Search

Aims Seeking to account for accessory atrioventricular conduction potentially leading to ventricular pre-excitation, Mahaim in the mid-20th century had described pathways between the atrioventricular conduction axis and the muscular ventricular septum. We aimed to look for such ‘paraspecific’ connections in adult human hearts. Methods and results We serially sectioned 21 hearts, covering the triangle of Koch and the aortic root, and assessing the atrioventricular node, the penetration of the conduction axis, and the bundle branches in our search for fasciculo-ventricular connections. We also calculated the length of the non-branching bundle, and if present the origin of the fasciculo-ventricular connections. The non-branching bundle was 3.6 ± 1.7 mmin length, varying from 1.7 mm to 7.2 mm. Fasciculo-ventricular connections were found in more than half of the hearts, making direct contact with the muscular septum at an average of 3.5 ± 1.7 mm from the origin of the left bundle branch, with the site of origin varying from 1.1 mm to 5.5 mm from the first fascicle of the left bundle branch. In three hearts, additional fasciculo-fascicular connections were observed in the left bundle branch. Two loops were small, but one loop extended over 9.5 mm. Conclusion We endorse the finding of Mahaim that fasciculo-ventricular pathways exist in most human hearts. We presume the identified connections had the capability of producing ventricular pre-excitation. More studies are needed to determine the potential clinical manifestations.

The recognition of the presence, location, and properties of unusual accessory pathways for atrioventricular conduction is an exciting, but frequently a difficult, challenge for the clinical cardiac arrhythmologist. In this third part of our series of reviews, we discuss the different steps required to come to the correct diagnosis and management decision in patients with nodofascicular, nodoventricular, and fasciculo-ventricular pathways. We also discuss the concealed accessory atrioventricular pathways with the properties of decremental retrograde conduction that are associated with the so-called permanent form of junctional reciprocating tachycardia. Careful analysis of the 12-lead electrocardiogram during sinus rhythm and tachycardias should always precede the investigation in the catheterization room. When using programmed electrical stimulation of the heart from different intracardiac locations, combined with activation mapping, it should be possible to localize both the proximal and distal ends of the accessory connections. This, in turn, should then permit the determination of their electrophysiologic properties, providing the answer to the question "are they incorporated in a tachycardia circuit?". It is this information that is essential for decision-making with regard to the need for catheter ablation, and if necessary, its appropriate site.

Introduction Much have been reported about esophago-left atrium fistula. However, esophago-mediastinal fistula, not reaching the left atrium, has not been studied as a different clinical entity, with different management. Methods and results We review and discuss the literature of esophago-mediastinum fistula after catheter ablation for atrial fibrillation with emphasis on the following points: the timing of its occurrence after ablation; the mechanisms and localization of the fistula; and its natural history. Conclusion We showed that esophageal stenting was associated with a better outcome in patients with esophagus-mediastinal fistula, introduced the concept of left atrial wall weakening during ablation, and suggest a possible role of contact force use in fistula formation.

The famous quotation of Winston Churchill, made in his radio broadcast of 1939 regarding Russia's next move, specifically "A riddle wrapped up in a mystery, inside an enigma," perfectly fits the current understanding of unusual accessory atrioventricular pathways, including the variants producing ventricular pre-excitation. It was many decades after their original descriptions that we came better to begin to understand most of their structure-function relationships. Their mysterious pathophysiology was sometimes unveiled after invasive treatments, such as surgical ablation of the atrioventricular conduction axis instead of the accessory pathway itself. Speculations made on this basis have largely been validated by subsequent clinical experience. Most of the names suggested for description of the pathways have stood well the test of time. For some of them, however, this is not the case, with the initial names becoming confusing. In a series of reviews, we re-visit those accessory pathways producing ventricular pre-excitation other than classical Wolff-Parkinson-White syndrome. To set the scene, in this initial review, we describe the development and anatomy of the normal atrioventricular conduction axis, along with the insulating tissues of the atrioventricular junctions. We have sought to illustrate our explanations by using virtual dissection of computerized tomographic datasets, since they retain the intact heart within the setting of the body. These images illustrate well the value of attitudinally appropriate terminology. Thereafter, we discuss the electrophysiological manifestations of the abnormal anatomical pathways which provide the potential for both accessory atrioventricular and intraventricular conduction.

Background The differential diagnosis of a supraventricular tachycardia (SVT) is accomplished using a number of pacing maneuvers. The incidence and mechanism of a single ventricular premature beat (VPB) on initiation and termination of tachycardia were evaluated during programmed electrical stimulation (PES) of the heart in patients with the two most common regular SVTs: atrioventricular re-entrant tachycardia (AVNRT) and orthodromic atrioventricular tachycardia (AVRT). Methods Three hundred and thirty-seven consecutive patients aged above 18 years with an inducible sustained AVNRT or AVRT were prospectively enrolled. Patients with more than one tachyarrhythmia mechanism were excluded. Two hundred and seventeen patients (64.4%) had typical slow/fast AVNRT and 120 (35.6%) had an orthodromic AVRT using a rapidly conducting accessory pathway for V-A conduction. In this cross-sectional study, we specifically report the analysis of tachycardia induction and termination by a single VPB. Results Tachycardia induction with a single VPB during sinus rhythm was seen in 7 of 120 AVRT and in only one of the 217 patients with AVNRT, (5.8% vs. 0.3%, p

A 28-year-old male patient with a 3-year history of re-current tachycardia was referred for electrophysiologic eval-uation and catheter ablation. The patient had no other co-morbidities. Propafenone was discontinued 7 days beforeadmission.Electrophysiologic study: normal baseline intervals dur-ing sinus rhythm (PA = 20, AH = 68, HV = 50 ms). Anarrow QRS tachycardia was repeatedly induced by a singleatrial premature beat following a pacing drive of 400 ms, orfollowing 2 premature beats delivered during sinus rhythm.In contrast, a wide QRS tachycardia was always inducedby 2 right ventricular premature beats delivered during sinusrhythm.Thisleftbundlebranchblock(LBBB)-liketachycar-dia with a cycle length of 330–340 ms would spontaneouslychange into a slower, narrow QRS tachycardia with a cyclelengthof370msafterstabilizationoftheRRinterval(Fig.1).Transitionfromwidetonarrowtachycardiawassudden.Thecycle length of the first RR interval after disappearance oftheLBBBpatternwas310msbutincreasedthereafter.Whatwas the mechanism of change in cycle length?

A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction.We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats.Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB.

Background— Epicardial mapping and ablation of accessory pathways through a subxiphoid approach can be an alternative when endocardial or epicardial transvenous mapping has failed. Methods and Results— We reviewed acute and long-term follow-up of 21 patients (14 males) referred for percutaneous epicardial accessory pathway ablation. There was a median of 2 previous failed procedures. All patients were highly symptomatic, 8 had atrial fibrillation (3 with cardiac arrest) and 13 had frequent symptomatic episodes of atrioventricular reentrant tachycardia. Six patients (28.5%) had a successful epicardial ablation. Five patients (23.8%) underwent a successful repeated endocardial mapping, and ablation after epicardial mapping yielded no early activation site. Epicardial mapping was helpful in guiding endocardial ablation in 2 patients (9.5%), showing that the earliest activation was simultaneous at the epicardium and endocardium. Four patients (19%) underwent successful open-chest surgery after failing epicardial/endocardial ablation. Two patients (9.5%) remained controlled under antiarrhythmic drugs after unsuccessful endocardial/epicardial ablation. Two patients had a coronary sinus diverticulum and one a right atrium to right ventricle diverticulum. Three patients acquired postablation coronary sinus stenosis. There was no major complication related to pericardial access. Conclusions— Percutaneous epicardial approach is an alternative when conventional endocardial or transvenous epicardial ablation fails in the elimination of the accessory pathway. A new attempt by endocardial approach was successful in a significant number of patients. Open-chest surgery may be required in symptomatic cases refractory to endocardial–epicardial approach.

Radiofrequency (RF) catheter ablation is the treatment of choice in patients with accessory pathways (APs) and Wolff-Parkinson-White syndrome. Endocardial catheter ablation has limitations, including the inability to map and ablate intramural or subepicardial APs. Some of these difficulties can be overcome using an epicardial approach performed through the epicardial venous system or by percutaneous catheterisation of the pericardial space. When a suspected left inferior or infero-paraseptal AP is refractory to ablation or no early activation is found at the endocardium, a transvenous approach via the coronary sinus is warranted because such epicardial pathways can be in close proximity to the coronary venous system. Associated congenital abnormalities, such as right atrial appendage, right ventricle diverticulum, coronary sinus diverticulum and absence of coronary sinus ostium, may also hamper a successful outcome. Percutaneous epicardial subxiphoid approach should be considered when endocardial or transvenous mapping and ablation fails. Epicardial mapping may be successful. It can guide and enhance the effectiveness of endocardial ablation. The finding of no epicardial early activation leads to a more persistent new endocardial attempt. When both endocardial and epicardial ablation are unsuccessful, open-chest surgery is the only option to eliminate the AP. info:eu-repo/semantics/publishedVersion

Background The electrophysiologic characteristics of decrementally conducting accessory pathways (APs) are well described; however, little is known about decrementally conducting APs caused by the radiofrequency ablation of a rapidly conducting AP. Objective To report the clinical, electrocardiographic, and electrophysiologic characteristics of 6 patients who developed a decremental AP after an attempt at ablation. Methods We compared the clinical and electrophysiologic characteristics of 295 consecutive patients with the Wolff-Parkinson-White syndrome who underwent radiofrequency ablation of 311 manifest APs (group A) with those of 6 patients with the Wolff-Parkinson-White syndrome in whom a decrementally conducting AP was detected after an attempt at ablation. Results The AP ablation site in group B patients was at the coronary sinus ostium region in 3 patients, middle cardiac vein in 2 patients, and left posteroseptal region in 1 patient. Sixty-two bypass tracts in group A patients and all 6 in group B patients were ablated at these locations, while 249 bypass tracts in group A patients and none in group B patients were ablated elsewhere ( P = .0001). Five of the 6 patients (83%) with acquired Mahaim physiology had an AP located in the venous system. The odds for developing an acquired decremental antegrade atrioventricular AP when it was located inside the venous system were 1 in 6. All group B decremental APs were sensitive to adenosine, but none in 85 group A patients ( P Conclusions The risk for developing decremental conduction after the ablation of a rapidly conducting AP is greater for APs inside the coronary venous system. Acquired decremental antegrade atrioventricular APs are electrophysiologically similar to de novo ones. They are capable of being part of an arrhythmia circuit and, therefore, should be targeted for ablation.