Ivan Cakulev

Simultaneous Biatrial High-Density (510-512 Electrodes) Epicardial Mapping of Persistent and Long-Standing Persistent Atrial Fibrillation in Patients: New Insights into the Mechanism of Its Maintenance

Background— The mechanism(s) of persistent and long-standing persistent (LSP) atrial fibrillation (AF) is/are poorly understood. We performed high-density, simultaneous, biatrial, epicardial mapping of persistent and LSP AF in patients undergoing open heart surgery (1) to test the hypothesis that persistent and LSP AF are due to ≥1 drivers, either focal or reentrant, and (2) to characterize associated atrial activation. Methods and Results— Twelve patients with persistent and LSP AF (1 month to 9 years duration) were studied at open heart surgery. During AF, electrograms were recorded from both atria simultaneously for 1 to 5 minutes from 510 to 512 epicardial electrodes with ECG lead II. Thirty-two consecutive seconds of activation sequence maps were produced per patient. During AF, multiple foci (QS unipolar atrial electrograms) of different cycle lengths (mean, 175±18 ms) were present in both atria in 11 of 12 patients. Foci (2–4 per patient, duration 5–32 s) were either sustained or intermittent, were predominantly found in the lateral left atrial free wall, and likely acted as drivers. Random and nonrandom breakthrough activation sites (initial r or R in unipolar atrial electrograms) were also found. In 1 of 12 patients, only breakthrough sites were found. All wave fronts emanated from foci and breakthrough sites, and largely either collided or merged with each other at variable sites. Repetitive focal QS activation occasionally generated repetitive wannabe reentrant activation in 5 of 12 patients. No actual reentry was found. Conclusions— During persistent and LSP AF in 12 patients, wave fronts emanating from foci and breakthrough sites maintained AF. No reentry was demonstrated.

Validation of novel 3-dimensional electrocardiographic mapping of atrial tachycardias by invasive mapping and ablation: A multicenter study

OBJECTIVES This study prospectively evaluated the role of a novel 3-dimensional, noninvasive, beat-by-beat mapping system, Electrocardiographic Mapping (ECM), in facilitating the diagnosis of atrial tachycardias (AT). BACKGROUND Conventional 12-lead electrocardiogram, a widely used noninvasive tool in clinical arrhythmia practice, has diagnostic limitations. METHODS Various AT (de novo and post-atrial fibrillation ablation) were mapped using ECM followed by standard-of-care electrophysiological mapping and ablation in 52 patients. The ECM consisted of recording body surface electrograms from a 252-electrode-vest placed on the torso combined with computed tomography-scan-based biatrial anatomy (CardioInsight Inc., Cleveland, Ohio). We evaluated the feasibility of this system in defining the mechanism of AT-macro-re-entrant (perimitral, cavotricuspid isthmus-dependent, and roof-dependent circuits) versus centrifugal (focal-source) activation-and the location of arrhythmia in centrifugal AT. The accuracy of the noninvasive diagnosis and detection of ablation targets was evaluated vis-à-vis subsequent invasive mapping and successful ablation. RESULTS Comparison between ECM and electrophysiological diagnosis could be accomplished in 48 patients (48 AT) but was not possible in 4 patients where the AT mechanism changed to another AT (n = 1), atrial fibrillation (n = 1), or sinus rhythm (n = 2) during the electrophysiological procedure. ECM correctly diagnosed AT mechanisms in 44 of 48 (92%) AT: macro-re-entry in 23 of 27; and focal-onset with centrifugal activation in 21 of 21. The region of interest for focal AT perfectly matched in 21 of 21 (100%) AT. The 2:1 ventricular conduction and low-amplitude P waves challenged the diagnosis of 4 of 27 macro-re-entrant (perimitral) AT that can be overcome by injecting atrioventricular node blockers and signal averaging, respectively. CONCLUSIONS This prospective multicenter series shows a high success rate of ECM in accurately diagnosing the mechanism of AT and the location of focal arrhythmia. Intraprocedural use of the system and its application to atrial fibrillation mapping is under way.

Confirmation of novel noninvasive high-density electrocardiographic mapping with electrophysiology study: Implications for therapy

Background—Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center’s clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. Methods and Results—Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart–torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff–Parkinson–White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. Conclusions—ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Cardioversion: Past, Present, and Future

Simplicity is the ultimate sophistication. — —Leonardo da Vinci Recent years have seen rapid proliferation of ablative and antiarrhythmic therapies for treating various ventricular and supraventricular arrhythmias. Yet cardioversion and defibrillation remain the main modalities to restore normal sinus rhythm. Their simplicity, reliability, safety, and, most important, their efficacy in promptly restoring normal sinus rhythm are unmatched in our current treatment armamentarium. ### The Early Work Contemporary cardiology has been significantly affected by the ready availability of this simple method for terminating atrial and ventricular tachyarrhythmias. However, fascination with electricity and its use in biological systems is hardly contemporary. The first capacitor that was able to store electric energy in a glass container was discovered in 1745. It was named the Leyden jar, and its use was shortly thereafter tested in the electrocution of small animals. There is a large body of literature in Italy, France, and England on biological and medical application of electricity dating from the 17th and 18th centuries. Although physicians across Europe started using electricity as an experimental treatment, the earliest recorded scientific approach with the use of electric shocks was that of Peter Abildgaard in 1775.1 He systematically shocked hens, delivering electric charges in different parts of their body. Electric stimuli applied anywhere across the body of the hen, particularly in the head, could render the animal lifeless, but subsequent shocks delivered to the chest could revive the heart. Abildgaard was only one of the several scientists who studied the effects of electricity on animals. Some reported similar findings, and others could not reproduce his results. However, Luigi Galvani in 1781 first clearly described the link between electricity and its presence in biological systems.2 He was the first to use the term animal electricity , coined after his famous experiments in which he caused the legs of …

Variable Clinical Features and Ablation of Manifest Nodofascicular/Ventricular Pathways

Background—Manifest nodofascicular/ventricular (NFV) pathways are rare. Methods and Results—From 2008 to 2013, 4 cases were identified with manifest NFV pathways from 3 centers. The clinical findings and ablation sites are reported. All 4 cases presented with a wide complex tachycardia but with different QRS morphologies. Case 1 showed a left bundle branch block/superior axis, case 2 showed a right bundle branch block/inferior axis, case 3 showed a left bundle branch block/inferior axis, and case 4 showed a narrow QRS tachycardia and a wide complex tachycardia with a left bundle branch block/inferior axis. Three of the 4 tachycardias had atrioventricular dissociation ruling out extranodal accessory pathways, including atriofascicular pathways. Programmed extrastimuli showed evidence of a decremental accessory pathway in 3 of the 4 cases. Coexisting tachycardia mechanisms were seen in 3 of the 4 cases (atrioventricular nodal reentry tachycardia [2] and atrioventricular reentrant tachycardia [1]). Ablation in the slow pathway region eliminated the NFV pathway in 3 (transient in 1) with the other responding to surgical closure of a large atrial septal defect. The NFV pathway was a critical part of the tachycardia circuit in 1 and proved to be a bystander in the other 3 cases. Conclusions—Manifest NFV pathways presented with variable QRS expression dependent on the ventricular insertion site and often coexisted with other tachycardia mechanisms (atrioventricular nodal reentry tachycardia and atrioventricular reentrant tachycardia). In most cases, the atrial insertion of the pathway was in or near the slow pathway region. The NFV pathways were either critical to the tachycardia circuit or served as bystanders.

Do Not Stop the Warfarin Until

Prevention of thromboembolism is a principal aim of atrial fibrillation management. Although the mechanisms underlying thrombogenesis in atrial fibrillation are clearly complex and remain only partly understood, it is intuitive that restoration and reliable maintenance of sinus rhythm is probably

Further refinement of torsades de pointes

The notion that patients can succumb to ventricular fibrillation as a consequence of complete heart block has been known for a long time. In the initial report, Schwartz et al have described in great detail the findings leading to such an event, including the variability in the ventricular rate preceding the episode of ventricular fibrillation, “the fibrillatory waves that always followed the premature beat,” and “the appearance of bizarre and deformed ventricular complexes with prolonged RS-T segments and progressively inverted T waves from beat-to-beat prior to the onset of ventricular fibrillation.” Schwartz et al postulated correctly that most Stokes-Adams attacks are, in fact, secondary to a ventricular arrhythmia we now call torsades de pointes. As an aside, they actually called it ventricular fibrillation. Almost 2 decades later, this type of ventricular arrhythmia was described officially and named torsades de pointes by Dessertenne. However, the initiation of this arrhythmia was not characterized clinically well until a report in the early eighties by Kay et al. A large group of patients with different clinical backgrounds who developed torsades de pointes was analyzed. In addition to the description of the classical initiation of the arrhythmia with a preceding longshort cycle length sequence, a clinically important observation was made that temporary pacing is the only consistently effective therapy that prevents torsades de pointes. The fact that the incidence of torsades de pointes in patients with complete heart block is not high but, nevertheless, represents the leading cause of death in these patients creates an important clinical dilemma. In which patients is urgent intervention with pacing needed? This becomes especially important when the decision on whether to insert a temporary pacemaker before the permanent one is contemplated. Although the ACC/AHA guidelines do not specifically address the issue of temporary pacing, in asymptomatic patients with persistent third-degree atrioventricular block with stable escape rates greater than 40 beats/ min, the permanent pacemaker implantation only has a clinical recommendation level of IIa.

Insights into new-onset atrial fibrillation following open heart surgery and implications for type II atrial flutter

AIMS Postoperative atrial fibrillation (POAF), new-onset AF after open heart surgery (OHS), is thought to be related to pericarditis. Based on AF studies in the canine sterile pericarditis model, we hypothesized that POAF in patients after OHS may be associated with a rapid, regular rhythm in the left atrium (LA), suggestive of an LA driver maintaining AF. The aim of this study was to test the hypothesis that in patients with POAF, atrial electrograms (AEGs) recorded from at least one of the two carefully selected LA sites would manifest a rapid, regular rhythm with AEGs of short cycle length (CL) and constant morphology, but a selected right atrial (RA) site would manifest AEGs with irregular CLs and variable morphology. METHODS AND RESULTS In 44 patients undergoing OHS, AEGs recorded from the epicardial surface of the RA, the LA portion of Bachmanns bundle, and the posterior LA during sustained AF were analysed for regularity of CL and morphology. Sustained AF occurred in 15 of 44 patients. Atrial electrograms were recorded in 11 of 15 patients; 8 of 11 had rapid, regular activation with constant morphology recorded from at least one LA site; no regular AEG sites were present in 3 of 11 patients. CONCLUSIONS Atrial electrograms recorded during sustained POAF frequently demonstrated rapid, regular activation in at least one LA site, consistent with a driver maintaining AF.

Response to Letter Regarding Article, “Variable Clinical Features and Ablation of Manifest Nodofascicular/Ventricular Pathways”

We thank Drs Papagiannis and Kanter1 for their interest and keen attention to our recent article. We shall address each of the points raised in their letter. Case 1: There is no difference between your description of the mechanism of case I and that provided in the article. Case 2: There is again no substantive difference with regards to tachycardia mechanism. You are correct. Figure 4A shows an obvious error in that we clearly show that stim A-V increases with A2. Thank you for pointing out this oversight. Case 3: We are well aware of the differential diagnoses of mechanisms resulting in reverse activation of the His bundle,2 but these points are moot …

Paul Zoll MD: The Pioneer Whose Discoveries Prevent Sudden Death

Stafford I. Cohen 216 pages. Salem, NH: Free People Publishing, 2014.