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J Almendral

Publications and source records attributed to J Almendral.

At least 37 records · Page 2Linked to original sources

[Electric treatment of atrial fibrillation].

In the present manuscript the information concerning electrical therapy of atrial fibrillation (AF) to prevent its development and to control its consequences (excluding ablation which will be covered in separate manuscripts of this series) is reviewed. Both presently conventional approaches and those undergoing investigation will be considered, under three general headings. Electrical stimulation to prevent the development of AF. Based on non controlled studies comparing VVI stimulation with other modalities that include stimulation of the atria, it was suggested that atrial stimulation could prevent AF recurrences in patients with sinus node dysfunction. This concept has been questioned in recent studies. In contrast, the hypothesis that specific ways of atrial stimulation (stimulation at sites other than the high right atrium, multisite simultaneous or with certain "delays" atrial stimulation) may be more efficacious is presently under enthusiastic assessment. Electrical stimulation to control ventricular response. Despite the evidence that ventricular stimulation may contribute to regularization and rate control during AF, its quantitative value seems to be scarce and, thus, is not of regular use in practice. Automatic implantable atrial defibrillator. Both animal experiments and clinical studies have demonstrated that the atria can be defibrillated using intracavitary electrodes with less than 3 joules in most cases, and without risk of inducing ventricular tachyarrhythmias as long as shocks are synchronized to the R wave and the preceding R-R interval is not short. Although an implantable atrial defibrillator is already undergoing clinical evaluation, the subject of tolerability of patients to shocks for non malignant arrhythmias is still controversial, since even low energy shocks seem to be painful.

Atrial Fibrillation↗

[Comparative study of 3 algorithms to localize the accessory pathway in Wolff-Parkinson-White syndrome].

BACKGROUND AND OBJECTIVES: Some electrocardiographic algorithms have been developed to predict the location of the accessory pathway in the WPW syndrome. Few studies address the interobserver variability of such algorithms and the possible observer-dependent changes of accuracy. This study analyzes three algorithms to localize accessory pathways recently published, comparing the inter-observer variability, their predictive value and the most frequent problems observed during their application. METHODS: Ninety-six electrocardiograms from patients who underwent successful ablation of a single accessory pathway were reviewed. The location of each pathway was predicted by two independent observers according to three different reported electrocardiographic algorithms. The interobserver agreement, percentage of correct predictions and critical steps of each algorithm were analyzed. RESULTS: The interobserver agreement varied between 64 and 79% and the accuracy between 38 and 67%. The best results were obtained in the left lateral accessory pathways (69 to 89% correctly located). All the algorithms presented critical steps at which more than 20% of pathways were incorrectly classified. CONCLUSIONS: The analyzed algorithms present a high interobserver variability. The accuracy obtained is clearly lower than that reported by the corresponding authors. These facts should be considered when being used them in clinical settings.

Adult↗

[Bradycardia and asystolia secondary to epileptic crisis. Report of a case].

We report the case of a 21 year old man with bradycardia and asystolia after a seizure. No cardiac disease could be demonstrated, but electroencephalography after sleep deprivation showed the presence of a temporal irritative focus. The importance of differential diagnosis between cardiogenic syncope and loss of consciousness due to epilepsy is discussed.

Adult↗

Evidence favoring the hypothesis that ventricular arrhythmias have prognostic significance in left ventricular hypertrophy secondary to systemic hypertension.

In the present review 6 lines of evidence will be discussed that suggest a prognostic significance for ventricular arrhythmias in patients with systemic hypertension and left ventricular hypertrophy: (1) in patients with systemic hypertension there is a statistical relation between asymptomatic ventricular arrhythmias and left ventricular hypertrophy; (2) in nonhypertensive left ventricular hypertrophy the prognostic value of ventricular arrhythmias is well known; (3) left ventricular hypertrophy is related to sudden death in patients with systemic hypertension; (4) it is generally acknowledged that ventricular arrhythmias are a frequent cause of sudden death; (5) there is experimental evidence to support the arrhythmic risk of left ventricular hypertrophy; and (6) it has been recently demonstrated that ventricular arrhythmias influence mortality in patients with left ventricular hypertrophy secondary to systemic hypertension. However, whether asymptomatic ventricular arrhythmias are specific markers for more severe sustained arrhythmias, or just markers for a more severe stage of the disease, remains to be determined.

Arrhythmias, Cardiac↗

[Radiofrequency ablation of a posteroseptal accessory pathway associated with coronary sinus diverticulum].

The case of a patient with a symptomatic Wolff-Parkinson-White syndrome undergoing attempted radiofrequency catheter ablation of a posteroseptal accessory pathway is described. Coronary sinus venography revealed the presence of a diverticulum attaching near the os. The electrogram recorded from a catheter placed in the narrow neck of the diverticulum revealed a short atrioventricular time during sinus rhythm. The pathway was easily ablated using radiofrequency energy applied in the neck of the diverticulum, after multiple failed attempts at catheter ablation from the endocardial surface of the posteroseptal space. Our report emphasizes the importance of searching for a coronary venous diverticulum in all patients with posterior accessory pathways undergoing catheter ablation.

Adult↗

Identification of concealed posteroseptal Kent pathways by comparison of ventriculoatrial intervals from apical and posterobasal right ventricular sites.

BACKGROUND: The differential diagnosis of supraventricular tachycardia with concentric atrial activation usually requires the inducibility of sustained tachycardia and needs a complex and time-consuming electrophysiological evaluation. To develop a simple test to establish if ventriculoatrial conduction uses a posteroseptal accessory pathway or the normal conduction system, we compared the ventriculoatrial intervals during right ventricular pacing from apical and posterobasal sites. METHODS AND RESULTS: Continuous pacing was performed from an apical and a posterobasal right ventricular site in 34 patients with retrograde conduction over the normal conduction system (group A) and in 22 patients with conduction over a posteroseptal accessory pathway (group B). During apical pacing, ventriculoatrial intervals in group A (176 +/- 40 milliseconds) were not significantly different than those in group B (197 +/- 47 milliseconds, P = NS). During posterobasal pacing, group B patients had significantly shorter ventriculoatrial intervals than group A patients (158 +/- 46 versus 197 +/- 39 milliseconds, P < .01). The difference between the ventriculoatrial interval obtained during apical pacing and that obtained during posterobasal pacing (ventriculoatrial index) discriminated between the two groups without overlapping: It was positive in all group B patients (39 +/- 19; range, +10 to +70 milliseconds) and negative in all except two group A patients (-21 +/- 13; range, -50 to +5 milliseconds; P < .001). CONCLUSIONS: This ventriculoatrial index can identify accurately and in the absence of tachycardia whether concentric retrograde conduction is proceeding over a posteroseptal accessory pathway or over the normal conduction system.

Adult↗

The importance of antitachycardia pacing for patients presenting with ventricular tachycardia.

The initial experience from electrophysiological studies showed that pacing induced termination of ventricular tachycardias is usually possible but requires a critical pacing sequence. Studies on the resetting phenomenon showed, in most instances of failure of termination, that the "limiting factor" to produce ventricular tachycardia termination is usually failure to produce block within the circuit rather than failure to access or interact with the ventricular tachycardia origin. The resetting response is related to tachycardia termination in a number of ways. Of note is that a steeply increasing resetting pattern usually predicts tachycardia termination. Between 50% and 90% of induced ventricular tachycardias will be terminated by trains of rapid ventricular pacing. The analysis of the pacing rate necessary for termination shows that it varies widely. Paced cycle lengths of < 80% of tachycardia cycle length are necessary in at least 20% of tachycardias. In contrast, the incidence of acceleration is closely related to the paced cycle length: it is negligible with paced cycle lengths over 80% of tachycardia cycle length and increases to 36% with paced cycle lengths below 76% of tachycardia cycle length. Present information about efficacy of antitachycardia pacing in spontaneous tachycardias suggests that it is extremely effective, with over 90% success. However, it is likely that these data correspond to a selected group of tachycardias.

Cardiac Pacing, Artificial↗

Ventricular fusion during resetting and entrainment of orthodromic supraventricular tachycardia involving septal accessory pathways. Implications for the differential diagnosis with atrioventricular nodal reentry.

BACKGROUND: Ventricular fusion during transient entrainment of orthodromic atrioventricular reciprocating tachycardias (OAVRT) was originally found to be absent and recently observed only with left ventricular stimulation. However, previous studies were restricted to cases with a left free wall accessory pathway. The hypothesis of the present study was that fusion is likely during resetting and entrainment of OAVRT with right ventricular stimulation if the accessory pathway is septally located, since its insertion is relatively close to the stimulation site. This phenomenon can help in the differential diagnosis with atrioventricular nodal reentry (AVNR). METHODS AND RESULTS: We performed programmed right ventricular stimulation during regular inducible supraventricular tachycardia with concentric atrial activation in 44 patients--20 with OAVRT and 24 with AVNR. Fusion in the ECG morphology of extrastimuli producing resetting was observed in 19 of 19 OAVRT but in 0 of 11 AVNR reset (P < .001). Transient entrainment was demonstrated in all 31 cases undergoing rapid ventricular pacing (14 OAVRT and 17 AVNR). Entrainment with fusion occurred in 13 of 14 OAVRT and in 0 of 17 AVNR (P < .001). Fusion was critically dependent on the coupling intervals or pacing rates, sometimes having a narrow window for its observation. CONCLUSIONS: The relative proximity (conduction time) among pacing site, site of entrance to a reentrant circuit, and site of exit from the circuit to the paced chamber are critical for the occurrence of fusion during resetting and/or entrainment. The presence or absence of fusion during these phenomena can help in the differential diagnosis of certain supraventricular tachycardias.

Adolescent↗

Prognostic significance of ventricular arrhythmias in the presence of pathological left ventricular hypertrophy.

It is well known that pathological left ventricular hypertrophy, either primary or secondary to cardiac overload, is associated with a high incidence of ventricular arrhythmias and sudden death, and that asymptomatic ventricular arrhythmias seem to be related to a high incidence of sudden death in patients with hypertrophic cardiomyopathy and ischaemic heart disease. However, this association has not been prospectively evaluated in patients with hypertensive LVH, where other factors, such as myocardial ischaemia, can play an important role. More studies are needed in this respect before establishing therapeutic implications.

Arrhythmias, Cardiac↗

Frequency and implications of resetting and entrainment with right atrial stimulation in atrial flutter.

Thirty-three patients (24 with typical and 9 with atypical flutter-wave morphology) were studied to evaluate the incidence and implications of resetting and entrainment of atrial flutter with right atrial stimulation. Resetting with single extrastimulus was present in 23 cases (group A) and absent in 10 (group B). Most cases of reset flutter were typical (20 of 23). Fixed fusion indicative of entrainment was observed in all 29 cases with pacing trains. Groups A and B did not differ significantly in flutter cycle length (230 +/- 20 vs 223 +/- 19 ms), atrial functional refractory period (165 +/- 18 vs 167 +/- 22 ms) or longest paced cycle length producing entrainment (213 +/- 19 vs 210 +/- 19 ms). In contrast, the return cycle after the longest paced cycle length producing entrainment was significantly shorter in group A (228 +/- 27 vs 284 +/- 56 ms; p = 0.001). The return cycle in group A was virtually identical to the flutter cycle length, whereas in group B it was greater (p = 0.002 compared with group A). Resetting was more frequent in typical than atypical flutter (20 of 24 vs 3 of 9; p = 0.01). Both typical and atypical flutter can be transiently entrained by right atrial pacing. Lack of resetting and longer return cycle, suggesting a longer conduction time between the reentrant circuit and the stimulation site, were mostly observed in atypical flutter. The data suggest a different location for both types of flutter, and may have implications for ablation techniques. A more cautious approach, with more extensive mapping, appears appropriate for ablation attempts of atypical flutter.

Adult↗

Rate-dependent failure of ventricular capture in patients treated with oral propafenone.

The effects of propafenone on ventricular excitability were studied in 18 patients after 9 +/- 6 days on oral propafenone (900 mg/day). Late diastolic double threshold right ventricular stimulation was performed at variable rates. In five patients (28%, group I) an intermittent, rate-dependent failure of ventricular capture was reproducibly observed during stimulation at rates above the sinus rhythm but not exceeding 150 beats min-1. In four patients loss of capture was preceded by gradual prolongation of the interval between the stimulus artifact and the local right ventricular bipolar electrogram. Such findings were not observed in the remaining 13 patients (group II) on propafenone nor in 28 studies in the same patients on different antiarrhythmic agents. Group I vs group II patients were older (72 +/- 4 vs 53 +/- 18 years, P = 0.002), had longer right ventricular effective refractory periods on the baseline (P = 0.004) and on propafenone (P = 0.0003), and had longer QRS duration on propafenone. The increase produced by propafenone in sinus rhythm QRS duration, paced QRS duration and ventricular effective refractory period was greater in group I than in group II: 42 +/- 36 vs 14 +/- 12 ms, P = 0.01, 94 +/- 43 vs 34 +/- 26 ms, P = 0.0002, 88 +/- 64 vs 22 +/- 37 ms, P = 0.025, respectively. Thus propafenone can produce rate-dependent failure of ventricular capture which is associated with marked prolongation of refractoriness and QRS duration suggesting a marked use-dependent drug effect in selected patients.

Administration, Oral↗