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A Sippensgroenewegen

Publications and source records attributed to A Sippensgroenewegen.

6 recordsLinked to original sources

Electrocardiographic analysis of ectopic atrial activity obscured by ventricular repolarization: P wave isolation using an automatic 62-lead QRST subtraction algorithm.

INTRODUCTION: Atrial activity on the surface ECG during premature beats and supraventricular arrhythmias frequently is obscured by the superimposed QRST complex of the previous cardiac cycle. This study examines the performance of a newly developed automatic QRST subtraction algorithm to isolate ectopic P waves from the preceding T-U wave. METHODS AND RESULTS: The 62-lead ECG recordings were obtained during (1) sinus rhythm and programmed right atrial stimulation in 12 patients (group A); and (2) sinus rhythm and atrial premature beats, atrial tachycardia, or paroxysmal atrial fibrillation in 5 patients (group B). Pacing in group A patients was conducted at a slow drive cycle length to generate an ectopic P wave not obscured by the previous QRST complex and by delivering single premature extrastimuli at progressively shorter coupling intervals to produce an ectopic P wave obscured by the upsloping (early T-U wave), peak (middle T-U wave), and downsloping component of the T-U wave (late T-U wave). All ectopic P waves in group B patients were concealed by the preceding T-U wave. Automatic QRST subtraction was attained using an adaptive template constructed from averaged QRST complexes (mean 83 +/- 25 complexes) obtained during sinus rhythm (groups A and B) or atrial overdrive pacing (group A). P wave integral maps subsequently were computed, visually compared, and mathematically correlated. A high correspondence in spatial map pattern was observed between integral maps of "nonobscured" and previously "obscured" paced P waves obtained in group A patients (mean r = 0.88 +/- 0.07) as well as between integral maps of two to three previously obscured P waves with the same atrial arrhythmia morphology obtained in group B patients (mean r = 0.94 +/- 0.05). Improved morphologic P wave replication in group A patients was acquired when concealment occurred in the early (mean r = 0.90 +/- 0.08) or late part of the T-U wave (mean r = 0.90 +/- 0.06) as opposed to the middle T-U wave (mean r = 0.85 +/- 0.07) (P = NS and P < 0.05 for early vs middle and late vs middle T-U wave, respectively). CONCLUSION: This novel automatic 62-lead QRST subtraction algorithm enables discrete isolation of T-U wave obscured ectopic atrial activity on the surface ECG while retaining the intricate spatial detail in P wave morphology. Future clinical application of the algorithm may enable improved ECG localization of focal triggers of paroxysmal atrial fibrillation, atrial tachycardia, and the atrial insertion of accessory pathways.

Adult↗

Low-power radiofrequency application and intracardiac echocardiography for creation of continuous left atrial linear lesions.

INTRODUCTION: Continuity of radiofrequency (RF) lesions for a catheter-based cure of atrial fibrillation is essential in order to avoid reentrant tachycardias. In the present study, we assessed the value of intracardiac echocardiography and preablation electrode-tissue interface parameters for creation of left atrial linear lesions. METHODS AND RESULTS: In six healthy dogs, two left atrial linear lesions (lesion 1, along the inferior posterior left atrium; lesion 2, from the appendage to the left atrial roof) were attempted via a transseptal approach using a deflectable catheter with six 7-mm coil electrodes. In a randomized fashion, one lesion was performed under echocardiographic guidance and one with blinded echocardiographic monitoring. The following preablation parameters were assessed for every coil electrode: (1) mean atrial electrogram amplitude of six consecutive sinus beats; (2) diastolic pacing threshold; and (3) temperature response to application of 5 W for 10 seconds. After ablation (target temperature 70 degrees C, maximum power 50 W, duration 60 sec), the excised left atrium was examined macroscopically and histologically for lesion length, continuity, and presence or absence of lesions associated with each coil. Out of 12 attempted RF lesions, 7 were continuous (length, 47+/-5 mm, lesion 2, n = 6) and 5 were discontinuous (lesion 1, n = 5). Fifty-two of 70 coil electrodes (74%) had pathologic evidence of lesion creation. Intracardiac echocardiography was superior to fluoroscopy with respect to the actual number of coil electrodes creating lesions, and lesion continuity was correctly predicted in 9 of 12 lesions. Intracardiac echocardiography was 85% sensitive and 54% specific in predicting lesions created by individual coils. The correlation between the mean 60-second ablation temperature and the preablation parameters was 0.45 for the electrogram amplitude, -0.67 for the pacing threshold, and 0.81 for the temperature response to low-power application. Sensitivity and specificity for prediction of lesions created by individual coils, respectively, were 84% and 48% for the electrogram amplitude, 90% and 68% for the pacing threshold, and 96% and 76% for the low-power RF application. CONCLUSION: Long linear lesions can be safely and effectively performed in the canine left atrium, using a tip-deflectable multielectrode catheter. Intracardiac echocardiography may be helpful for positioning the ablation catheter in some parts of the left atrium, and preablation parameters, especially a nontraumatic low-power RF application, are able to predict ultimate lesion creation with high accuracy.

Animals↗

Electrocardiographic identification of abnormal ventricular depolarization and repolarization in patients with idiopathic ventricular fibrillation.

OBJECTIVES: We sought to gain more insight into the arrhythmogenic etiology of idiopathic ventricular fibrillation (VF) by assessing ventricular depolarization and repolarization properties by means of various electrocardiographic (ECG) techniques. BACKGROUND: Idiopathic VF occurs in the absence of demonstrable structural heart disease. Abnormalities in ventricular depolarization or repolarization have been related to increased vulnerability to VF in various cardiac disorders and are possibly also present in patients with idiopathic VF. METHODS: In 17 patients with a first episode of idiopathic VF, 62-lead body surface QRST integral maps, QT dispersion on the 12-lead ECG and XYZ-lead signal-averaged ECGs were computed. RESULTS: All subjects of a healthy control group had a normal dipolar QRST integral map. In patients with idiopathic VF, either a normal dipolar map (29%,), a dipolar map with an abnormally large negative area on the right side of the thorax (24%) or a nondipolar map (47%) were recorded. Only four patients (24%) had increased QT dispersion on the 12-lead ECG and late potentials could be recorded in 6 (38%) of 16 patients. During a median follow-up duration of 56 months (range 9 to 136), a recurrent arrhythmic event occurred in 7 patients (41%), all of whom had an abnormal QRST integral map. Five of these patients had late potentials, and three showed increased QT dispersion on the 12-lead ECG. CONCLUSIONS: In patients with idiopathic VF, ventricular areas of slow conduction, regionally delayed repolarization or dispersion in repolarization can be identified. Therefore, various electrophysiologic conditions, alone or in combination, may be responsible for the occurrence of idiopathic VF. Body surface QRST integral mapping may be a promising method to identify those patients who do not show a recurrent episode of VF.

Adult↗

Value of body surface mapping in localizing the site of origin of ventricular tachycardia in patients with previous myocardial infarction.

OBJECTIVES: This study examined the performance of the 62-lead body surface electrocardiogram (ECG) in identifying the site of origin of ventricular tachycardia in patients with a previous myocardial infarction. BACKGROUND: Because the accuracy of ECG localization of ventricular tachycardia using standard 12-lead recordings is restricted to the identification of rather large ventricular areas, application of multiple torso lead recordings may augment the resolving power of the surface ECG and result in more discrete localization of arrhythmogenic foci. METHODS: Thirty-two patients were selected for electrophysiologically guided ablative therapy for drug-resistant postinfarction ventricular tachycardia. In these patients, QRS integral maps of distinct monomorphic ventricular tachycardia configurations were correlated with a previously generated infarct-specific reference data base of paced QRS integral maps. Each paced pattern in the data base corresponded with ectopic endocardial impulse formation at 1 of 18 or 22 discrete segments of the left ventricle with a previous anterior or inferior myocardial infarction, respectively. Electrocardiographic localization was compared with the results obtained during intraoperative or catheter endocardial activation sequence mapping. RESULTS: Body surface mapping was performed during 101 distinct ventricular tachycardia configurations. Compared with the activation mapping data that were acquired in 64 of 101 ventricular tachycardias, body surface mapping identified the correct segment of origin in 40 (62%) of 64 tachycardias, a segment adjacent to the segment where the arrhythmia actually originated in 19 (30%) of 64 tachycardias and a segment disparate from the actual segment of origin in 5 (8%) of 64 tachycardias. With respect to infarct location, the segment of origin was correctly identified in 28 (60%) of 47 ventricular tachycardias in patients with anterior, 7 (70%) of 10 tachycardias in patients with inferior and 5 (71%) of 7 tachycardias in patients with combined anterior and inferior myocardial infarction. CONCLUSIONS: This study shows that body surface mapping enables precise localization of the origin of postinfarction ventricular tachycardia in 62% and regional approximation in 30% of tachycardias. The multiple-lead ECG may be used to guide and shorten catheter-based mapping procedures during ventricular tachycardia and to provide relevant information on the origin of tachycardias that cannot be mapped with conventional single-site mapping techniques because of unfavorable characteristics.

Body Surface Potential Mapping↗