A Simple Method to Differentiate Atrioventricular Node Reentrant Tachycardia from Orthodromic Reciprocating Tachycardia.

Discrimination between atrioventricular node reentry tachycardia (AVNRT) and orthodromic reciprocating tachycardia (ORT) during an electrophysiological study is sometimes challenging. This study aimed to investigate if the difference in the local VA (ventricle-atrium) interval during ventricular entrainment pacing and during tachycardia (DVA, defined as the shortest local VA interval of coronary sinus [CS] during entrainment minus the shortest local VA interval of CS during tachycardia) was different in patients with AVNRT and patients with ORT.Diagnoses of AVNRT or ORT through a concealed accessory pathway (AP) were made according to conventional electrophysiological criteria and ablation results. Entrainment by right ventricular (RV) pacing was performed in each patient before ablation and patients with successful entrainment were included in the study. The DVA was compared between patients with AVNRT and patients with ORT. The DVA in patients with AVNRT was significantly longer than that in patients with ORT (120 ± 20 versus 5.7 ± 9; P < 0.001). In each patient with AVNRT of slow-fast type, fast-slow type, and slow-slow type, the DVA was more than 48 ms. In each patient with ORT using a left free wall accessory pathway (AP), right free wall AP, and septal AP, the DVA was less than 20 ms.DVA was found to be a rapid, useful test in distinguishing patients with AVNRT from those with ORT.

Palpitations in a 72-year-old woman.

CLINICAL INTRODUCTION: A 72-year-old woman presented with an 8-year history of palpitations occurring every few weeks. They were sudden in onset, were associated with dizziness and could last for up to 2 hours. She was prescribed bisoprolol which reduced the frequency of events but did not abolish them. Baseline ECG and echocardiography were normal. She was referred for electrophysiological study. Despite initial difficulties, diagnostic catheters were placed in the right ventricular (RV) apex and in the coronary sinus (CS) via the right internal jugular vein and superior vena cava (SVC) (figure 1A). A narrow complex tachycardia was easily induced, and ablation was then delivered during tachycardia with the ablation catheter positioned as shown in (figure 1A). This terminated tachycardia 4 s after onset of energy delivery and on follow-up she has remained asymptomatic. She later underwent a CT scan (figure 1B,C; online supplementary video).DC1SP110.1136/heartjnl-2017-311734.supp1Supplementary file 1 heartjnl;103/19/1554/F1F1F1Figure 1(A) Fluoroscopy of catheter placement. (B) Sagittal contrast-enhanced CT image. (C) Axial contrast-enhanced CT. QUESTION: What anatomical abnormality caused difficulty in catheter placement during the procedure?Azygous continuation of the inferior vena cava (IVC)Giant Eustachian valveDextrocardiaRenal tumour compressing IVC.

Pathophysiology of ventricular tachyarrhythmias : From automaticity to reentry.

Ventricular arrhythmias are a heterogeneous group of arrhythmias and may arise in patients with cardiomyopathy or structurally normal hearts. The electrophysiologic mechanisms responsible for the initiation and maintenance of ventricular tachycardia include enhanced automaticity, triggered activity, and reentry. Differentiating between these three mechanisms can be challenging and usually requires an invasive electrophysiology study. Establishing the underlying mechanism in a particular patient is helpful to define the optimal therapeutic approach, including the selection of pharmacologic agents or delineation of an ablation strategy.

Sinus Node Dysfunction and Atrial Fibrillation: A Reversible Phenomenon?

BACKGROUND: Symptomatic sinus node dysfunction (SND) consists of a variety of manifestations, including tachycardia-bradycardia syndrome. Atrial fibrillation (AF) is commonly associated with SND, which complicates the management of both conditions. This paper reviews the epidemiology, pathophysiology, and clinical trial data investigating therapeutic approaches for treatment of patients with both SND and AF. METHODS: The authors reviewed articles published in English describing the epidemiology, pathophysiology, and therapeutic approaches for patients with SND and AF. The search was conducted using PubMed. Keywords included: sick sinus syndrome, sinus node dysfunction, atrial fibrillation, pacing, and pulmonary vein isolation. RESULTS: SND affects up to one in five patients with AF. AF can lead to anatomical and electrophysiological remodeling in both atria, including the region of sinoatrial node. Changes including atrial fibrosis, altered calcium channel metabolism, and transformed gene expression have been demonstrated in patients with AF and SND. Nonrandomized clinical trial data have failed to demonstrate whether any pacing strategy can reduce the risk of AF. Pulmonary vein isolation appears to decrease episodes of tachybrady syndrome and sinus pauses. CONCLUSIONS: SND affects up to one in five patients with AF. The pathophysiological derangements in gene expression, ion channel metabolism, and alterations in myocardial architecture associated with AF may lead to anatomic and electrical changes in the region of the sinoatrial node. Ablation may improve symptoms associated with SND in patients with AF. Future randomized trials are needed to clarify the epidemiology and optimal management of patients with SND and AF.

Effect of anisotropy on ventricular vulnerability to unidirectional block and reentry by single premature stimulation during normal sinus rhythm in rat heart.

Single high-intensity premature stimuli when applied to the ventricles during ventricular drive of an ectopic site, as in Winfree's "pinwheel experiment," usually induce reentry arrhythmias in the normal heart, while single low-intensity stimuli barely do. Yet ventricular arrhythmia vulnerability during normal sinus rhythm remains largely unexplored. With a view to define the role of anisotropy on ventricular vulnerability to unidirectional conduction block and reentry, we revisited the pinwheel experiment with reduced constraints in the in situ rat heart. New features included single premature stimulation during normal sinus rhythm, stimulation and unipolar potential mapping from the same high-resolution epicardial electrode array, and progressive increase in stimulation strength and prematurity from diastolic threshold until arrhythmia induction. Measurements were performed with 1-ms cathodal stimuli at multiple test sites (n = 26) in seven rats. Stimulus-induced virtual electrode polarization during sinus beat recovery phase influenced premature ventricular responses. Specifically, gradual increase in stimulus strength and prematurity progressively induced make, break, and graded-response stimulation mechanisms. Hence unidirectional conduction block occurred as follows: 1) along fiber direction, on right and left ventricular free walls (n = 23), initiating figure-eight reentry (n = 17) and tachycardia (n = 12), and 2) across fiber direction, on lower interventricular septum (n = 3), initiating spiral wave reentry (n = 2) and tachycardia (n = 1). Critical time window (55.1 ± 4.7 ms, 68.2 ± 6.0 ms) and stimulus strength lower limit (4.9 ± 0.6 mA) defined vulnerability to reentry. A novel finding of this study was that ventricular tachycardia evolves and is maintained by episodes of scroll-like wave and focal activation couplets. We also found that single low-intensity premature stimuli can induce repetitive ventricular response (n = 13) characterized by focal activations.NEW & NOTEWORTHY We performed ventricular cathodal point stimulation during sinus rhythm by progressively increasing stimulus strength and prematurity. Virtual electrode polarization and recovery gradient progressively induced make, break, and graded-response stimulation mechanisms. Unidirectional conduction block occurred along or across fiber direction, initiating figure-eight or spiral wave reentry, respectively, and tachycardia sustained by scroll wave and focal activations.

New Validated Signal-averaging-based Electrocardiography Method to Determine His-ventricle Interval.

BACKGROUND/AIM: The signal-averaging (SA) technique is used to record high-resolution electrocardiograms (HRECGs) showing cardiac micropotentials. We aimed to develop a non-invasive signal-averaging-based portable bedside device to determine His-ventricle interval. PATIENTS AND METHODS: After amplifying the HRECG recordings, signal duration and voltage can be measured up to four decimal precision. To validate our system, comparison of the invasively and non-invasively determined HV intervals has been performed in 20 patients. RESULTS: Our workgroup has developed a system capable of displaying and measuring cardiac micropotentials on storable ECG. Neither related paired-sample T-test (p=0.263) nor Wilcoxon's non-parametric signed ranks test (p=0.245) showed significant deviations of the HV intervals. Furthermore, related paired-sample T-test showed strong correlation (corr=0.910, p<0.001) between HV intervals determined by electrophysiology (EP) and non-invasive measurements. CONCLUSION: Our research group managed to assemble and validate an easy to use device capable of determining HV intervals even under ambulatory conditions.

Delayed afterdepolarizations generate both triggers and a vulnerable substrate promoting reentry in cardiac tissue.

BACKGROUND: Delayed afterdepolarizations (DADs) have been well characterized as arrhythmia triggers, but their role in generating a tissue substrate vulnerable to reentry is not well understood. OBJECTIVE: The purpose of this study was to test the hypothesis that random DADs can self-organize to generate both an arrhythmia trigger and a vulnerable substrate simultaneously in cardiac tissue as a result of gap junction coupling. METHODS: Computer simulations in 1-dimensional cable and 2-dimensional tissue models were performed. The cellular DAD amplitude was varied by changing the strength of sarcoplasmic reticulum calcium release. Random DAD latency and amplitude in different cells were simulated using gaussian distributions. RESULTS: Depending on the strength of spontaneous sarcoplasmic reticulum calcium release and other conditions, random DADs in cardiac tissue resulted in the following behaviors: (1) triggered activity (TA); (2) a vulnerable tissue substrate causing unidirectional conduction block and reentry by inactivating sodium channels; (3) both triggers and a vulnerable substrate simultaneously by generating TA in regions next to regions with subthreshold DADs susceptible to unidirectional conduction block and reentry. The probability of the latter 2 behaviors was enhanced by reduced sodium channel availability, reduced gap junction coupling, increased tissue heterogeneity, and less synchronous DAD latency. CONCLUSION: DADs can self-organize in tissue to generate arrhythmia triggers, a vulnerable tissue substrate, and both simultaneously. Reduced sodium channel availability and gap junction coupling potentiate this mechanism of arrhythmias, which are relevant to a variety of heart disease conditions.

Clinical and electrophysiological characteristics of typical atrioventricular nodal reentrant tachycardia in the elderly - changing of slow pathway location with aging.

BACKGROUND: The aim of this study was to retrospectively evaluate the clinical and electrophysiological characteristics of elderly patients with typical atrioventricular nodal reentrant tachycardia (AVNRT), and to assess the acute safety and efficacy of slow-pathway radiofrequency (RF) ablation in this specific group of patients. METHODS AND RESULTS: The present study retrospectively included a total of 1,290 patients receiving successful slow-pathway RF ablation for typical slow-fast AVNRT. Patients were divided into 2 groups: group I included 1,148 patients aged <65 years and group II included 142 patients aged >65 years. The required total procedure duration and total fluoroscopy exposure time were significantly higher in group II vs. group I (P=0.005 and P=0.0001, respectively). The number of RF pulses needed for a successful procedural end-point was significantly higher in group II than in group I (4.4 vs. 7.2, P=0.005). While the ratio of the anterior location near to the His-bundle region was significantly higher in group II, the ratio of posterior and midseptal locations were significantly higher in group I (P=0.0001). The overall procedure success rates were similar. There was no significant difference between the 2 groups in respect of the complications rates. CONCLUSIONS: This experience demonstrates that RF catheter ablation, targeting the slow pathway, could be considered as first-line therapy for typical AVNRT patients older than 65 years as well as younger patients, as it is very safe and effective in the acute period of treatment.

Coronary sinus activation pattern in the differential diagnosis of regular atrial tachyarrhythmias during catheter ablation of atrial fibrillation.

BACKGROUND: Prompt diagnosis and management of atrial tachyarrhythmias (ATAs) during catheter ablation of atrial fibrillation (AF) is still challenging. METHODS AND RESULTS: In 88 patients undergoing catheter ablation of AF, 128 regular ATAs were induced or converted from AF. The coronary sinus activation time (CSAT) around the mitral annulus (MA) was measured as the difference in activation time between the most proximal and distal poles of the coronary sinus (CS) electrodes. Entrainment pacing was performed around the MA, roof area, or cavotricuspid isthmus (CTI) depending on the CSAT result. Mechanisms of tachycardias included macro-reentry around the MA (perimitral atrial flutter [PM-AFL], n=63), roof-dependent AFL (Roof-AFL, n=14), CTI-dependent AFL (CTI-AFL, n=25), and atrial tachycardia (AT, n=26). When the CSAT was ≥ 45 ms, the MA activation sequence was sequential, either proximal to distal or distal to proximal. When the CSAT was <45 ms, the MA activation sequence was mainly non-sequential with converging or diverging patterns. CSAT <45 ms was highly sensitive in ruling out PM-AFL from other left ATAs. When combined with PPI data from the MA, roof area or CTI, PM-, Roof-, CTI-AFL and AT was successfully differentiated with a high predictive accuracy. CONCLUSIONS: A diagnostic algorithm combining CSAT and entrainment pacing is helpful to assess the mechanism of ATAs during catheter ablation of AF.

Phase-2 reentry in cardiac tissue: role of the slow calcium pulse.

Phase-2 re-entry is thought to underlie many causes of idiopathic ventricular arrhythmias as, for instance, those occurring in Brugada syndrome. In this paper, we study under which circumstances a region of depolarized tissue can re-excite adjacent regions that exhibit shorter action potential duration (APD), eventually inducing reentry. For this purpose, we use a simplified ionic model that reproduces well the ventricular action potential. With the help of this model, we analyze the conditions that lead to very short action potentials (APs), as well as possible mechanisms for re-excitation in a cable. We then study the induction of re-entrant waves (spiral waves) in simulations of AP propagation in the heart ventricles. We show that re-excitation takes place via a slow pulse produced by calcium current that propagates into the region of short APs until it encounters excitable tissue. We calculate analytically the speed of the slow pulse, and also give an estimate of the minimal tissue size necessary for allowing reexcitation to take place.

Instability in action potential morphology underlies phase 2 reentry: a mathematical modeling study.

BACKGROUND: Phase 2 reentry occurs when electrotonic current propagates from sites of normal notch-and-dome action potentials (APs) to loss-of-dome abbreviated AP sites, causing abnormal reexcitation. The existence of two neighboring regions exhibiting these two different AP morphologies is believed to be sufficient for local reexcitation and development of phase 2 reentry. OBJECTIVE: The purpose of this study was to investigate the mechanism of phase 2 reentry development in simulated tissues having no gradient or continuous gradients of ionic currents that affect phase 2. In particular, we investigated gradients of the transient outward current conductance G(to), representing hypothesized right ventricular G(to) gradients. METHODS: Single-cell simulations of Luo-Rudy dynamic model cells with a range of G(to) values were performed. In addition, one-dimensional fiber simulations were used to investigate the spatiotemporal phenomenon of phase 2 reentry. RESULTS: In single-cell simulations, low and normal values of G(to) produced the notch-and-dome morphology, whereas high values of G(to) produced abbreviated APs with loss-of-dome morphology. However, intermediate values of G(to) caused cells to switch intermittently between the two morphologies during constant pacing. Phase 2 reentry occurred in homogeneous and heterogeneous cable simulations, but only when a mass of cells had G(to) values close to the unstable "switching" behavior range. CONCLUSION: A main factor underlying phase 2 reentry apparently is not the presence of two different stable morphologies in adjacent regions but rather unstable switching AP morphology within a significant subset of cells.

Focal activities and re-entrant propagations as mechanisms of gastric tachyarrhythmias.

BACKGROUND & AIMS: Gastric arrhythmias occur in humans and experimental animals either spontaneously or induced by drugs or diseases. However, there is no information regarding the origin or the propagation patterns of the slow waves that underlie such arrhythmias. METHODS: To elucidate this, simultaneous recordings were made on the antrum and the distal corpus during tachygastrias in open abdominal anesthetized dogs using a 240 extracellular electrode assembly. After the recordings, the signals were analyzed, and the origin and path of slow wave propagations were reconstructed. RESULTS: Several types of arrhythmias could be distinguished, including (1) premature slow waves (25% of the arrhythmias), (2) single aberrant slow waves (4%), (3) bursts (18%), (4) regular tachygastria (11%), and (5) irregular tachygastria (10%). During regular tachygastria, rapid, regular slow waves emerged from the distal antrum or the greater curvature, whereas, during irregular tachygastria, numerous variations occurred in the direction of propagation, conduction blocks, focal activity, and re-entry. In 12 cases, the arrhythmia was initiated in the recorded area. In each case, after a normal propagating slow wave, a local premature slow wave occurred in the antrum. These premature slow waves propagated in various directions, often describing a single or a double loop that re-entered several times, thereby initiating additional slow waves. CONCLUSIONS: Gastric arrhythmias resemble those in the heart and share many common features such as focal origin, re-entry, circular propagation, conduction blocks, and fibrillation-like behavior.

Ablación de la taquicardia intranodal: cuando la fisiología cuenta en la era de la anatomía / Intranodal tachycardia ablation: when physiology is important in the era of anatomy

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Two atrial reentrant tachycardias originating from the superior vena cava: electrophysiological characteristics and radiofrequency ablation.

A case with two different types of atrial reentrant tachycardia of superior vena cava (SVC) origin is presented. Recent clinical studies have shown that the origin of focal atrial tachycardia typically lies in the venous structures connecting to both atria--the coronary sinus, the superior and inferior vena cava, and the pulmonary vein. These foci have atrial muscle fiber extensions which have electrophysiological characteristics essential to generation of focal ectopic firing. However, little is known about reentrant mechanism of these venous structures. In this report, we present a case of two atrial tachycardias (SVT1 and SVT2) independently originating from the SVC. SVT1 had 430 ms of tachycardia cycle length, and SVT2 had 390 ms of tachycardia cycle length. Both of them showed the character of reentry, and their earliest activations were recorded in the SVC. They were successfully eliminated by focal radiofrequency ablation in the SVC.