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M López-Gil

Publications and source records attributed to M López-Gil.

14 recordsLinked to original sources
PubMed1998

Mechanisms of induction of typical and reversed atrial flutter.

INTRODUCTION: Typical flutter is due to reentry around caval veins and terminal crest. In patients with typical flutter, reversed (clockwise) reentry can be induced. We studied mechanisms of typical and reversed flutter induction. METHODS AND RESULTS: Thirteen patients (11 men) underwent 16 radiofrequency (RF) ablation procedures for typical (12) or reversed flutter (1). High right atrium (RA) stimulation included 1 to 3 extrastimuli over cycle lengths 600 to 250 msec, and burst. We recorded simultaneously from three levels of septal and anterior RA. RF was delivered to the inferior vena cava-tricuspid isthmus (CTI). Of 25 inductions, 4 were a result of single, 9 double, and 11 triple extrastimuli, and 1 burst. Clinical basal flutter was induced (7 typical, 1 reversed). After RF, typical flutter was reinduced in 9 cases and reversed flutter in 7, with only typical flutter seen clinically. All flutters were interrupted by ablation or catheter pressure on the CTI. Typical flutter began by low RA septal activation block, preceded by repetitive responses in 12 instances, atypical flutter in 1, and directly from stimuli in 4. Reversed flutter started in 8 instances by low RA block of a stimulated front descending the anterior wall and in 1 by repetitive responses. CONCLUSION: Septal activation block was the usual mechanism of typical flutter induction by RA extrastimuli. Facilitation of reversed flutter after RF application is probably due to a new area of block in the CTI. Flutter induction without intermediate rhythms confirms the presence of block at the terminal crest at baseline.

Atrial Flutter↗
PubMed1997

The upper link of human common atrial flutter circuit: definition by multiple endocardial recordings during entrainment.

Common atrial flutter is due to a macroreentry circuit in the right atrium, but the cranial path of the circuit has not been defined. The objectives of this article are to determine the cranial turning point of flutter activation in relation to a hypothetic obstacle, the superior vena cava opening, by examining the changes in activation sequence produced by entrainment from different points. In 13 cases of common atrial flutter with typical counter-clockwise right atrial circuits confirmed by endocardial mapping the atrium was paced from the high posterior and mid-septal walls. Entrainment was confirmed by simultaneous recordings of 6-7 right atrial electrograms. Changes in sequence of electrograms from high septum and high anterolateral walls was sought. Electrogram sequence and morphology did not change with entrainment at the posterior wall with respect to the basal flutter or mid-septal wall entrainment. Pacing "below" the superior vena cava did not advance the anterior wall electrogram in relation to the septal electrogram. These findings support the concept that common flutter activation turned around (cranial and anterior to) the superior vena cava opening, and not around the free end of a line of block below the superior vena cava in the posterior wall. Common atrial flutter activation rotates cranial (and anterior) to the superior vena cava opening, through the "right atrial roof." The line of functional block should span from inferior to superior vena cava openings.

Adult↗
PubMed1996

Atrial flutter mapping and ablation. I. Studying atrial flutter mechanisms by mapping and entrainment.

Endocardial mapping has led to a detailed knowledge of reentry mechanisms in atrial flutter. Multipolar and deflecting tip catheters allow recording local electrograms from multiple areas of the right atrium, and from the coronary sinus. In common flutter, with the typical "sawtooth" pattern, there is circular activation of the right atrium in a "counterclockwise" direction, descending in the anterior and lateral walls, and ascending in the septum and posterior wall. Superior and inferior vena cava, linked by a "line" of functional block in the posterolateral wall, make the central obstacle for circular activation. The cranial and caudal turning points are the atrial "roof," and the isthmus between the inferior vena cava and the tricuspid valve. Complex conduction patterns, probably including slow conduction are detectable in the low septal area, around the coronary sinus. Atypical flutter, without the sharp negative deflections of common flutter, sometimes shows circular activation in the right atrium, rotating in the opposite direction of common flutter (clockwise). Other atypical flutters show no circular right atrial activation, and only partial data from coronary sinus activation, combined with the response to atrial stimulation (entrainment) allow the diagnosis of left atrial reentry, without a precise delimitation of the circuits. In patients having undergone cardiac surgery, atypical flutter may be based on reentry around surgical scars. To our knowledge, the mechanism of type II flutter has not been disclosed in humans.

Atrial Flutter↗
PubMed1996

Atrial flutter mapping and ablation II. Radiofrequency ablation of atrial flutter circuits.

The definition of the anatomical substrate of reentry in atrial flutter has allowed the recognition of narrow, critical areas of the circuit, where radiofrequency ablation can interrupt reentry. In common flutter the isthmus between the inferior vena cava and the tricuspid valve appears the best target, but ablation between the coronary sinus and tricuspid valve can also be effective in some cases. In atypical flutter using the same circuit as common flutter in a "clockwise" direction, ablation of the same isthmus is effective. Flutter interruption is the main objective, but it does not mean complete isthmus ablation. If flutter remains inducible, new applications are delivered in the isthmus, until it is made noninducible. Complications are rare. Despite attaining noninducibility, flutter may recur, and new procedures may be needed to prevent recurrence. Atrial fibrillation can occur in up to 30% of the cases during follow-up, but it is generally well controlled with antiarrhythmic drugs, that were ineffective to treat flutter before ablation. In reentry circuits based on surgical atrial scars, ablation of an isthmus between the scar and the inferior vena cava can also be effective. Left atrial circuits are not known well enough to guide successful ablation.

Animals↗
PubMed1996

Radiofrequency catheter ablation of atrial flutter circuits.

Common atrial flutter is due to reentrant activation of the right atrium, rotating around anatomic structures and areas of functional block, in counterclockwise direction in the frontal plane. The myocardium between the inferior vena cava and the tricuspid valve is critical to close the activation circuit, and ablation of this isthmus by catheter-delivered radiofrequency can interrupt flutter, and eventually destroy the circuit, preventing recurrence of the arrhythmia. Flutter interruption does not mean complete isthmus ablation, and the procedure endpoint is to attain flutter non-inducibility, and isthmus block. Despite non-inducibility, flutter may recur, and new procedures may be needed for complete ablation. Atrial fibrillation can occur in up to 35% of the cases during follow-up but is generally well controlled with drugs that were ineffective against flutter before ablation. Some atypical atrial flutters show circular right atrial activation, using the same circuit in a clockwise direction, and these can also be interrupted by ablation of the inferior vena cava-tricuspid valve isthmus. Other atypical flutters can have different anatomic substrates in the right or left atrium, and mapping has to define specific isthmuses as ablation targets in each case. Left atrial flutter remains inaccessible to ablation.

Atrial Flutter↗
PubMed1995

Wolff-Parkinson-White syndrome presenting as the permanent form of junctional reciprocating tachycardia.

The substrate of the permanent form of junctional reciprocating tachycardia is an accessory pathway with no spontaneous anterograde conduction, usually located in the posteroseptal area. We report a case of this type of tachycardia with overt anterograde ventricular preexcitation. Electrophysiologic study confirmed that tachycardia was due to an accessory pathway with long retrograde conduction time; electrophysiologic findings suggested longitudinal dissociation of the accessory pathway. Radiofrequency application at the coronary sinus os resulted in disappearance of preexcitation and cure of the tachycardia.

Catheter Ablation↗
PubMed1995

Atrial flutter ablation: electrophysiological landmarks.

Understanding the configuration of the whole flutter circuit is for us the only valid parameter allowing the design of an ablation strategy. Fragmented or double electrograms may have different meanings in different parts of the circuit, and full activation mapping is the best clue to their interpretation. Correlation of anatomy with activation sequence will mark the best ablation target (isthmus) in each case. Multiple simultaneous recordings from the septum and right atrial anterior wall are very helpful to rapidly diagnose circular activation of the right atrium. In cases without this type of activation, coronary sinus recordings and the study of postentrainment cycles are helpful to localize the reentry circuit.

Atrial Flutter↗
PubMed1993

Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter.

Endocardial mapping has suggested that common atrial flutter (AF) is based on right atrial reentry surrounding the inferior vena cava (IVC). The isthmus between the IVC and the tricuspid valve (TV) appears essential to close the circuit. To test this hypothesis, radiofrequency was applied to the IVC-TV isthmus, with catheter electrodes, in 9 patients with AF. Mapping confirmed a right atrial circuit surrounding the IVC in all. In 4 patients another type of AF was induced that followed the circuit in the opposite direction. Radiofrequency interrupted AF in all patients. Multiple endocardial recordings showed that interruption was due to activation block at the point of application. Radiofrequency produced very brief or sustained, atrial fibrillation in 2 patients, which resulted in sinus rhythm. AF recurred in 4 patients with the same activation pattern and was interrupted again with radiofrequency in the IVC-TV isthmus in 3. AF was noninducible in 7 patients after 1 to 4 sessions. AF-free periods of 2 to 18 months without drugs were observed after radiofrequency, but 2 patients had paroxysmal atrial fibrillation. These results confirm that the IVC-TV isthmus is an essential part of the AF circuit. Ablation of this area may be of therapeutic value, but technical improvements are needed. Long-term efficacy of the procedure is uncertain.

Aged↗
PubMed1993

Catheter ablation of atrial flutter circuits.

Atrial flutter (AF) mapping has shown circular activation in the right atrium (RA), with a "counterclockwise" rotation in a frontal view. The myocardial isthmus between the inferior vena cava and the tricuspid valve (IVC-T) closes the activation circuit in its caudal end. The reproducibility of this activation pattern, and the fact that some "rare" AF with a "clockwise" rotation of activation use the same circuit, suggests that reentry is greatly facilitated by the anatomical arrangement of the caudal end of the RA. This suggested that ablation of the IVC-T isthmus may interrupt AF and prevent its recurrence. We have applied radiofrequency (RF) current to the IVC-T isthmus in nine patients, producing sudden interruption of activation at this point in five (all those treated with large surface electrode catheters). In three others, RF produced acceleration or disorganization, leading to interruption. Preliminary follow-up data suggest a favorable effect on AF recurrence, either by preventing it, or by making antiarrhythmic drugs effective.

Atrial Flutter↗
PubMed1992

Electrophysiologic studies in atrial flutter.

The clinical electrophysiologic approaches to atrial flutter (F) have been activation mapping and the observation of changes induced by programmed stimulation. Sequential endocardial activation mapping has recently yielded information indicating that common F is produced by a large right atrial (RA) reentry circuit, with counterclockwise rotation in the frontal plane, including the inferior vena cava in its center. Functional block in the crista terminalis and conduction slowing in the approaches to the atrioventricular node seem to be important to support reentry. F inscribing positive deflections in the inferior leads usually follows the same path, but in a clockwise direction. Atypical F may be produced by left atrial circuits. Atrial stimulation during F entrains the circuit, resetting it with each stimulus. Collision between antidromic and orthodromic activation during entrainment produces fusion that can be identified in the surface electrocardiogram. The last paced activation restarts F, unless circuit penetration has been enough to modify it by block or disorganization. Entrainment may result in F acceleration, with changes in activation sequence, suggesting a different type of reentry, possibly based on functional factors.

Atrial Flutter↗
PubMed1990

Atrial endocardial mapping in the rare form of atrial flutter.

Endocardial atrial activation mapping was performed in 7 patients with rare atrial flutter (AF), inscribing predominantly positive deflections on leads II, III and aVF. In 2 cases both a rare and a common AF were mapped on different occasions. Every case displayed circular right atrial activation. In 5 of the 7 cases rare AF direction was clockwise (craniocaudal in the septum and posterior wall and caudocranial on the lateral and anterior walls). In 2 cases rare AF direction was counterclockwise (caudocranial in the septum and posterior wall and craniocaudal in the lateral and anterior walls). Both common AF rotated counterclockwise. A "line" of conduction delay or block was present in both clockwise and counterclockwise circuits between the posterior and lateral walls, in the probable location of the crista terminalis. This line of block extended the central obstacle made by the inferior vena cava toward, but perhaps not all the way to, the superior vena cava, making activation rotate roughly around the tricuspid ring. The ridge between the inferior vena cava and the tricuspid ring was a critical anatomic "closing" point in all clockwise and counterclockwise circuits. Right atrial macroreentry underlies rare AF. Direction of activation tends to be opposite to that in common AF. The cause of the positive deflection is unclear.

Adult↗
PubMed1990

Intracardiac coiling of permanent atrial leads.

We have observed intracardiac movement of permanently implanted atrial pacing leads in two patients with AAI pacemakers. This resulted in looping of the lead body into the right atrium and ventricle, without displacement of the tip or changes in the pacing or sensing thresholds. At surgery only a single fixation ligature was found and allowed sliding of the lead through the suture sheath, in both cases. The position was corrected by gently pulling the lead. Multiple ligature fixation may avoid this complication.

Aged↗
PubMed1990

[Permanent atrial stimulation (AAI) in the sick sinus syndrome].

A consecutive series of 18 patients (5 males, 13 females, mean age +/- DS 65 +/- 12 and 66 +/- 13 years, respectively, and mean +/- DS Wenckebach point of 162 +/- 20 ppm) given arterial pacemakers for sinus node dysfunction (SND) were followed to study the incidence of lead failure, atrioventricular conduction disturbances and chronic atrial tachyarrhythmias. The mean follow up time +/- SD was 18 +/- 10 months. There was not lead dislodgement. Chronic voltage output was reduced to 2.5 volts in 73% of patients because of a reduced chronic pacing threshold. One patient presented acute transient rise of pacing threshold and temporary loss of atrial detection. Progression to AV block was not documented. One patient had asymptomatic Wenckebach AV block during the night while on digoxin plus amiodarone. The AV block disappeared after cessation of drug therapy. Patients with previous episodes of paroxysmal atrial fibrillation did not presented the arrhythmia during follow up, while 75% of patients with previous atrial flutter presented the arrhythmia. None of the patients had systemic embolism. In conclusion, AAI pacing is a reliable and safe mode of pacing in patients with SND.

Aged↗