Long term follow up of radiofrequency catheter ablation of atrial flutter: clinical course and predictors of atrial fibrillation occurrence.

OBJECTIVES: To evaluate the time to onset and the predictors of atrial fibrillation (AF) during long term follow up of patients with typical atrial flutter (AFL) treated with transisthmic ablation. DESIGN: Prospective multicentre study. METHODS AND RESULTS: 383 patients (75.4% men, mean (SD) age 61.7 (11.1) years) who underwent transisthmic ablation for typical AFL were investigated. In 239 patients (62.4%) AF was present before ablation. Ablation proved successful in 367 patients (95.8%). During a mean (SD) follow up of 20.5 (12.4) months, 41.5% of patients reported AF. The cumulative probability of postablation AF increased continuously as time passed: it was 22% at six months, 36% at one year, 50% at two years, 58% at three years, and 63% at four years. CONCLUSIONS: AF occurred in a large proportion of patients after transisthmic catheter ablation of typical AFL. The occurrence of AF was progressive during follow up. Preablation AF, age < 65 years, and left atrial size > 50 mm are associated with postablation AF occurrence.

Low-energy internal cardioversion in patients with long-lasting atrial fibrillation refractory to external electrical cardioversion: results and long-term follow-up.

AIM: Low-energy internal cardioversion is a new electrical treatment for patients with persistent atrial fibrillation. This paper evaluates the efficacy and safety of low-energy internal cardioversion in patients with long-lasting atrial fibrillation refractory to external electrical cardioversion, and the clinical outcome of such patients. METHOD AND RESULTS: The study population consisted of 55 patients [32 male, mean age 65 +/- 10 years, 48 (87%) with underlying heart disease] with long-lasting (mean 18 +/- 34 months) atrial fibrillation in whom external cardioversion had failed to restore sinus rhythm. Two custom-made catheters were used: one positioned in the right atrium and one in the coronary sinus or the left pulmonary artery. A standard catheter was inserted into the right ventricular apex to provide R wave synchronization. Sinus rhythm was restored in 52 patients (95%) with a mean defibrillating energy of 6.9 +/- 2.6 J (320 +/- 60 V). No complications were observed. During follow-up (mean 18 +/- 9 months), 16 patients (31%) suffered early recurrence (< or = 1 week) of atrial fibrillation and 20 patients (38%) had late recurrence (> 1 week, mean 3.5 +/- 3.6 months) of atrial fibrillation. Six patients with a late recurrence again underwent cardioversion and five of these maintained sinus rhythm. Therefore, a total of 21/52 patients (40%) were in sinus rhythm at the end of follow-up. No clinical difference was found between patients with and without recurrences. CONCLUSIONS: Low-energy internal cardioversion is a useful means of restoring sinus rhythm in patients with long-lasting atrial fibrillation refractory to external electrical cardioversion. More than one-third of patients maintained sinus rhythm during long-term follow-up.

Pacemapping of the triangle of Koch: a simple method to reduce the risk of atrioventricular block during radiofrequency ablation of atrioventricular node reentrant tachycardia.

Slow pathway ablation in common AVNRT can be complicated by total AV block. When radiofrequency energy is delivered to the posterior aspect of the triangle of Koch, total AV block may be the consequence of the absence of anterograde conduction along the fast pathway or of inadvertent damage to a fast pathway abnormally located close to the slow pathway. To localize the anterogradely conducting fast pathway, the triangle of Koch was pacemapped in 72 patients who underwent the ablation of common AVNRT. In all cases, before ablation the St-H interval was calculated by stimulating the anteroseptal (AS), mid-septal (MS), and posteroseptal (PS) aspect of the triangle of Koch at a rate slightly faster than the sinus rate. In all patients, common AVNRT was induced. In 64 (89%) of 72 patients (group A) the shortest St-H interval was recorded on stimulating the AS region. In six (8%) patients (group B) the shortest St-H interval was recorded on stimulating the MS region. Finally, in two (3%) patients (group C) the shortest St-H interval was recorded stimulating in the PS region. In group C, AH interval, calculated on stimulating in the AS region, was significantly longer than in patients of groups A and B (200 +/- 99 ms vs 64 +/- 18 and 62 +/- 3, respectively). In group A, on stimulating in the AS, MS, and PS regions, the AH interval remained constant in all patients. In contrast, in groups B and C on stimulation in the MS and PS regions, AH interval shortened (in group B from 56 +/- 8 to 27 +/- 37 and 37 +/- 14, respectively; in group C from 200 +/- 99 to 170 +/- 100 and to 137 +/- 109, respectively). In groups A and B, a posteroseptal slow pathway, and in group C, an anteroseptal retrograde fast pathway were successfully ablated without AV block. Pacemapping of the triangle of Koch can help to recognize patients in whom the anterograde conducting fast pathway is abnormally located far from the anteroseptal region or in whom anterograde conduction of the fast pathway is absent. In these cases the risk of AV block can be reduced by performing slow pathway ablation in a site sufficiently far from the site of the anterograde fast pathway or ablating the retrogradely conducting fast pathway.

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.

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.

Successful catheter ablation by radiofrequency energy of posteroseptal accessory pathway in a patient with drug refractory Wolff-Parkinson-White syndrome.

A 45-year-old patient with the Wolff-Parkinson-White syndrome suffering from recurrent intractable reciprocating atrioventricular tachycardia (RAVT) is reported. He used amiodarone, sotalol, quinidine, propafenone and flecainide unsuccessfully. An electrophysiological study (EPS) performed with four catheters localized the site of the anomalous pathway in the ostium of the coronary sinus. In this region we could also record a Kent potential. In the ostium of the coronary sinus, radiofrequency energy was repeatedly applied until the conduction over the accessory pathway was abolished both in the anterograde and the retrograde direction. The Kent deflection detectable before ablation, could not be detected after it. During follow-up (1 month) the patient remained asymptomatic and the control EPS showed no evidence of pre-excitation, either anterogradely or retrogradely.

[The endocavitary and transesophageal electrophysiological findings in idiopathic atrial fibrillation]. / Rilievi elettrofisiologici endocavitari e transesofagei nella fibrillazione atriale idiopatica.

BACKGROUND: We studied 105 patients (pts) in order to help clarify the pathogenetic mechanisms of idiopathic atrial fibrillation (AF). Eighty of these pts (Group I) had experienced paroxysmal AF, and 25 were normal control subjects (Group II). Twenty-two pts out of Group I had idiopathic paroxysmal AF (Group IA), while the remaining 58 (Group IB) presented with a heart disease or a WPW pattern. METHODS: All pts underwent endocavitary (EEPS) (69) or transesophageal (TEPS) (36) electrophysiologic study. In all pts the inducibility of a sustained AF (greater than 1 min) was tested by aggressive stimulation protocols including high frequency atrial bursts. RESULTS: In Group I a sustained AF was induced in 82% of cases vs 4% of Group II cases (p less than 0.001). In Group I there was no difference between pts with or without idiopathic AF (IA 73% vs IB 86%, NS). In two pts with idiopathic AF a concealed Kent bundle was identified and a reciprocating atrioventricular tachycardia was induced, which in one case spontaneously degenerated into AF. Four athletes with idiopathic AF were studied before and after autonomic blockade. AF was induced in all during the basal state, lasting several hours, and after autonomic blockade in 3 pts, lasting again for several hours. In 1 patient (pt) the arrhythmia spontaneously resolved within 50 sec. CONCLUSIONS: 1) The induction of a sustained AF by EEPS or TEPS is a pathologic phenomenon which is frequently observed in pts with clinical episodes of paroxysmal AF, while it is very rare in normal control subjects. 2) Pts with idiopathic AF have an electrophysiologic behaviour similar to pts with non-idiopathic AF. This fact suggests that among the former, most cases probably have a concealed atrial anomaly. In some cases this atrial anomaly can be related to the existence of a Kent bundle. 3) In athletes with paroxysmal AF the inducibility of a sustained AF both in the basal state and after autonomic blockade suggests that the vagal prevalence typical of such subjects probably plays a secondary role.

[Supraventricular paroxysmal reentry tachycardia. Empirical and guided therapy]. / Tachicardie parossistiche sopraventricolari da rientro. Terapia empirica e mirata.

The empirical therapy of reentrant supraventricular tachycardias (A-V and junctional tachycardia) is based on a preliminary diagnosis through standard ECG to evaluate, whenever possible, the relationship between P wave and QRS. In order to distinguish atrial tachycardias from other types, we must employ vagal manoeuvres or drugs. Often we use methods of recording and stimulation such as Holter monitoring and transesophageal technique which can provide useful information about the electrophysiological mechanisms and therefore can better guide our choice of drugs. The decision of undertaking pharmacologic treatment takes into account frequency, duration and tolerability of the crises and the patient's compliance. The most commonly used drugs are verapamil, diltiazem, propafenone, flecainide, sotalol and amiodarone. The percentage of success at 1 year ranges from 30 to 60%. Particularly in the Wolff-Parkinson-White (WPW) therapy must follow an accurate evaluation of the electrophysiological pattern through effort test, drugs test, transesophageal (ETS) or endocavitary (EPS) electrophysiological study. Indeed therapy aims not only at reducing arrhythmic relapses, but also preventing the potential risk of either death or severe damage. The useful drugs must have the property of acting at the same time upon at least one branch of the A-V circuit, on the atrium reducing its vulnerability and finally modifying the conductive anterograde capacity of the Kent bundle. They are quinidine, procainamide, propafenone (group I) sotalol and amiodarone (group III). The limitations of the empirical therapy are a high percentage of relapses and the difficulty in foreseeing the pro-arrhythmic effects. The guided by serial electrophysiologic testing implies artificial induction of spontaneous arrhythmia by repeating the test after acute or chronic assumption of drugs. Is this way it can be evaluated the efficacy as well as the tolerability of an antiarrhythmic drug which later will be taken for chronic prophylaxis. The percentage of inducibility of clinical arrhythmias is next to 100% both for EPS and TES. The number of patients for whom we can find an effective pharmacologic regimen through acute testing ranges from 30 to 100%, but is influenced by several factors such as aggressiveness of therapeutic protocol and type and dosage of drugs. The predictive value is high as it approaches 100% for a positive acute test. The elective indications for serial electrophysiologic study are: failure of empirical therapy; disabling and very frequent arrhythmias; arrhythmias provoking major disturbances (lipothymia, syncope, hypotension, shock); symptomatic WPW.

[Treatment of malignant ventricular tachyarrhythmia with amiodarone: comparison of empirical administration and administration guided by Holter or ventricular stimulation. Results of the parallel test]. / Trattamento delle tachiaritmie ventricolari maligne con amiodarone: confronto tra somministrazione empirica e somministrazione guidata da Holter o da stimolazione ventricolare. Risultati del test parallelo.

To assess the most appropriate method of administering amiodarone and predicting its efficacy (empiric vs guided by Holter or by ventricular stimulation), 19 patients with sustained ventricular tachycardia or ventricular fibrillation underwent a "parallel study". Fifteen patients were men and 4 women, with a mean age of 65 years. A coronary artery disease with previous myocardial infarction was present in 15 patients, dilated cardiomyopathy in 3 and arrhythmogenic right ventricular dysplasia in 1 (mean left ventricular ejection fraction = 35%). All 19 patients had, as inclusion criteria, 1) frequent (greater than or equal to 30/hour) and/or repetitive (greater than or equal to 10/24 hours) ventricular premature beats during 24-hour Holter monitoring and 2) inducible sustained (greater than 30/sec) ventricular arrhythmias during programmed ventricular stimulation (1-3 extrastimuli from 2 right ventricular sites). Amiodarone was given at an initial dosage of 15 mg/kg/day for 2 weeks and then at a dosage of 5 mg/kg/day. After 15 days 24-hour Holter monitoring and programmed ventricular stimulation were repeated. The data of these tests, however, were not used to guide the therapy that remained empiric, but served only to assess retrospectively the predictive value of Holter monitoring and ventricular stimulation. The following main results were obtained: The mean duration of follow-up was 25 +/- 13 months. During this period 6 patients (32%) died, 3 from sudden and 3 from non-sudden cardiac death. Two other patients had recurrence of sustained ventricular arrhythmias. After 15 days of therapy amiodarone was effective at Holter monitoring in 15 patients (79%) and not effective in 4 (21%). Two of the 15 patients considered responders died suddenly during the follow-up and 2 had arrhythmic recurrence, vs 1 of the 4 non-responder patients who died suddenly (negative predictive value of Holter monitoring: 73%; positive predictive value: 25%; predictive accuracy: 63%). After 15 days of therapy amiodarone was effective at ventricular stimulation in 10 patients (53%) and not effective in 9 (47%). None of the 10 patients considered responders had arrhythmic events during the follow-up, vs 5 of the 9 non-responders, 3 of whom died suddenly and 2 of whom had arrhythmic recurrences (negative predictive value of ventricular stimulation: 100%; positive predictive value: 56%; predictive accuracy: 79%). Only 1 patient discontinued amiodarone after 25 months of follow-up because of development of an important blue-grey skin discoloration.(ABSTRACT TRUNCATED AT 400 WORDS)

[Idionodal reciprocal tachycardia irresponsive to pharmacological prophylaxis. Description of a case successfully treated with radio frequency]. / Tachicardia reciprocante idionodale insensibile alla profilassi farmacologica. Descrizione di un caso trattato con successo con la radiofrequenza.

The case of a 63-year old female suffering from recurrent paroxysmal supraventricular tachycardia for 30 years is reported. In the past she was treated unsuccessfully with multiple drugs. Electrophysiological study showed dual nodal pathways and the inducibility of a junctional reciprocating tachycardia with RR and V-A intervals respectively 360-410 and 40 msec. Radiofrequency was applied for 30" in the nodal region during induced reciprocating tachycardia. The arrhythmia was interrupted after a few seconds and a 1st degree A-V block persisted for a few minutes. Repeated electrophysiological studies were performed 30 minutes and 20 days after the ablating procedure. They showed a slight increase in AH interval from 55 msec to 90 and 65 msec respectively, as well as the persistence of anterograde dual nodal pathways and the disappearance of retrograde conduction of the A-V node. No reentry arrhythmia could be induced. After six months the patient is asymptomatic and drug free.

[Empiric treatment with amiodarone in patients with sustained ventricular tachyarrhythmia. Results of a long-term follow-up]. / Trattamento empirico con amiodarone in pazienti con tachiaritmie ventricolari sostenute. Risultati a medio e lungo termine.

The long-term follow-up of 52 pts (36 M, 16 F, mean age: 62 years) with sustained ventricular tachyarrhythmias (SVT) was analyzed to assess the efficacy and feasibility of empiric amiodarone treatment. Forty-five pts had organic heart disease (mean EF: 38.3%) and 7 pts no overt heart disease. Twenty pts suffered from syncope or cardiac arrest secondary to sustained ventricular tachyarrhythmias (mean: 2.35 episodes) and 32 did not. All pts were given amiodarone empirically (mean dose: 390 mg) and followed-up for a mean period of 29.5 months (range 1-137). Two pts (3.8%) died of non cardiac causes, 5 (9.6%) of non sudden cardiac death and 7 (13.4%) of sudden death. Fifteen pts (28.8%) experienced non fatal arrhythmic recurrences. Four out of 7 pts who died suddenly experienced non fatal arrhythmic recurrence before death. The actuarial incidence of cardiac death was 10.8, 22.7, 31.5, 31.5% at 1, 2, 3 and 5 years; the actuarial incidence of sudden death was 8.9, 12, 22.1, 22.1% at 1, 2, 3 and 5 years; the actuarial incidence of non fatal arrhythmic recurrences was 17.4, 26.3, 26.3, 26.3, 44.7% at 1, 2, 3, 4 and 5 years. Univariate analysis identified recent myocardial infarction, NYHA functional class, detection of frequent and/or repetitive premature ventricular contractions on Holter monitoring and non fatal arrhythmic recurrences as predictors of cardiac death (p less than 0.05), while only non fatal arrhythmic recurrences were associated with sudden death (p less than 0.05). Twenty-two pts (42.3%) developed side effects. Nine (17.3%) discontinued amiodarone: 6 pts (11.5%) because of side effects and 3 inadvertently.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of head-up tilt test in evaluating patients with syncope of unknown origin and negative electrophysiologic study.

The vasovagal nature of syncope, which remained unexplained despite full clinical and electrophysiologic investigation, was evaluated by means of 60 degrees head-up tilt test for 60 minutes. Thirty patients (17 men and 13 women, mean age 65 years, 19 with and 11 without organic heart disease) with 1 to 28 (mean 5) episodes of syncope of unknown origin were studied. Head-up tilt test was considered positive if syncope developed in association with hypotension, bradycardia, or both. During baseline head-up tilt 15 patients (50%) had a positive response. Ten patients had a vasodepressor response (marked hypotension without marked bradycardia) and 5 had a mixed response (marked hypotension with marked bradycardia). None of 8 control subjects became symptomatic during the test. Baseline head-up tilt test was positively reproducible in 10 of 14 patients (71%). Nine of these 10 patients underwent serial head-up tilt tests after drug administration to determine the pathogenesis of vasovagal syncope. Atropine prevented tilt-induced syncope in 3 of 8 patients (37.5%), propranolol in 2 of 8 (25%) and etilephrine in 7 of 7 (100%). Seven patients received long-term drug treatment with drugs selected on the basis of acute drug testing. One responder to atropine received transdermal scopolamine and 6 received etilephrine. None of these 7 patients had syncopal recurrences or death during a mean follow-up of 12 months. Head-up tilt is a very sensitive and highly specific test to unmask susceptibility to vasovagal reaction in patients with syncope of unknown origin. Withdrawal of alpha-sympathetic stimulation is a principal mechanism responsible for vasodilation and syncope during head-up tilt.(ABSTRACT TRUNCATED AT 250 WORDS)

[Clinical and prognostic value of evaluation of atrial vulnerability in an electrophysiological endocavitary and transesophageal study]. / Valore clinico e prognostico della valutazione della vulnerabilità atriale con lo studio elettrofisiologico endocavitario e transesofageo.

UNLABELLED: Atrial fibrillation or flutter is frequently inducible during endocavitary or transesophageal electrophysiologic study. However, its clinic and prognostic significance has not yet been clarified. We studied 443 patients: 276 underwent endocavitary electrophysiologic study, 228 underwent transesophageal electrophysiologic study and 61 underwent both methods. In 343 of them a satisfactory echocardiogram was obtained. Patients were divided in three groups: gr. I, 93 patients with documented episodes of paroxysmal atrial fibrillation or flutter; gr. II, 257 patients with or without heart disease without clinical atrial fibrillation or flutter; gr. III, 93 symptomatic or asymptomatic Wolff-Parkinson-White patients without clinical atrial fibrillation or flutter. Gr. I included patients without overt heart disease (20), with WPW (11), mitral valve prolapse (4), and miscellaneous (58). Gr. II included patients without overt heart disease (49), with concealed Kent bundles (7), Mahaim (1) or James fibers (1) mitral valve prolapse (6), sick sinus syndrome (40), miscellaneous (91), or syncope of an unknown origin (62). Atrial vulnerability was evaluated both by endocavitary and transesophageal electrophysiologic study using two different protocols; the first protocol was moderately aggressive (prot. A), while the second was aggressive (prot. B). Endocavitary electrophysiologic study. Prot. A: single and double extrastimuli at the three heart rates (sinus, 100 and 150/m'), 10/m' incremental atrial pacing from 160 to 250/m; prot. B: prot. A + incremental atrial pacing from 260/m' up to 2:1 St-A block. Transesophageal electrophysiologic study. Prot. A: 10" atrial burst at 100-600/m' prot. B: prot. A + 6-9" increasing rate bursts from 200 to 800/m'. End point of all protocols: initiation of greater than 1' atrial fibrillation or atrial flutter. RESULTS: Endocavitary electrophysiologic study. A greater than 1' atrial fibrillation or atrial flutter was induced with the two protocols respectively in 67% (52/78) and 85% (51/60) of gr. I, in 17% (26/150) and 36% (38/105) of gr. II and in 35% (17/48) and 44% (21/48) of gr. III (gr. I vs gr. II p less than 0.001 for prot. A and p less than 0.01 for prot. B; gr. II vs gr. III p less than 0.001 for prot. A and NS for prot. B). Induced atrial fibrillation or atrial flutter using the two protocols had a greater than 5' duration respectively in 83 and 78% of gr. I, 62 and 42% of gr. II and in 41 and 38% of gr. III.(ABSTRACT TRUNCATED AT 400 WORDS)

[Syncope of undetermined nature after electrophysiologic study. Usefulness of the head-up tilt test in the diagnosis of vaso-vagal origin and in the choice of treatment]. / Sincopi di natura indeterminata dopo studio elettrofisiologico. Utilità dell'head-up tilt test nella diagnosi di origine vaso-vagale e nella scelta della terapia.

The vaso-vagal nature of syncopes which remained unexplained despite full clinical and electrophysiological investigation was evaluated by means of 60 degrees head-up tilt test for 60 minutes. Thirty patients (16 men and 14 women, mean age 63.6 years, 19 with and 11 without organic heart disease) with 1 to 28 (mean 5.1) episodes of syncope of unknown origin were studied together with 11 asymptomatic control subjects. Head-up tilt test was considered positive if syncope developed in association with hypotension and/or bradycardia. During baseline head-up tilt 15 patients (50%) showed a positive test, with vasodepressor response (marked hypotension without marked bradycardia) in 10 cases and with mixed response (marked hypotension with marked bradycardia) in 5 cases. None of the control subjects became symptomatic during the test. Mean time to syncope was 24.9 minutes. Baseline head-up tilt test was reproducibly positive in 10 out of 14 patients (71%). Eight of these 10 patients underwent serial head-up tilt tests after atropine (0.04 mg/Kg i.v. in 1 minute), propranolol (0.2 mg/Kg i.v. in 3 minutes) and etilefrin (15-30 mg/day orally for 2-3 days) to determine the pathogenesis of vaso-vagal syncope. Atropine prevented tilt-induced syncope in 3 out of 7 patients (43%), propranolol in 2 out of 7 (29%) and etilephrine in 6 out of 6 (100%). Seven patients were chronically treated with drugs selected on the basis of acute drug testing. One patient-responder to atropine received transdermal scopolamine and the other 6 received etilephrine. None of these 7 patients had syncopal recurrences or death during a mean follow-up of 7.7 months, except 1 who experienced another episode of syncope after having discontinued etilephrine 4 months before. These results suggest that: 1) head-up tilt is a very sensitive and highly specific test to unmask susceptibility to vaso-vagal reaction in patients with syncope of unknown origin; 2) withdrawal of alpha-sympathetic stimulation is the principal mechanism responsible for vasodilation and syncope during head-up tilt; 3) alpha-sympathomimetic agents, such as etilephrine, are effective in preventing spontaneous episodes of vaso-vagal syncope during a short-term follow-up.

Electrogenesis of the S1S2S3 electrocardiographic pattern. A study in humans based on body surface potential and right ventricular endocardial mapping.

To study the electrogenesis of the S1S2S3 pattern, seven patients had body surface potential mapping and endocardial mapping of inflow tract, outflow tract, and apex of the right ventricle. QRS duration was longer in S1S2S3 versus controls (94 +/- 14 vs. 84 +/- 14 msec). Surface mapping was similar in S1S2S3 patients and in controls during the first 30-40 msec of QRS, but S1S2S3 patients subsequently presented the following differences: (1) earlier time of onset (34 +/- 3 vs. 44 +/- 6 msec) and a lower voltage (1,242 +/- 468 vs. 1,649 +/- 31 mV) of peak positive anterior maximum; (2) earlier dorsal migration (45 +/- 3 vs. 55 +/- 7 msec) of the maximum; (3) a second peak positive maximum at 58 +/- 3 msec, located on the dorsal spine; (4) the appearance of a right subclavicular positive area at 51 +/- 6 msec, which in controls was absent or appeared later (66 +/- 7 msec). At the end of QRS, the maximum was located in all but two S1S2S3 cases on the upper sternum. Right ventricular endocardial mapping showed a similar activation time of the apex in S1S2S3 patients and controls, but in the former a significant inflow (56 +/- 21 vs. 36 +/- 9 msec) and outflow tract (79 +/- 13 vs. 39 +/- 8 msec) activation delay was documented. The data obtained using body surface potential mapping suggest that an anomalous wavefront rightward and superiorly oriented is present in the S1S2S3 pattern, which is able to oppose the electrical forces of ventricular free walls.(ABSTRACT TRUNCATED AT 250 WORDS)

[Usefulness of transesophageal electrophysiological study during the ergometric test in the evaluation of supraventricular paroxysmal tachycardia occurring during exertion]. / Utilità dello studio elettrofisiologico transesofageo durante test ergometrico nella valutazione delle tachicardie parossistiche sopraventricolari insorgenti sotto sforzo.

Transesophageal electrophysiologic study has recently been proposed for the evaluation of supraventricular arrhythmias. In this report we present 13 cases, with palpitations occurring only during effort, due to a suspected supraventricular tachycardia, in which the usefulness of the transesophageal electrophysiologic study performed during stress test was evaluated. Of these 13 patients, nine were male and four were female, mean age was 29 yrs. Twelve cases had no heart disease, one had a moderate mitral valve insufficiency. Nine cases had a normal ECG, four had a WPW pattern. In 9/13 cases no significant arrhythmia was ever documented, in 1/13 ventricular premature beats were present in the basal ECG, in 1/13 a atrial fibrillation and in 2/13 a supraventricular reciprocating tachycardia was recorded. In all cases a maximal exercise test and a 24-hour Holter monitoring were performed. In all pts a transesophageal electrophysiologic study was performed both at rest and during extra-stimuli and incremental atrial pacing. The end point of transesophageal study was the induction of a sustained (greater than 30") supraventricular tachycardia. RESULTS. Maximal exercise test was negative in 11/13 cases; it showed ventricular premature beats in one case and initiated a supraventricular tachycardia in one. The 24 hour Holter monitoring was negative in 12/13 cases while it showed frequent ventricular premature beats in one. Resting transesophageal electrophysiologic study revealed dual A-V nodal pathways in six pts: in one of them a junctional re-entry was induced; in two a single echo beat was observed, while in three no reentry was observed. In three cases a supraventricular tachycardia was induced which was sustained in one and unsustained (7" and 24") in two cases. In 4 cases transesophageal electrophysiologic study gave no information. Transesophageal stimulation during exercise induced a greater than 30" reciprocating tachycardia in all patients, at work loads of 30-180 watts. Six pts had an intranodal tachycardia (V-A less than 70 msec) a further six pts had a atrioventricular tachycardia involving a Kent bundle (V-A greater than or equal to 70 msec), which was concealed in two, and one had a atrial tachycardia. In four cases (3 with intranodal and 1 with atrioventricular tachycardia), exercise transesophageal study was repeated after chronic therapy with betablockers (sotalol 240 mg/die or metoprolol 200 mg/die). In all cases, after therapy, the induced tachycardia had a longer cycle and in two cases it was induced at a higher work load. In a further two cases flecainide (200 mg/die) was tested. In one case (with atrial tachycardia), the arrhythmia was no longer inducible after therapy, in another case (with intranodal tachycardia) the drug had no effect. CONCLUSIONS. In patients with paroxysmal supraventricular tachyarrhythmias occurring during effort the basal ECG is normal or shows a WPW pattern. The maximal exercise test and 24 hour Holter monitoring give no information in over 90% of cases.(ABSTRACT TRUNCATED AT 400 WORDS)

[Different degrees of risk of high-frequency atrial fibrillation in symptomatic and asymptomatic WPW syndrome. Electrophysiologic evaluation]. / Diverso rischio di fibrillazione atriale ad alta frequenza nel WPW sintomatico e asintomatico. Valutazione elettrofisiologica.

Sudden death in WPW pattern can occur when atrial fibrillation (a.f.) with rapid ventricular response develops. This event seems to be the final result of three concomitant conditions: the appearance of an orthodromic atrio-ventricular reciprocating tachycardia, the most common form of tachycardia in these patients; a high atrial vulnerability, which makes possible that reciprocating tachycardia degenerates into atrial fibrillation and a short anterograde refractory period of the Kent bundle. With the purpose of evaluating the risk to develop high frequency a.f., 36 WPW subjects were electrophysiologically studied. 22 were symptomatic for palpitations (Group I) and 14 were totally asymptomatic (Group II). 3/22 patients of Group I had experienced clinical atrial fibrillation (Subgroup I A), which was never documented in the remaining 19/22 (Subgroup I B). In all cases the following parameters were analyzed: the presence or absence of the retrograde conduction of the anomalous pathway, essential for the occurrence of orthodromic reciprocating atrio-ventricular tachycardia; the presence or absence of a high atrial vulnerability and the presence of RR intervals between pre-excited complexes during induced a.f. less than 250 msec. As an index of atrial vulnerability were considered the spontaneous degeneration into atrial fibrillation of an electrophysiologically induced reciprocating tachycardia and/or the induction of a sustained a.f. by programmed right atrial stimulation during sinus rhythm and/or during 600 and 400 ms atrial driving and/or by 160-250/m' atrial bursts. Results--Retrograde conduction of Kent bundle was documented in 100% of Gr. I vs 22% of Gr. II (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

[The Italian Group for the Study of Streptokinase in Myocardial Infarct: Study of electrocardiographic changes]. / G.I.S.S.I.: Studio delle alterazioni elettrocardiografiche.

The twofold purpose of the ECG sub-group study of G.I.S.S.I. (Gruppo Italiano per lo Studio della Streptokinasi nell'Infarto miocardico) is to evaluate whether exist different ECG evolution in pts with AMI treated with streptokinase (SK YES) and/or with coronary reperfusion (early CK peak) with respect to pts non treated with streptokinase (SK NO) and/or without coronary reperfusion (late CK peak) and to establish whether the ECG is useful to recognize the patients in which reperfusion occurs. Among 365 pts randomized for G.I.S.S.I., 209 pts with first myocardial infarction, admitted within 6 hours from the onset of pain, alive for at least 24 hours, were included. 98 were SK YES and 111 SK NO: 48 cases (group A) had the CK peak before 15th hour; 59 cases (group B) had the CK peak between 15th and 21th hour: 102 cases (group C) had the CK peak after 21th hour. In all the patients ECG was analyzed on admission and thereafter at 3rd, 6th, 9th, 12th, 24th hours and on 2nd, 3rd, 7th and 14th days. RESULTS--Anterior myocardial infarction--SK YES pts had in respected to SK NO pts a significantly lower sum of ST elevation on anterior leads (sigma ST increases V1-V6) at all times after admission starting from 6th hour. A similar behaviour was observed in groups A and B in respect to group C. SK YES pts when compared to SK NO pts had an earlier loss of the sum of R wave in anterior leads (sigma RV1-V6), although the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)