Argentina's most important contributions in the field of electrophysiology.

Latin American electrocardiology emerged internationally thanks to the Argentine School of Electrocardiology. All started when the idea of a different anatomy of the conduction system was not only necessary to change the paradigm of a bifascicular system, but also to question diagnostic electrocardiographic criteria adopted by the scientific community without dispute. Almost every scientific contribution coming from the Argentine School of Electrocardiology represented a significant step forward in the understanding of the electrophysiology of the heart and its electrocardiographic counterpart. There is another reason that increases their value: the noticeable simplicity of the technical facilities with which these studies were done from the modest laboratory in Argentina, whose production was purely and genuinely Latin American. In the following lines we summarize what we consider to be the greatest contributions of the Argentine school to world electrophysiology.

Fascicular Blocks: Update 2019.

Many advances in the knowledge of medical science are due to the observation of an unknown phenomenon that remains an open question. A plausible hypothesis must be demonstrated and proved through a scientific method in order to be accepted by the scientific community and the same results must be reached by following either the same or different techniques. The original case described by Rosenbaum MB et al., in this review triggered a series of anatomic and physiologic investigations with clinical and experimental observations that supported the trifascicular nature of the intraventricular conduction system of the heart and the concept of hemiblocks. The recognition and description of the left fascicular blocks made by the Argentinian School of Electrocardiology bridged an important gap in electrocardiography and many electrocardiograms that could not be explained until that moment could finally be understood. This review intends to redefine reliable criteria for the electrocardiographic and vectorcardiographic diagnosis of left fascicular blocks [hemiblocks]. The anatomy of the left bundle branch is also discussed to better understand the incidence, prevalence, clinical significance and main causes of left anterior and left posterior hemiblock either isolated or associated with right bundle branch block. This review offers the reader a reappraisal of the trifascicular nature of the intraventricular conduction system regarding the anatomy of the left bundle branch system and its pathophysiological and clinical significance.

Cardiac automaticity: basic concepts and clinical observations.

PURPOSE: The purpose of this report was to review the basic mechanisms underlying cardiac automaticity. Second, we describe our clinical observations related to the anatomical and functional characteristics of sinus automaticity. METHODS: We first reviewed the main discoveries regarding the mechanisms responsible for cardiac automaticity. We then analyzed our clinical experience regarding the location of sinus automaticity in two unique populations: those with inappropriate sinus tachycardia and those with a dominant pacemaker located outside the crista terminalis region. RESULTS: We studied 26 patients with inappropriate sinus tachycardia (age 34 ± 8 years; 21 females). Non-contact endocardial mapping (Ensite 3000, Endocardial Solutions) was performed in 19 patients and high-density contact mapping (Carto-3, Biosense Webster with PentaRay catheter) in 7 patients. The site of earliest atrial activation shifted after each RF application within and outside the crista terminalis region, indicating a wide distribution of atrial pacemaker sites. We also analyzed 11 patients with dominant pacemakers located outside the crista terminalis (age 27 ± 7 years; five females). In all patients, the rhythm was the dominant pacemaker both at rest and during exercise and located in the right atrial appendage in 6 patients, in the left atrial appendage in 4 patients, and in the mitral annulus in 1 patient. Following ablation, earliest atrial activation shifted to the region of the crista terminalis at a slower rate. CONCLUSIONS: Membrane and sub-membrane mechanisms interact to generate cardiac automaticity. The present observations in patients with inappropriate sinus tachycardia and dominant pacemakers are consistent with a wide distribution of pacemaker sites within and outside the boundaries of the crista terminalis.

[Trigeminy of ventricular bigeminy caused by reentrant mechanism: reentry of reentry]. / Trigeminia de la bigeminia ventricular por mecanismo reentrante: reentrada de la reentrada.

The process that follows an acute myocardial infarction generates an appropriate substrate for the formation of reentry circuits, considered to be the most frequent mechanism of ventricular extrasystoles and tachyarrhythmias. We present the case of a patient with an acute myocardial infarction unusually concurring with ventricular trigeminy coupled to ventricular bigeminated extrasystoles giving rise to a trigeminy sequence over the bigeminy, which indicates the existence of two reentry circuits (reentry of reentry) that trigger ventricular flutter.

Trigeminia de la bigeminia ventricular por mecanismo reentrante: reentrada de la reentrada / Trigeminy of ventricular bigeminy caused by reentrant mechanism: reentry of reentry

El proceso post-infarto agudo de miocardio genera el sustrato apropiado para la formación de circuitos de reentrada, los cuales son considerados como el mecanismo más frecuente de las extrasístoles y taquiarritmias ventriculares. Presentamos el trazado electrocardiográfico de un paciente con infarto agudo de miocardio en quien se observó la inusual concurrencia de una trigeminia ventricular acoplada a extrasístoles ventriculares bigeminadas, que originó una secuencia de trigeminia sobre la bigeminia, evidenciando la existencia de dos circuitos reentrantes (reentrada de la reentrada); después de una dupla de la extrasístole bigeminada se genera un aleteo ventricular.

The process that follows an acute myocardial infarction generates an appropriate substrate for the formation of reentry circuits, considered to be the most frequent mechanism of ventricular extrasystoles and tachyarrhythmias. We present the case of a patient with an acute myocardial infarction unusually concurring with ventricular trigeminy coupled to ventricular bigeminated extrasystoles giving rise to a trigeminy sequence over the bigeminy, which indicates the existence of two reentry circuits (reentry of reentry) that trigger ventricular flutter.

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.

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 features of complete and partial left anterior and left posterior hemiblock.

The aim of this study is to present the criteria for the diagnosis of incomplete or partial block within the anterior and posterior divisions of the left bundle-branch (LBB). To disclose incomplete left anterior hemiblock (LAH) and incomplete left posterior hemiblock (LPH), clinical cases of pathologic and physiologic intermittent or transient block in the divisions of the LBB are analyzed. When dealing with the diagnosis of incomplete LAH, an ÂQRS shift in the same or in successive tracings in a patient, showing electrical axis at +50°, +40°, +30°, and 0° covering the whole range up to -45° or even more negative, makes the diagnosis of incomplete to complete block in the anterior division of the LBB. Conversely, when LPH is the case, a progressive change of the ÂQRS from a normal axis to the right, up to +120° in the same or subsequent tracings in a short period, can only be explained by increasing the degrees of LPH. When a partial or incomplete LAH or LPH is present and the ÂQRS direction can be considered normal in clinical practice, it is difficult or even impossible to reach a diagnosis. That is, small degrees of block in the divisions of the LBB totally overlap normal variants.

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.

Antibodies with beta-adrenergic activity from chronic chagasic patients modulate the QT interval and M cell action potential duration.

AIMS: The aim of this study was to investigate whether the sera from chronic chagasic patients (CChPs) with beta-1 adrenergic activity (Ab-beta) can modulate ventricular repolarization. Beta-adrenergic activity has been described in CChP. It increases the L-type calcium current and heart rate in isolated hearts, but its effects on ventricular repolarization has not been described. METHODS AND RESULTS: In isolated rabbit hearts, under pacing condition, QT interval was measured under Ab-beta perfusion. Beta-adrenergic activity was also tested in guinea pig ventricular M cells. Furthermore, the immunoglobulin fraction (IgG-beta) of the Ab-beta was tested on Ito, ICa, and Iks currents in rat, rabbit, and guinea pig myocytes, respectively. Beta-adrenergic activity shortened the QT interval. This effect was abolished in the presence of propranolol. In addition, sera from CChP without beta-adrenergic activity (Ab-beta) did not modulate QT interval. The M cell action potential duration (APD) was reversibly shortened by Ab-beta. Atenolol inhibited this effect of Ab-beta, and Ab- did not modulate the AP of M cells. Ito was not modulated by isoproterenol nor by IgG-beta. However, IgG-beta increased ICa and IKs. CONCLUSION: The shortening of the QT interval and APD in M cells and the increase of IKs and ICa induced by IgG-beta contribute to repolarization changes that may trigger malignant ventricular arrhythmias observed in patients with chronic chagasic or idiopathic cardiomyopathy.