The right ventricular end-diastolic pressure decreased during AF (5.6 +/- 2 vs 3.8 +/- 2 mmHg, P < 0.01), whereas mean right atrial pressure showed a trend toward an increase. Stroke volume markedly decreased (P < 0.001) while the cardiac index did not significantly change. Systemic vascular resistance, pulmonary arteriolar resistance, and the arteriovenous O2 difference showed no significant variations after the induction of AF. These results suggest that in subjects without organic heart disease, paroxysmal AF is well tolerated hemodynamically, and the rise in the atrial pressures during AF is not related to an increase in the ventricular end-diastolic pressure.

The effect of exogenous adenosine in patients with neurally-mediated syncope and sick sinus syndrome.

The effects of a 20-mg i.v., bolus of adenosine 5' triphosphate (ATP) on the heart rhythm was studied in 79 patients affected by neurally-mediated syncope (26 cases) or sick sinus syndrome (22 cases) or both syndromes (31 cases) and in 31 healthy control subjects in order to examine the sensitivity of cardiac purinoceptors in such circumstances. During ATP infusion, the sinus cycle lengthened to > 2 seconds in no control, in 1 (4%) patient with neurally-mediated syncope, in 5 (23%) patients with sick sinus syndrome, and in 13 (42%) patients with both neurally-mediated and sick sinus syndromes (P = 0.01). Atrioventricular block occurred in 14 (45%) of controls, in 10 (38%) patients with neurally-mediated syncope, in 4 (18%) patients with sick sinus syndrome, and in 13 (42%) patients with both neurally-mediated syncope and sick sinus syndrome (n.s.). Thus, exogenous ATP exerts different effects on patients with neurally-mediated syncope and patients with sick sinus syndrome. In fact, intrisic disease of the sinus node is necessary to modulate an abnormal adenosine-mediated sinus arrest, whereas patients affected by neurally-mediated syncope alone show a normal sensitivity to the drug administration. The effect of ATP on atrioventricular conduction is greater than that on sinus node and is of similar magnitude in patients and controls; thus the clinical meaning of ATP induced atrioventricular block remains uncertain.

Hemodynamic effects of oral sotalol during both sinus rhythm and atrial fibrillation.

OBJECTIVES: This study investigated the hemodynamic effects of oral sotalol during both sinus rhythm and paroxysmal atrial fibrillation. BACKGROUND: The hemodynamic effects of most antiarrhythmic drugs have been characterized in subjects during sinus rhythm. However, there are no data concerning these effects on the paroxysmal tachyarrhythmias. METHODS: In 17 patients with paroxysmal atrial fibrillation and without heart failure (aged 62 +/- 11 years, ejection fraction 51 +/- 4%), an electrophysiologic-hemodynamic study was performed twice. In the first study, hemodynamic variables were evaluated both during sinus rhythm and after the induction of atrial fibrillation. Sotalol (160 or 240 mg/day) was administered for 6 to 7 days and the study was then repeated with the same methods. RESULTS: The drug significantly diminished heart rate during both sinus rhythm and atrial fibrillation. During sinus rhythm, sotalol did not change systemic pressures and significantly increased left and right ventricular end-diastolic, left and right atrial and pulmonary pressures. Cardiac index decreased, whereas stroke volume was unchanged after the drug. Ejection fraction and left ventricular end-diastolic and end-systolic volumes evaluated by echocardiography were unchanged after sotalol. During atrial fibrillation, the drug had less evident effects on cardiac function. Left ventricular end-diastolic, left atrial and pulmonary pressures did not increase significantly. CONCLUSIONS: The hemodynamic changes induced by oral sotalol appear to be mainly related to an involvement of ventricular distensibility; this effect is less evident during atrial fibrillation than during sinus rhythm. In patients with paroxysmal atrial fibrillation without heart failure treated with oral sotalol, a recurrence of the tachyarrhythmia is hemodynamically well tolerated.

Long-term effects of theophylline in atrial fibrillation with a slow ventricular response.

In 17 patients (aged 78 +/- 9 years) with symptomatic atrial fibrillation and a slow ventricular response not related to drugs, a resting electrocardiogram and 24-hour Holter recording were obtained before and 5 to 6 days after administration of slow-release theophylline (700 mg/day), and successively every 3 months during the long-term phase. Fourteen patients had organic heart disease, and 13 complained of syncope or presyncope, and 4 of asthenia and easy fatigability. At the steady-state evaluation, theophylline significantly increased resting heart rate (HR) by 42%, mean 24-hour HR by 31% and minimal 24-hour HR by 34%. Cardiac pauses > 2,500 ms disappeared or markedly decreased. The daily number of wide QRS complexes increased. Serum theophylline level was 13 +/- 5 ng/ml. During the follow-up period (20 +/- 18 months), the mean daily theophylline dosage was 450 mg and the mean serum theophylline level 9 ng/ml. Seven patients died: 1 because of heart failure, and 6 because of noncardiac death. One patient complained of a syncopal episode during 1 visit. The drug markedly reduced asthenia and easy fatigability. During the long-term phase, HR increased spontaneously in 3 patients, and the treatment was interrupted. In 2 patients, theophylline had to be discontinued because of gastric intolerance. During long-term therapy, HR was similar to that observed at the steady-state evaluation, despite the reduction in daily dosage. The data suggest that theophylline is an effective therapy in most patients with symptomatic atrial fibrillation and a slow ventricular response.

An abnormal neural reflex plays a role in causing syncope in sinus bradycardia.

OBJECTIVES: This study investigates the role of an abnormal neural reflex in causing syncope in patients with sinus bradycardia. BACKGROUND: Syncope is commonly considered an indication of severity in sinus bradycardia. However, the occurrence of syncope is unpredictable, and the prognosis appears to be similar in patients with and without syncope. METHODS: Head-up tilt testing (60 degrees for 60 min), carotid sinus massage in the supine and standing positions, 24-h Holter ambulatory electrocardiographic (ECG) recording and electrophysiologic study before and after pharmacologic autonomic blockade were performed in 25 patients with sinus bradycardia and syncope (group I, sinus rate < 50 beats/min, age 71 +/- 12 years) and 25 patients with sinus bradycardia and no neurologic symptoms (group II, sinus rate < 50 beats/min, age 67 +/- 16 years). RESULTS: Clinical characteristics and ambulatory ECG monitoring data were similar in the two study groups. A positive response (induction of syncope or presyncope with hypotension and/or bradycardia) was obtained by head-up tilt testing in 15 group I (60%) and in 3 group II (12%) patients (p < 0.001) and by carotid sinus massage in 11 group I (44%) and 6 group II (24%) patients (p = NS). Results of at least one test (head-up tilt testing or carotid sinus massage, or both) were positive in 19 group I (76%) and 9 group II (36%) patients (p < 0.01). Basal and intrinsic corrected sinus node recovery time did not differ significantly between the two groups. An abnormal intrinsic heart rate was present in 66% of group I and 26% of group II patients (p < 0.01). The different percentage of positive findings on head-up tilt testing and carotid sinus massage in the two groups was independent of the presence of intrinsic sinus node dysfunction. CONCLUSIONS: These results indicate that an abnormal neural reflex plays a role in causing syncope in patients with sinus bradycardia. This reflex seems to be unrelated to the severity of sinus node dysfunction, even if the latter could enhance the cardioinhibitory response.

[Effects of vagal tone on Kent bundle conduction in patients with Wolff-Parkinson-White syndrome]. / Effetti del tono vagale sulla conduzione nel fascio di Kent in soggetti con sindrome di Wolff-Parkinson-White.

BACKGROUND: The influences of the sympathetic tone on the conduction in the Kent bundle have been widely investigated; on the contrary, very little is known about the effects of the vagal tone on such a bypass. Vagal influences on Kent bundle can be adequately investigated only after sympathetic blockade. METHODS: An electrophysiological study was performed in 12 subjects with Wolff-Parkinson-White syndrome (7 F and 5 M, age: 30 +/- 17 years) during basal state, after beta-blockade (propranolol 0.2 mg/Kg iv) and after atropine (0.04 mg/Kg iv). RESULTS: In no subject were signs of organic heart disease present. The anterograde effective refractory period of the bypass significantly lengthened after propranolol (291 +/- 65 ms vs 313 +/- 52 ms, p < .01), and shortened after atropine (313 +/- 52 ms vs 290 +/- 46 ms, p < .01). This parameter showed no significant differences in the basal state nor after complete autonomic blockade. The longest pacing atrial cycle length for a second degree atrio-ventricular block in the bypass significantly lengthened after propranolol (322 +/- 55 ms vs 383 +/- 44 ms, p < .01) and shortened after atropine, even if the variation was not statistically significant (383 +/- 44 ms vs 368 +/- 39 ms, p: NS); such a parameter was significantly more prolonged after complete autonomic blockade than in the basal state (p < .05). The retrograde conduction in the bypass showed a similar behaviour: the retrograde effective refractory period and the longest ventricular pacing cycle length for a second degree ventriculo-atrial block significantly lengthened after propranolol (434 +/- 133 ms vs 532 +/- 188 ms, p < .01 and 398 +/- 150 ms vs 492 +/- 179 ms, p < .01, respectively) and shortened after atropine (532 +/- 188 ms vs 464 +/- 157 ms, p < .01, and 492 +/- 179 ms vs 431 +/- 158 ms, p < .05, respectively). These parameters were more prolonged after complete autonomic blockade than in the basal state (p < .05). CONCLUSIONS: These data evidence a vagal influence on the conduction in the resting Kent bundle; the vagal effect appears, however, less marked than the sympathetic one.