The mechanisms of spontaneous termination of reentrant supraventricular tachycardias.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) often terminate spontaneously, presumably due to changes in the electrophysiological properties of the reentrant circuit. However, the mechanism of spontaneous termination of these arrhythmias is incompletely understood. METHODS: We included 70 consecutive patients with reentrant supraventricular tachycardias (35 AVNRT, 35 AVRT) in whom the arrhythmia ended spontaneously during the electrophysiologic study. We determined in each patient the duration of the induced arrhythmia, site of block, beat-to-beat oscillations in tachycardia cycle-length (CL), A-H, H-V, H-A and V-A intervals. RESULTS: In 21/34 (62%) patients with AVNRT and 19/30 (63%) with orthodromic AVRT, tachycardia termination was preceded by progressive increase in tachycardia CL due to prolongation of the A-H interval (Mobitz type-I pattern). In 13/34 patients with AVNRT (38%) and 11/30 with orthodromic AVRT (37%), termination occurred suddenly without a preceding change in CL, with block ensuing retrogradely either in the fast AV nodal pathway or the accessory pathway (Mobitz type-II pattern). In 4/5 patients with antidromic AVRT the tachycardia ended at the retrograde limb with previous prolongation of the VA interval. CONCLUSION: Spontaneous termination of AVNRT and AVRT is a time-related phenomenon. Despite different pathways being involved in these two reentrant tachycardias, termination can follow antegrade or retrograde block in similar ratio (60% antegradely and 40% retrogradely). Antegrade block is preceded by prolongation of the AH interval (Mobitz type-I), whereas retrograde block occurs unexpectedly in the retrograde limb (Mobitz type-II). Fatigue of conduction appears to be involved in this phenomenon.

Accelerated idioventricular rhythm unmasking the brugada electrocardiographic pattern.

It has recently been reported that a high-degree right bundle branch block (RBBB) may conceal the electrocardiographic manifestations of the Brugada ECG pattern. An 82-year-old with recent onset palpitations was seen in clinic. The resting ECG showed sinus rhythm, high-degree RBBB, and an irregular idioventricular rhythm. Some fusion beats between sinus rhythm and idioventricular rhythm occurred spontaneously depicting incomplete RBBB pattern and a clear cut elevation of the ST-segment was unveiled, giving rise to a suspicious Brugada ECG pattern. The mechanisms and implications of these findings are discussed.

Short-term amiodarone therapy after reversion of persistent atrial fibrillation reduces recurrences at 18 months.

BACKGROUND: The aim of this study was to compare the outcome of 3 months vs. 18 months of amiodarone treatment after atrial fibrillation (AF) conversion in patients who experienced the first episode of persistent AF. METHODS: We included 51 patients who experienced the first episode of persistent AF receiving amiodarone (600 mg) daily for 4-6 weeks. If AF persisted, electrical cardioversion (ECV) was performed. All patients received amiodarone (200 mg daily) for 3 months and then were randomized to amiodarone (Group I) or placebo (Group II) and followed for 15 months. The control group comprised 9 untreated patients undergoing ECV. Treatment effectiveness was evaluated using a Bayesian model. RESULTS: Eighteen months after AF reversion, 22 (81.5%) patients in Group I, 13 (54.2%) patients in Group II, and 1 (11.1%) patient in the control group remained in sinus rhythm. No differences were found between Group I patients who required ECV and Group II patients. Sinus rhythm was preserved in all Group I patients when it was achieved during amiodarone administration. Limiting adverse effects occurred in 3 (11.1%) patients in Group I. CONCLUSIONS: In patients regaining sinus rhythm after the first episode of persistent AF, a 3-month amiodarone treatment after reversion is a reasonable option for rhythm control.

Right bundle branch block and middle septal fiber block with or without left anterior fascicular block manifested as aberrant conduction in apparent healthy individuals: Electro-vectorcardiographic characterization.

BACKGROUND: Right bundle branch block (RBBB) evident in the precordial ECG leads may be associated with evidence of left bundle branch involvement in the limb leads. Any of the components of the left bundle can be involved, and this complex interventricular conduction abnormality has previously been described in patients with underlying heart disease. OBJECTIVES: To analyze the electro-vectorcardiographic manifestations of RBBB with left middle septal fiber block (LMSFB), with or without left anterior fascicular block (LAFB) in premature atrial beats of patients without apparent structural heart disease. METHODS: Twelve patients (8 men/4 women; mean age: 32±8years) with premature atrial contractions with this conduction abnormality were included. Surface 12 simultaneous lead ECG recordings and the corresponding vectorcardiographic loops were analyzed. RESULTS: The QRS complexes with RBBB and also LMSFB persisted for between 150 and 190ms. There were no q waves in lead I. The maximum spatial vector (72-86ms) was directed posteriorly, superiorly, and leftward, and the terminal forces were oriented anteriorly, inferiorly and rightward. In 10 patients, small q waves were apparent in leads V1-V2 and the frontal QRS axis was -60° and -70°, with the 46ms vector located at -50°±5. All of these patients most probably had LAFB in addition to LMSFB. In two patients, the initial electrical forces were directed anteriorly, inferiorly, and leftward, and the 46ms vector axis in the frontal plane was 6° and 11°, respectively, indicating absence of LAFB. CONCLUSIONS: The combination of RBBB and LMSFB occurring in patients without apparent structural heart disease may be related to the simultaneous occurrence of block of conduction through these components of the Purkinje network. The anterior fascicle of the left bundle may also be involved.

A reappraisal on lidocaine-sensitive repetitive, uniform atrial tachycardia.

BACKGROUND: Lidocaine sensitive, repetitive atrial tachycardia is an unusual arrhythmia whose electrophysiologic substrate remains undefined. We aimed to analyze the electropharmacologic characteristics of this arrhythmia with emphasis on its cellular substrate and response to drug challenges. METHODS: We retrospectively analyzed a series of 18 patients from an electrocardiographic and electrophysiologic perspective and the response to pharmacological challenge. RESULTS: There was no evidence of structural heart disease in 12 patients, 4 patients presented with systemic hypertension; one patient had a prior myocardial infarction and one a mitral valve prolapse. The arrhythmia depicted a consistent pattern in nine patients. The first initiating ectopic beat showed a long coupling interval, the cycle length of the second atrial ectopic beat presented the shortest cycle length and a further prolongation was apparent towards the end of the atrial salvos. Conversely, in the other nine cases, the atrial tachycardia cycle length was erratic. The arrhythmia was suppressed by asynchronous atrial pacing at cycle lengths longer than those of the atrial tachycardia. Intravenous lidocaine eliminated the arrhythmia in all patients, but intravenous verapamil suppressed the atrial tachycardia in only two patients while adenosine caused a transient disappearance in 2/8 patients. Only one patient responded to all the three agents. Radiofrequency ablation was successfully performed in 10 patients. CONCLUSIONS: Repetitive uniform atrial tachycardia can be sensitive to lidocaine. In few cases, this rare focal arrhythmia may be also suppressed by adenosine and/or verapamil, which suggests a diversity of electrophysiologic substrates that deserve to be accurately identified.

Masquerading bundle branch block: a variety of right bundle branch block with left anterior fascicular block.

The so-called 'masquerading' type of right bundle branch block is caused by the simultaneous presence of a high-degree left anterior fascicular block often accompanied with severe left ventricular enlargement and/or fibrotic block in the anterolateral wall of the left ventricle. These conditions tend to reorient the terminal electrical forces of the QRS complex towards the left and upwards, in such a way that the characteristic slurred S wave in lead I becomes smaller or even disappears. In many cases of standard masquerading right bundle branch block, a small Q wave in lead I is present due to the initial forces of the left anterior fascicular block, which are oriented rightwards and inferiorly. However, in some cases, the Q wave in lead I also vanishes, and the mimicking of a left bundle branch block becomes perfect in standard leads. This is commonly associated with an inferior myocardial infarction or severe inferior fibrosis in cardiomyopathies. The typical QRS changes of right bundle branch block may eventually be concealed even in the right precordial leads; under such circumstances, the ECG diagnosis may be mistaken and the right bundle branch block totally missed. The masquerading right bundle branch block carries a poor prognosis, since it always implies the presence of a severe underlying heart disease.

The electrocardiographic diagnosis of intraventricular blocks coexisting with ventricular preexcitation.

The electrocardiographic diagnosis of intraventricular conduction disturbances may be hindered by the coexistence of ventricular preexcitation. In fact, the premature depolarization of ventricular myocardium through an accessory pathway tends to conceal any electrocardiographic manifestation of a bundle-branch block. However, there are several conditions favoring the diagnosis of bundle-branch block associated with ventricular preexcitation: intermittency of ventricular preexcitation and/or bundle-branch block, fast atrioventricular (AV) nodal impulse propagation, slow conduction over the accessory pathway or between its ventricular insertion site and the remaining myocardium, and presence of atrioventricular junctional ectopic beats exposing the intraventricular conduction disturbance. This article reexamines the available data on preexcitation in patients with intraventricular blocks and presents clinical examples to emphasize the importance of a thorough examination of the electrocardiogram to attain the correct diagnosis of this association.

Distinct pharmacologic substrate in lidocaine-sensitive, repetitive atrial tachycardia.

Lidocaine-sensitive, repetitive atrial tachycardia is an uncommon arrhythmia. The electrophysiologic substrate is still unknown, and the pharmacologic responses have not been fully explored. The aim of this study was to investigate the effects of intravenous adenosine and verapamil in patients with lidocaine-sensitive atrial tachycardia. In 9 patients with repetitive uniform atrial tachycardia, the response to intravenous adenosine (12 mg), lidocaine (1 mg/kg body weight), and verapamil (10 mg) were sequentially investigated. Simultaneous 12-lead electrocardiogram (ECG) was recorded at baseline and continuously monitored thereafter. Tracings were obtained at regularly timed intervals right after the administration of each drug to evaluate changes in the arrhythmia characteristics. Repetitive atrial tachycardia was abolished by intravenous lidocaine in the 9 patients within the first 2 minutes after the end of injection. Adenosine suppressed the arrhythmia in 2 patients and shortened the runs of atrial ectopic activity in 1 patient, while verapamil was effective in 2 patients, 1 of them insensitive to adenosine and the other 1 sensitive to this agent. In 5 patients, the arrhythmia was abolished by radiofrequency ablation at different sites of the right atrium. Lidocaine-sensitive atrial tachycardia may eventually be also suppressed by adenosine and/or verapamil. This suggests that this enigmatic arrhythmia may be caused by different underlying electrophysiologic substrates and that at least in some cases, delayed afterdepolarizations seem to play a determining role.

Reversal of primary and pseudo-primary T wave abnormalities by ventricular pacing. A novel manifestation of cardiac memory.

AIMS: "Cardiac memory" refers to abnormal T waves (TW) appearing after transient periods of altered ventricular depolarization. The aim of the study was to test the hypothesis that in the presence of abnormal TW, short periods of tailored ventricular pacing (VP) can be followed by normalization of ventricular repolarization. METHODS: Ten patients with normal TW (control group) and 18 patients with abnormal TW (study group) underwent 15 min of VP at a cycle length of 500 ms. In the control group, VP was performed from the right ventricular apex, and in the study group from right or left ventricular sites that resulted in paced QRS complexes of opposite polarity to that of the abnormal TW. Before and after VP, atrial pacing was maintained at a stable cycle length. Simultaneous 12-lead electrocardiography (ECG) was recorded before, during, and following VP to assess changes in TW polarity, amplitude, electrical axis, QTc interval, and QTc interval dispersion. RESULTS: As expected, VP was followed by memory-induced changes in TW in eight of ten patients in the control group. Mean T wave axis shifted from +60 degrees + or - 21.2 degrees to +23.5 degrees + or - 50.7 degrees (p = 0.01) in the frontal plane. In the study group, complete or partial normalization of TW occurred in 17 of 18 patients. Mean T wave axis shifted from -23.7 degrees + or - 22.9 degrees to +19.7 degrees + or - 34.7 degrees (p < 0.0002) in the frontal plane when paced from right ventricular outflow tract. The QTc interval shortened after VP both in the control group (424 + or - 25 vs. 399 + or - 27 ms; p = 0.007) and in the study group (446 + or - 26 vs. 421 + or - 22 ms; p < 0.0002). No significant changes were found in QTc interval dispersion. CONCLUSIONS: Transient changes in the sequence of ventricular activation may either induce or normalize abnormal TW. The background of preceding ventricular depolarization needs to be taken into account before determining the clinical significance of a given pattern of ventricular repolarization.

Implantable cardioverter defibrillators and Chagas' disease: results of the ICD Registry Latin America.

AIMS: Chagas' disease is an endemic parasitic affliction in Latin America. It is frequently associated with ventricular tachyarrhythmia and sudden death. The aim of this study is to assess the evolution of patients with Chagas' disease treated with an implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: Eighty-nine chagasic patients with ICD were included for analysis from the Medtronic ICD Registry Latin America. At implant, mean age was 59 +/- 10 years, and 72% were male. Eighty-one patients (91%) had secondary prevention indications. Mean left ventricular ejection fraction was 40 +/- 11%, and mean follow-up was 12 +/- 7 months. During follow-up, six patients died (6.7%); three due to congestive heart failure, one due to sudden death, and two due to non-cardiac cause. Hospitalization occurred in seven patients. Thirty-eight patients (42%) received appropriate ICD therapies. A total of 737 episodes were detected by the ICD. The mean period between ICD implantation and the first appropriate therapy was 104 days. Electrical storms were observed in 14 of the 89 patients (15.7%). Inappropriate therapies were observed in seven patients. CONCLUSION: This registry confirms that ICD therapy provides protection by effectively terminating life-threatening arrhythmias in patients with Chagas' disease. This is especially so when patients receive the device for secondary prevention.