Atrial activation

Diastolic dysfunction was also the only independent predictor of asymmetry ASI , suggesting a common pathophysiologic pathway of the electromechanic and anatomic LA remodeling.

The present data add to our knowledge by studying the missing links between electrical, mechanical and anatomical LA remodeling in AF patients. These results invigorate previous studies showing an association between AF and the interatrial delay biphasic P wave caused by deterioration of the BB conduction or more prominent inferiorly located interatrial connections.

In accordance with the study of Xia et al, our study found that advanced age and diastolic dysfunction i. This represents a prominent increase of the anterior LA and has been previously proven to be an independent predictor for AF recurrence after CA. This is further supported by our recent findings that emphasize the pathophysiological importance of diastolic dysfunction LVDD on the asymmetric LA remodeling.

An increased LV stiffness or a decreased relaxation translates into higher LA pressure with reduced LA emptying and finally atrial dilatation, all promoting electromechanical delay and the risk for AF. These characteristics specify advanced AF that might necessitate changes in management to address the developing substrate, for example, radiofrequency ablation instead of cryoablation.

Therefore, comprehensive evaluation of the remodeling should take into account variables such as asymmetrical dilatation and changes in activation sequence. This study demonstrates that a pathologic electromechanical activation is associated with LA remodeling and that both share the casual pathway of diastolic dysfunction. Since the usual risk factors for AF progression have limited predictive value, the implementation of new and more sensitive predictors could help frame earlier and more appropriate therapeutic decisions.

Cardioversion prior to ablation and inclusion of more patients with persistent AF may have drawn a different picture. Our group is working on an automated shape analysis in a larger cohort, but ASI in this study was calculated manually, with good inter and intraobserver agreement, limiting the size of the study. Finally, since impaired LV systolic function, severe hypertrophy and valvular disease were exclusion criteria, the results of this study may not be valid for patients with these conditions.

Diastolic dysfunction is a common cause of this pathologic activation and remodeling. Left atrial activation and asymmetric anatomical remodeling in patients with atrial fibrillation: The relation between anatomy and function. Clin Cardiol. Data are available upon reasonable request from the corresponding author.

National Center for Biotechnology Information , U. Journal List Clin Cardiol v. Published online Nov Harry J.

Author information Article notes Copyright and License information Disclaimer. Sotirios Nedios, Email: moc. Corresponding author. Email: moc. This article has been cited by other articles in PMC.

Hypothesis This study aimed to identify echocardiographic parameters associated with changes in anatomy and conduction properties of the left atrium LA. Patients We prospectively studied a total of patients from to Imaging All patients underwent a comprehensive transthoracic echocardiographic examination in sinus rhythm Vivid 7, General Electric, Milwaukee, Wisconsin , according to the guidelines of the American Society of Echocardiography.

Open in a separate window. Electrophysiological study and catheter ablation An electrophysiological study was performed in all patients as previously described. Statistics Categorical variables are reported as frequencies and percentage. It is obvious, therefore, that classification based on earliest atrial retrograde activation is inappropriate.

Figure 5 and Figure 6 depicts fast-slow and slow-slow AVNRT, respectively, with earliest retrograde atrial activation at the His bundle electrode. However, both absolute and relative values may be meaningless in certain occasions. They depend on autonomic status, age, use of isoprenaline and sedatives and conduction properties of pathways involved, and may change during a single electrophysiology study.

Furthermore, when a His bundle electrogram cannot be recorded during tachycardia, a diagnosis based exclusively on them is impossible. Early studies have considered the possibility of additional AV nodal tissue extrinsic to the tachycardia circuit in order to explain various electrophysiologic phenomena observed during AVNRT,[ 20 ] and the concepts of upper and lower common pathways have been longstanding controversies of AVNRT. The breakthrough is whatever leads to atrial activation via transitional tissue; thus there are many possibilities see Figures 3 — 6.

The lower common pathway, as initially considered by Mendez and Moe,[ 24 ] has a more sound physiological basis. The notion of a lower common pathway has been utilised in order to explain phenomena of AV block without recording of a His electrogram as well as retrograde Wenckebach periodicity during AVNRT. The conduction time over the lower common pathway has been usually estimated by subtracting the His to atrium interval during tachycardia measured from the onset of the His electrogram to the onset of the atrial electrogram from that during ventricular pacing measured from the end of the His electrogram to the onset of the atrial electrogram at the same cycle length and considered a measurable interval in the majority of typical AVNRT cases.

This is often seen at the onset of very fast AVNRT, which may expose the His-Purkinje tissue to long-short periods and can lead to functional phase 3 block, having nothing to do with the reentrant circuit. The electrophysiological proof of the existence of a lower common pathway depends on several assumptions that may not be valid, in a way that even if a lower common pathway exists, applied methodologies are unable to accurately detect and measure it.

Atrial and, mainly, ventricular pacing manoeuvres during sinus rhythm or tachycardia have been used with variable success rate. In clinical practice, these techniques cannot be applied to all cases, and multiple criteria have to be used for the differential diagnosis of narrow complex tachycardias with atypical characteristics.

In Table 4 we summarise our experience with various techniques and manoeuvres for the differential diagnosis of narrow-QRS tachycardias in the electrophysiology laboratory. Usually, a combined anatomical and mapping approach is employed with ablation lesions delivered at the inferior or mid part of the triangle of Koch.

Ablation should be only directed towards the anatomic position of the slow pathway. There is no mortality associated with this procedure. National Center for Biotechnology Information , U. Journal List Arrhythm Electrophysiol Rev v. Arrhythm Electrophysiol Rev. Demosthenes G Katritsis. Author information Article notes Copyright and License information Disclaimer.

Corresponding author. Disclosure : The authors have no conflicts of interest to declare. Received Feb 7; Accepted May This article has been cited by other articles in PMC. Keywords: Atrioventricular, nodal, reentrant, tachycardia. Open in a separate window. Figure Table 1: Atrioventricular Junctional Arrhythmias.

Atrioventricular nodal reentrant tachycardia Non-reentrant junctional tachycardia Non-paroxysmal junctional tachycardia Focal junctional tachycardia Other non-reentrant variants. Electrophysiological Features Earliest Atrial Retrograde Activation Heterogeneity of both fast and slow conduction patterns has been well described, and all forms of AVNRT may display anterior, posterior and middle retrograde activation patterns.

Upper and Lower Common Pathways Early studies have considered the possibility of additional AV nodal tissue extrinsic to the tachycardia circuit in order to explain various electrophysiologic phenomena observed during AVNRT,[ 20 ] and the concepts of upper and lower common pathways have been longstanding controversies of AVNRT. References 1. Atrioventricular nodal reentrant tachycardia. DOI: Katritsis DG, Becker A. The atrioventricular nodal reentrant tachycardia circuit: A proposal.

Heart Rhythm. Connexin 43 expression delineates two discrete pathways in the human atrioventricular junction. Anat Rec. Hoboken DOI: Structure-function relationship in the sinus and atrioventricular nodes. Pediatr Cardiol. Classification of electrophysiological types of atrioventricular nodal reentrant tachycardia: a reappraisal.

Characterization of subforms of AV nodal reentrant tachycardia. Pacing Clin Electrophysiol. Patient with atrioventricular node reentrant tachycardia with eccentric retrograde left-sided activation: treatment with radiofrequency catheter ablation.

Jpn Heart J. Unusual variant of atrioventricular nodal reentrant tachycardia. Electrophysiologic characteristics of atrioventriicular nodal reentrant tachycardia: implications for reentrant circuits. Cardiac Electrophysiology: From Cell to Bedside.

Fifth edition. US: Saunders, ; pp. Heterogeneity of anterograde fast-pathway and retrograde slow-pathway conduction patterns in patients with the fast-slow form of atrioventricular nodal reentrant tachycardia: electrophysiologic and electrocardiographic considerations. Methods: Using this system, we performed intraoperative atrial activation mapping in 10 patients with chronic atrial fibrillation who were undergoing isolated mitral valve operations.

Results: Regular and repetitive activation cycle length ranged from to milliseconds originated in the left atrium in all 10 patients.

Two patterns of repetitive activation in 2 patients and three patterns in 1 patient appeared alternately during the observation period in the left atrium. In contrast to the repetitive activation in the left atrium, the activation sequence of the right atrium was extremely complex and chaotic.