Initiation Of Tachycardia Research Articles

Initiation and termination of a wide complex tachycardia by an atrial beat

Initiation and termination of a wide complex tachycardia by an atrial beat

Mechanisms of Vein of Marshall-Related Tachyarrhythmias and the Impact of Ethanol Infusion.

The Ligament of Marshall (LOM) is a remnant of the embryonic sinus venosus and the left cardinal vein, containing a combination of fat, fibrous tissue, blood vessels, muscle bundles, nerve fibers, and ganglia. Various muscular connections exist between the LOM and the left atrium (LA) and the coronary sinus (CS). The LOM is richly innervated by autonomic nerves, with ganglion cells distributed around it. The unique characteristics of the LOM are responsible for generating focal electrical activities and enable it to serve as a substrate for micro- and macro-reentrant circuits. This, in turn, leads to the initiation and perpetuation of atrial fibrillation (AF) and atrial tachycardia (AT). Endocardial ablation in this region does not consistently succeed due to anatomical constraints within the left lateral LA, including the presence of a thicker and longer mitral isthmus (MI), anatomical variations between the MI and epicardial structures such as the CS and vein of Marshall (VOM) and circumflex artery, and the presence of fibrofatty tissue insulating the LOM. Furthermore, epicardial ablation is challenging for inexperienced institutions because of its invasive nature. Ethanol infusion into the VOM (EI-VOM) represents an effective and safe approach that can be employed in conjunction with radiofrequency ablation to eliminate this arrhythmogenic structure.

Successful caudal vena cava and pulmonary vein isolation in healthy horses using 3D electro-anatomical mapping and a contact force-guided ablation system.

Recently, treatment of equine atrial tachycardia by three-dimensional electro-anatomical mapping (3D EAM) and radiofrequency catheter ablation (RFCA) has been described. Myocardial sleeves in the caudal vena cava and pulmonary veins are a potential trigger for initiation and perpetuation of atrial tachycardia and atrial fibrillation in the horse. Isolation of these myocardial sleeves by RFCA may be an effective treatment for these arrhythmias. To describe the feasibility of 3D EAM and RFCA to isolate caudal vena cava and pulmonary veins in adult horses using 3D mapping and a contact force (CF)-guided ablation system. In vivo experiments. 3D EAM and RFCA was performed in five horses without cardiovascular disease under general anaesthesia, using the CF-guided system CARTO®3. Point-by-point RFCA aimed for isolation of caudal vena cava and pulmonary veins. Radiofrequency energy was delivered in power-controlled mode with a target power of 45 W, CF between 10 and 15 g and 30 mL/min irrigation rate, until an ablation-index of 450-500 was reached. In the right atrium, myocardial sleeves of the caudal vena cava were isolated (n = 5). In the left atrium, isolation of ostium II (n = 3), ostium III (n = 1) and ostium I, II and III en bloc (n = 1) was performed. Successful isolation was confirmed by entrance and exit block. Horses were euthanised at the end of the procedure, so long term effects such as potential reconnection of isolated veins could not be studied. This is the first description of 3D EAM and RFCA with CARTO®3 in horses, thereby showing the technical feasibility and successful caudal vena cava and pulmonary vein isolation. CF measurement allowed monitoring of catheter-tissue contact, resulting in efficient acute lesion creation as confirmed by entrance and exit block. This is a promising treatment for cardiac arrhythmias in horses.

Initiation of a wide complex tachycardia: What is the mechanism?

Initiation of a wide complex tachycardia: What is the mechanism?

AP-452681-4 UNUSUAL INITIATION OF ORTHODROMIC ATRIOVENTRICULAR REENTRANT TACHYCARDIA WITH A JUNCTIONAL BEAT

Spontaneous initiation of orthodromic atrioventricular reentrant tachycardia (AVRT) is commonly noted with premature ventricular beat (PVC). In the lab it can be initiated with programmed atrial or ventricular stimulation. We report the initiation of AVRT (with left lateral accessory pathway) with a junctional beat. Case report A 69-year-old male with history of Parkinson’s, HTN, who has had palpitations for few years. Event monitor showed narrow and wide complex tachycardia and he was scheduled for electrophysiology (EP) study and catheter ablation. He presented in sinus rhythm. EP study revealed normal AH and HV intervals with no evidence of preexcitation. Narrow complex supraventricular tachycardia (SVT) initiated spontaneously as noted in the Figure. SVT (short RP) was also initiated with ventricular and atrial extra stimuli without critical AH dependence. There was eccentric atrial activation during SVT with the earliest atrial activation on distal CS. Ventricular overdrive pacing (VOD) during SVT lead to VAV response ruling out atrial tachycardia. There was LBBB during SVT that increased the VA time from 94 ms to 170 ms. The tachycardia terminated with single fused PVC with VA block. Based on these findings a diagnosis of AVRT was made and the concealed left lateral accessory pathway was ablated at 1’o clock on mitral annulus via transseptal catheterization. This case illustrates spontaneous initiation of AVRT using a left lateral accessory pathway with a junctional beat that conducted retrogradely through the accessory pathway. This is a novel finding that has not been demonstrated prior to this. Hence a junctional beat can spontaneously initiate AVRT similar to a PVC. Similarly JPC can initiate AVNRT especially during ablation at the slow pathway region and should not be presumed to be junctional tachycardia.

Substrate Mapping Alters Ventricular Tachycardia Inducibility.

Initiation of ventricular tachycardia (VT) by programmed electrical stimulation (PES) has an important role to allow mapping and assess ablation end points. We hypothesized that substrate mapping may alter VT inducibility by mechanical bumping of critical sites. Subjects with left ventricular scar-related VT that was inducible by PES who were undergoing ablation were included. PES was repeated after substrate mapping (Group I) or after time under sedation/anesthesia during which additional imaging and transeptal puncture were performed without substrate mapping (Group II). The response to the second PES was categorized as type I if the same VT was induced, type II if a different VT was induced, and type III if VT was not inducible. Twenty-eight patients (median age 66 years, 61% ischemic cardiomyopathy), 14 in Group I and 14 in Group II, were included. Age, time between initial and second PES, type of cardiomyopathy, ejection fraction, and anesthesia methods were not different between the 2 groups. Initial VT cycle length, however, was shorter in Group I (305 millisecond [range, 235-600] versus 350 millisecond [range, 235-600], P=0.016). Also, Group I required more extrastimuli to induce VT in PES 1 (2 [1-4] versus 2 [1-3], P=0.022). In Group I, following substrate mapping, the second PES induced the same VT in 3 patients (21%), a different VT in 9 (64%), and no VT in 2 (14%) patients. In contrast, in Group II the same VT was induced in 10 (71%) patients, a different VT in 3 (21%) and no VT in 1 (7%) patient (P=0.017). Mechanical effects of substrate mapping commonly alter inducibility of VT. This has important implications for catheter ablation procedure planning and acute assessment of outcome and can potentially account for some recurrent VTs that are not recognized at the time of the procedure.

A case series of very slow atrioventricular nodal reentrant tachycardia resembling junctional tachycardia.

IntroductionThe surface electrocardiography of typical atrioventricular nodal reentrant tachycardia (AVNRT) shows simultaneous ventricular‐atrial (RP) activation with pseudo R′ in V1 and typical heart rates ranging from 150 to 220/min. Slower rates are suspicious for junctional tachycardia (JT). However, occasionally we encounter typical AVNRT with slow ventricular rates. We describe a series of typical AVNRT cases with heart rates under 110/min.MethodsA total of 1972 patients with AVNRT who underwent slow pathway ablation were analyzed. Typical AVNRT was diagnosed when; (1) evidence of dual atrioventricular nodal conduction, (2) tachycardia initiation by atrial drive train with atrial‐His‐atrial response, (3) short septal ventriculoatrial time, and (4) ventricular‐atrial‐ventricular (V‐A‐V) response to ventricular overdrive (VOD) pacing with corrected post pacing interval‐tachycardia cycle length (cPPI‐TCL) > 110 ms. JT was excluded by either termination or advancement of tachycardia by atrial extrastimuli (AES) or atrial overdrive (AOD) pacing.ResultsWe found 11 patients (age 20−78 years old, six female) who met the above‐mentioned criteria. The TCL ranged from 560 to 782 ms. Except for one patient showing tachycardia termination, all patients demonstrated a V‐A‐V response and cPPI‐TCL over 110 ms with VOD. AES or AOD pacing successfully excluded JT by either advancing the tachycardia in 10 patients or by tachycardia termination in one patient. Slow pathway was successfully ablated, and tachycardia was not inducible in all patients.ConclusionsThis case series describes patients with typical AVNRT with slow ventricular rate (less than 110/min) who may mimic JT. We emphasize the importance of using pacing maneuvers to exclude JT.

Shorter post pacing interval during initiation of regular narrow QRS tachycardia. What is the mechanism?

Shorter post pacing interval during initiation of regular narrow QRS tachycardia. What is the mechanism?

Short-Long Heart Rate Variation Increases Dispersion of Action Potential Duration in Long QT Type 2 Transgenic Rabbit Model

The initiation of polymorphic ventricular tachycardia in long QT syndrome type 2 (LQT2) has been associated with a characteristic ECG pattern of short-long RR intervals. We hypothesize that this characteristic pattern increases APD dispersion in LQT2, thereby promoting arrhythmia. We investigated APD dispersion and its dependence on two previous cycle lengths (CLs) in transgenic rabbit models of LQT2, LQT1, and their littermate controls (LMC) using random stimulation protocols. The results show that the short-long RR pattern was associated with a larger APD dispersion in LQT2 but not in LQT1 rabbits. The multivariate analyses of APD as a function of two previous CLs (APDn = C + α1CLn−1 + α2CLn−2) showed that α1 (APD restitution slope) is largest and heterogeneous in LQT2 but uniform in LQT1, enhancing APD dispersion under long CLn−1 in LQT2. The α2 (short-term memory) was negative in LQT2 while positive in LQT1, and the spatial pattern of α1 was inversely correlated to α2 in LQT2, which explains why a short-long combination causes a larger APD dispersion in LQT2 but not in LQT1 rabbits. In conclusion, short-long RR pattern increased APD dispersion only in LQT2 rabbits through heterogeneous APD restitution and the short-term memory, underscoring the genotype-specific triggering of arrhythmias in LQT syndrome.

A 43-year-old man with an unusual initiation of a long RP tachycardia

A 43-year-old man with an unusual initiation of a long RP tachycardia

When and howdoes a single ventricular premature beat initiate and terminate supraventricular tachycardia?

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). Three hundred and thirty-seven consecutive patients aged above 18years 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. 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<0.05). When a single VPB was delivered during basic ventricular pacing these values were 28% versus 4%, respectively, (p<0.001). Termination of tachycardia by a single VPB was observed in nine (4.1%) patients with AVNRT and in 57 (47.5%) with AVRT (p<0.001). Initiation of SVT by a single VPB during sinus rhythm was uncommon and favored AVRT. Termination of SVT by a single VPB was commonly seen in AVRT but rarely in AVNRT. These findings can be of help when interpreting a noninvasive arrhythmia event recording.

Drivers of the dive response in trained harbour porpoises (Phocoena phocoena).

Pronounced dive responses through peripheral vasoconstriction and bradycardia enable prolonged apnoea in marine mammals. For most vertebrates, the dive response is initiated upon face immersion, but little is known about the physical drivers of diving and surfacing heart rate in cetaceans whose faces are always mostly submerged. Using two trained harbour porpoises instrumented with an ECG-measuring sound-and-movement tag (DTAG-3), we investigated the initiation and progression of bradycardia and tachycardia during apnoea and eupnoea for varying levels of immersion. We show that paranasal wetting drives bradycardia initiation and progression, whereas apnoea leads to dive-level bradycardia eventually, but not instantly. At the end of dives, heart rate accelerates independently of lung expansion, perhaps in anticipation of surfacing; however, full tachycardia is only engaged upon inhalation. We conclude that breathing drives surface tachycardia, whereas blowhole wetting is an important driver of bradycardia; however, anticipatory/volitional modulation can overrule such responses to sensory inputs.

Defining the pattern of initiation of monomorphic ventricular tachycardia using the beat-to-beat intervals recorded on implantable cardioverter defibrillators from the RAFT study: A computer-based algorithm

Arrhythmia onset pattern may have important implications on morbidity, recurrent implantable cardioverter defibrillator (ICD) shocks, and mortality, given the proposed correlation between initiation pattern and arrhythmia mechanism. Therefore, we developed and tested a computer-based algorithm to differentiate the pattern of initiation based on the beat-to-beat intervals of the ventricular tachycardia (VT) episodes in ICD recordings from the Resynchronization-Defibrillation for Ambulatory Heart Failure Trial (RAFT). Intervals on intracardiac electrograms from ICDs were analyzed backwards starting from the marker of VT detection, comparing each interval with the average tachycardia cycle length. If the morphology of the beat initiating the VT was similar to the morphology of the VT itself, the episode was considered sudden. If the morphology of the beat initiating the VT was not similar to the morphology of the VT itself, the episode was considered non-sudden. The capability of the algorithm to classify the pattern of initiation based only on the beat-to-beat intervals allows for the classification and analysis of large datasets to further investigate the clinical importance of classifying VT initiation. If analysis of the VT initiation proves to be of clinical value, this algorithm could potentially be integrated into ICD software, which would make it easily accessible and potentially helpful in clinical decision-making.

A single electrical pulse within the protective zone of each cardiac cycle prevented reperfusion-induced ventricular tachycardia in conscious mice.

Early pioneering investigators discovered, in anesthetized dogs, a protective period within the cardiac cycle. The protective period was a time within the cardiac cycle when a precisely timed stimulus prevented the initiation of ventricular fibrillation caused by an earlier stimulus. Thus, in addition to the susceptible period of repolarization discussed by Wiggers and Wegria (Am. J. Physiol. 131:296, 1940; Am. J. Physiol. 128:500, 1940), there is also a nearby protective period. This report describes a protective period within the cardiac cycle of conscious mice when a precisely timed stimulus prevented the initiation of ventricular tachycardia caused by an earlier stimulus. In addition, we tested the hypothesis that this precisely timed pulse within the protective period prevents reperfusion‐induced ventricular tachyarrhythmias in conscious mice. Mice (n = 6) were prepared to record arterial blood pressure and the electrocardiogram. In addition, a vascular occluder was placed around the left main coronary artery, and stimulating electrodes were secured onto the left ventricle. A single precisely timed electrical pulse (5 msec pulse width and 2.5 V) to the left ventricle arriving 13.9 ± 1.1 msec after the R‐wave, caused ventricular tachycardia occurring 24.9 ± 0.9 msec after the R‐wave. Importantly, a second precisely timed electrical pulse arriving 18.8 ± 0.5 msec after the first stimulus blocked the induction of ventricular tachycardia caused by the earlier stimulus. On an alternate day, the susceptibility to sustained ventricular tachycardia produced by 3.5 min of occlusion and reperfusion of the coronary artery was determined in conscious mice by use of the vascular occluder. Reperfusion resulted in ventricular tachycardia in all six mice. A precisely timed pulse within the protective period prevented ventricular tachycardia in all mice.

32 Global high density mapping of re-entry vulnerability index aids risk stratification and identifies sites of arrhythmia initiation in brugada syndrome and arvc

Introduction Initiation of reentrant ventricular tachycardia (VT) involves complex interactions between activation (AT) and repolarization times (RT). Recently, an algorithm has been developed to generate a spatial map (designated the re-entry vulnerability index-RVI) from intervals between local ATs and RTs at adjacent points over a multielectrode grid. The algorithm has been shown to accurately identify the region of a macro-reentrant circuit in two animal models (1). The aim of this study was to test the feasibility of RVI mapping in the right ventricle (RV) to aid ablation strategy of reentrant arrhythmias. Methods Patients with Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) (n=10), Brugada Syndrome (BrS) (n=14) and normal heart RV outflow tract (RVOT) VT (n=6) underwent electrophysiological studies and were followed up for 113±21 months post procedure. Unipolar electrograms were recorded from a non-contact array (St Jude Medical) placed in the RVOT and geometry created with the Ensite system. Recordings were made during a programmed electrical stimulation protocol consisting of a 600 ms drive train and S2 extras. ATs and RTs were computed from the unipolar electrograms and the RVI calculated as previously described (1). Minimum 10% of global RVI values corrected for cycle length ( RVI c 10% ) and distance between region of lowest 5% of RVI values and region of earliest activation during VT ( D min ) were computed for each patient. Results Shortest values of RVI, which represent sites of highest susceptibility to re-entry, co-localised with earliest activation point during VT in the 9 patients with ARVC/BrS where VT was initiated (figure 1). In the ARVC patients this corresponded with location of RV scar as seen on MRI. In the 6 patients with normal heart focal VT, regions of lowest RVI did not co-localise with VT origin. Distance between region of lowest RVI and region of earliest activation during VT, D min , was significantly lower in BrS and ARVC than in normal heart VT (Fig 2A). In both ARVC patients D min =0, indicating region of lowest RVI overlapped with region of earliest VT activation. Of the patients with ARVC/BrS, those with inducible VT or clinical VT at follow-up had significantly lower minimum values of RVI c than those without (−61.0±13.8 ms vs −37.1±7.1 ms) (Fig 2B). Patients with normal heart VT had highest values of RVI c (−27.0±11.3 ms). Conclusion An algorithm based on relative local ATs and RTs identifies localised regions of high susceptibility to conduction block and re-entry, with lowest RVI values localising VT origin of reentrant but not focal arrhythmias. This index could be applied to: 1. Risk stratify ARVC/BrS patients to target ICD prophylaxis. 2. Target ablation for reentrant arrhythmias which are difficult to induce or are haemodynamically unstable, without need for arrhythmia initiation. Reference . Child Net al. Heart Rhythm2015;12:1644–1653

Role of His Refractory Premature Ventricular Complexes in the Differential Diagnosis of a Left Bundle Branch Block Morphology Tachycardia

A 65-year-old man, with no significant past medical history, presented with an episode of sudden onset palpitations and lightheadedness. He was hemodynamically stable and the ECG revealed a left bundle branch block (LBBB) morphology tachycardia at 214 beats per minute (Figure 1A). The tachycardia terminated spontaneously with conversion to normal sinus rhythm and LBBB (Figure 1B). Further evaluation included a 2-dimensional echocardiogram showing a left ventricular ejection fraction of 40% to 45%, left heart catheterization showing angiographically normal coronaries, and cardiac magnetic resonance imaging revealing atypical septal motion with left ventricular ejection fraction of 60% to 65% and no scar or ischemia. The patient underwent an electrophysiology study. At baseline, the sinus cycle length was 890 ms, atrial-His interval was 64 ms, His-ventricular interval was 108 ms, and QRS duration was 120 ms. Spontaneous onset of the LBBB morphology tachycardia after a sinus beat is shown in Figure 2. The tachycardia cycle length is 306 ms, and the His-ventricular interval is 120 ms. The QRS while similar to the LBBB seen during sinus rhythm shows change in axis and the morphology in aVR is predominantly positive. There is no ventriculo-atrial conduction during the tachycardia. Attempts at entrainment from right ventricle (RV) led to termination of the tachycardia. His refractory premature ventricular complexes (PVCs) delivered from RV apex during tachycardia after the His depolarization advances the next H and V (Figure 3). What is the mechanism of the tachycardia? See Editor's Perspective by Asirvatham and Stevenson Figure 1. A , ECG showing wide complex tachycardia with left bundle branch block (LBBB) morphology. B , ECG showing sinus rhythm and LBBB. Figure 2. Spontaneous initiation of tachycardia during sinus rhythm. The first sinus complex does not conduct because of a premature ventricular complexes. The second sinus complex conducts with a His-ventricular (HV) interval of 108 …

Pathophysiology of ventricular tachyarrhythmias : From automaticity to reentry.

Ventricular arrhythmias are aheterogeneous 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 aparticular patient is helpful to define the optimal therapeutic approach, including the selection of pharmacologic agents or delineation of an ablation strategy.

Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

Atrioventricular nodal reentrant tachycardia is the most common type of supraventricular tachycardia. The initiation and maintenance of tachycardia is caused by the characteristic anatomic and electrophysiologic properties of the atrioverntricular node. Acute management for the termination of tachycardia includes pharmacologic and non-pharmacologic management. There are several options for preventing recurrence of tachycardia, and radiofrequency ablation for modulation of tachycardia circuit can be considered as a primary strategy. A thorough understanding of the unique electrophysiologic features is very essential for optimal management and best possible outcome in cases of invasive management. Key words: Supraventricular Tachycardia; AVNRT

Pattern of initiation of monomorphic ventricular tachycardia and implications on tachycardia mechanism

The incidence of sudden cardiac death, predominantly caused by ventricular tachycardia and ventricular fibrillation, is high in patients with congestive heart failure. Implantable cardiac defibrillators have improved survival in this population but defibrillator shocks can lead to low quality of life and heart failure progression. The current management of recurrent ventricular tachycardia includes ablation and anti-arrhythmic drugs and both are associated with high recurrence rates. Better understanding the mechanism of ventricular tachycardia allowing individualization of treatment may improve outcomes. Re-entry is currently accepted as the mechanism of the majority of monomorphic ventricular tachycardias in patients with congestive heart failure, being responsible for more than 90% of the ventricular tachycardia in patients with ischemic cardiomyopathy. On the other hand, some studies show a greater participation of focal arrhythmias in the genesis of ventricular tachycardia in this population. The pattern of initiation of ventricular tachycardia is divided into sudden, when the first beat of the tachycardia is morphologically similar to the rest of the tachycardia, and non-sudden, when its morphology is dissimilar. An association between the pattern of the initiation and the mechanism of ventricular tachycardia has been proposed. The pattern of initiation of ventricular tachycardia is a readily available from data stored in current generation implantable cardiac defibrillators. The association with tachycardia mechanism may allow individualization of the therapy, however evidence is lacking and further research is required.

Initiation of tachycardia with longitudinal dissociation: What is the mechanism?

Case presentation A 61-year-old man with hypertension, diabetes, and obstructive sleep apnea had a history of intermittent palpitations for 30 years that progressively increased in frequency and duration. The patient underwent an invasive electrophysiologic study, during which pacing from the right ventricular apex demonstrated earliest retrograde atrial activation along the posterior paraseptal region. Administration of intravenous adenosine (12 mg) during ventricular pacing is shown in Figure 1. There was no evidence of anterograde dual atrioventricular (AV) nodal physiology or anterograde preexcitation. Sustained supraventricular tachycardia (SVT) at a cycle length of 370 ms was induced in the baseline state with a single premature ventricular extrastimulus (Figure 2). An example of tachycardia response to a premature extrastimulus is shown in Figure 3A. What is the mechanism of the tachycardia?