Anees Thajudeen

Arrhythmias After Heart Transplantation: Mechanisms and Management

Heart transplantation (HT) has significantly altered the treatment paradigm for end-stage heart disease. With current surgical techniques and postoperative immunosuppression, 1-year survival after HT is ≈90%, 5-year survival is ≈70%, and median survival exceeds 10 years.[1][1]–[3][2] These

Iron Deposition following Chronic Myocardial Infarction as a Substrate for Cardiac Electrical Anomalies: Initial Findings in a Canine Model

Purpose Iron deposition has been shown to occur following myocardial infarction (MI). We investigated whether such focal iron deposition within chronic MI lead to electrical anomalies. Methods Two groups of dogs (ex-vivo (n = 12) and in-vivo (n = 10)) were studied at 16 weeks post MI. Hearts of animals from ex-vivo group were explanted and sectioned into infarcted and non-infarcted segments. Impedance spectroscopy was used to derive electrical permittivity () and conductivity (). Mass spectrometry was used to classify and characterize tissue sections with (IRON+) and without (IRON-) iron. Animals from in-vivo group underwent cardiac magnetic resonance imaging (CMR) for estimation of scar volume (late-gadolinium enhancement, LGE) and iron deposition (T2*) relative to left-ventricular volume. 24-hour electrocardiogram recordings were obtained and used to examine Heart Rate (HR), QT interval (QT), QT corrected for HR (QTc) and QTc dispersion (QTcd). In a fraction of these animals (n = 5), ultra-high resolution electroanatomical mapping (EAM) was performed, co-registered with LGE and T2* CMR and were used to characterize the spatial locations of isolated late potentials (ILPs). Results Compared to IRON- sections, IRON+ sections had higher, but no difference in. A linear relationship was found between iron content and (p<0.001), but not (p = 0.34). Among two groups of animals (Iron (<1.5%) and Iron (>1.5%)) with similar scar volumes (7.28%±1.02% (Iron (<1.5%)) vs 8.35%±2.98% (Iron (>1.5%)), p = 0.51) but markedly different iron volumes (1.12%±0.64% (Iron (<1.5%)) vs 2.47%±0.64% (Iron (>1.5%)), p = 0.02), QT and QTc were elevated and QTcd was decreased in the group with the higher iron volume during the day, night and 24-hour period (p<0.05). EAMs co-registered with CMR images showed a greater tendency for ILPs to emerge from scar regions with iron versus without iron. Conclusion The electrical behavior of infarcted hearts with iron appears to be different from those without iron. Iron within infarcted zones may evolve as an arrhythmogenic substrate in the post MI period.

Correlation of Scar in Cardiac MRI and High‐Resolution Contact Mapping of Left Ventricle in a Chronic Infarct Model

Endocardial mapping for scars and abnormal electrograms forms the most essential component of ventricular tachycardia ablation. The utility of ultra‐high resolution mapping of ventricular scar was assessed using a multielectrode contact mapping system in a chronic canine infarct model.

Mapping and Ablation of Ventricular Tachycardia From the Left Upper Fascicle How to Make the Most of the Fascicular Potential

Triggered activity or localized reentry in the fascicular system can give rise to premature impulses or ventricular tachycardia (VT). The diagnosis of fascicular rhythms relies on the recording of the His bundle potential before the onset of surface ventricular activation.1 Radiofrequency catheter ablation can be performed successfully by identification of the earliest fascicular potential (FP).2 The following cases illustrate how the comparison of the FP-V interval between sinus rhythm (SR) and VT can help to identify the successful ablation site. ### Case 1 A 50-year-old man presented with symptoms of fatigue and frequent premature ventricular contractions (PVC) that were refractory to medical therapy. Left ventricular systolic function was normal as measured by echocardiography. On a 12-lead ECG, the PVCs were relatively narrow with an incomplete right bundle branch block morphology and normal axis, suggestive of origin from the proximal left fascicular system (Figure 1A). Electrophysiology study and mapping were performed during PVCs with a 4-mm catheter electrode via a retrograde aortic approach. Right bundle branch block was noted because of inadvertent mechanical block of the right bundle branch during manipulation of the right ventricular catheter. The ablation catheter was positioned near the distal His bundle or proximal left bundle with H-V (His-V) interval of 52 ms during SR and 24 ms during PVCs (Figure 2A). The catheter was then positioned at the proximal left anterior fascicle (LAF) with recordings of FP-V (fascicular potential-V) interval of 38 ms during SR and PVCs (Figure 2C). Radiofrequency was applied at this site with 30 W at 60°C that resulted in complete elimination of PVCs and LAF block (Figure 1B). The proximal left posterior fascicle (LPF) and distal LAF were also mapped before radiofrequency application. FP-V interval was measured as 29 ms during SR versus 17 ms during PVCs at the site of the proximal …Triggered activity or localized reentry in the fascicular system can give rise to premature impulses or ventricular tachycardia (VT). The diagnosis of fascicular rhythms relies on the recording of the His bundle potential before the onset of surface ventricular activation. Radiofrequency catheter ablation can be performed successfully by identification of the earliest fascicular potential (FP). The following cases illustrate how the comparison of the FP-V interval between sinus rhythm (SR) and VT can help to identify the successful ablation site.

Paradoxical Increase in Stimulus to Atrium Interval During Para-Hisian Pacing

A 40-year-old gentleman has undergone electrophysiological study for paroxysmal palpitation. Surface electrocardiogram during sinus rhythm showed no preexcitation. The AH and HV intervals during sinus rhythm were 104 and 40 ms, respectively. There was no dual AV node physiology demonstrated. Para-Hisian pacing was performed to exclude a septal bypass tract which showed an interesting response (Fig. 1). Para-Hisian pacing demonstrated relatively broader (104 ms) and narrow (60 ms) QRS morphologies with stimulus to atrium (S–A) intervals of 156 and 175 ms, respectively. The atrial activation sequence with the 2 QRS morphologies is not similar (Fig. 2). The ventricular activation has also changed from the left to the right panels, with the proximal left ventricle (as suggested by the V electrogram [EGM] in the coronary sinus [CS] electrodes 5, 6, 3, 4, 1, and 2) and para-Hisian right ventricle are relatively early when the QRS

“Classical” Response in a Pre-excited Tachycardia What Are the Pathways Involved?

A 24-year-old patient presented with history of recurrent palpitation and was diagnosed as wide QRS tachycardia which was cardioverted. The sinus rhythm ECG and the tachycardia ECG are shown in Figure 1. During the electrophysiological study, 2 morphologies of tachycardia were inducible, 1 with right bundle branch block (RBBB) morphology (Figure 2A) and another with left bundle branch block (LBBB) morphology (Figure 2B), which was her clinical tachycardia. The LBBB type wide QRS tachycardia was faster (Figure 2B). During the RBBB morphology tachycardia, ventricular entrainment showed a V–A–V response and a His refractory ventricular extrastimulation advanced the retrograde atrial activation, resetting the tachycardia. Figure 1. Twelve-lead electrocardiograms of the patient in sinus rhythm ( A ) and during clinical tachycardia ( B ). Figure 2. Surface leads I, III, and V1 and intracardiac electrograms from right atrium (HALO 1, 2 at lateral right atrium to HALO 17, 18), His bundle (His bundle distal [HBED] and His bundle middle [HBEm]), the coronary sinus (coronary sinus distal [CSD] and coronary sinus proximal [CSP]) and right ventricular apex (RVA). A , The orthodromic tachycardia with right bundle branch block aberrancy. B , The left bundle branch block tachycardia of shorter cycle length and long ventricular–His of 80 ms with the same retrograde eccentric atrial activation as in the initial tachycardia. The LBBB morphology tachycardia showed variation in cycle length with a constant Ventriculo–Atrial (VA) interval. Atrial entrainment did not change the QRS morphology or VA relationship. An early premature atrial extrastimulation from the lateral right atrium showed an interesting finding (Figure 3). Very late atrial extrastimulus from the same location did not advance the V without affecting the septal A. What are the mechanisms of the two tachycardia? Figure 3. Surface leads I, III, and V1 and intracardiac electrograms from right atrium (HALO 1, 2 at lateral right atrium to HALO …

Radiofrequency Ablation of Left Atrial Reentrant Tachycardias in Rheumatic Mitral Valve Disease: A Case Series.

Left atrial (LA) reentrant tachycardias are not uncommon in regions where rheumatic heart disease is prevalent. Some of these arrhythmias may be curable by radiofrequency ablation (RFA). However, there are limited data pertaining to this in existing literature.

Radial left ventricular dyssynchrony by speckle tracking in apical versus non apical right ventricular pacing- evidence of dyssynchrony on medium term follow up

Introduction: To study effects of various sites of right ventricular pacing lead implantation on left ventricular function by 2-dimensional (2D) speckle tracking for radial strain and LV dyssynchrony. Methods: This was retrospective prospective study. Fifteen patients each with right ventricular (RV) apical (RV apex and apical septum) and non-apical (mid septal and low right ventricular outflow tract [RVOT]) were programmed to obtain 100% ventricular pacing for evaluation by echo. Location and orientation of lead tip was noted and archived by fluoroscopy. Electrocardiography (ECG) was archived and 2D echo radial dyssynchrony was calculated. Results: The baseline data was similar between two groups. Intraventricular dyssynchrony was significantly more in apical location as compared to non-apical location (radial dyssynchrony: 108.2 ± 50.2 vs. 50.5 ± 24, P < 0.001; septal to posterior wall delay [SLWD] 63.5 ± 27.5 vs. 34 ± 10.7, P < 0.001, SPWD 112.5 ± 58.1 vs. 62.7 ± 12.1, P = 0.003). The left ventricular ejection fraction was decreased more in apical location than non apical location. Interventricular dyssynchrony was more in apical group but was not statistically significant. The QRS duration, QTc and lead thresholds were higher in apical group but not statistically significant. Conclusion: Pacing in non apical location (RV mid septum or low RVOT) is associated with less dyssynchrony by specific measures like 2D radial strain and correlates with better ventricular function in long term.

Response to letter to editor titled “Para-Hisian Pacing Maneuver: A Pitfall in the Pitfall”: MOHANAN NAIR et al .

To the Editor We thank Ali et al.1 for reading our article and giving their interpretations and comments. In the EP image, we presented an interesting response to para-Hisian pacing. We know thatwith para-Hisian pacing it is possible to capture atrial myocardium, theHis bundle (H), and ventricularmyocardium (V) in any combination. With ventricular capture alone, QRS is wider with morphology of left bundle branch block (LBBB). His bundle and ventricular capture is associated with a narrower QRS and with pure His bundle capture, the QRS morphology is very narrow and the same as a sinus beat. In addition, there will be a delay between the pacing stimulus and local ventricular activation on the distal His electrodes, suggesting that local ventricular myocardium was not captured and “pulled in” by the pacing stimulus.1 In our case, the second paced QRS was very narrow with a duration of 60 ms with delayed activation of local ventricular myocardium at the His electrode suggesting pure His capture. The first paced QRS was broader (with QRS duration of 104 ms) than the second but without any complete LBBB morphology, suggesting His andmyocardial capture.2 A change in atrial activation as well as ventricular activation pattern was seen with pure His versus His and myocardial capture.3 With para-Hisian pacing (beat 1), the activation in atria is through the rightsided accessory pathway. With pure Hisian Capture (beat 2), the activation pattern is different and consistent with mixed pathway and nodal conduction as interpreted by Ali et al.Here, retrograde AV nodal conduction is thought to be delayed because of the shorter H-H interval as pointed out in the letter. Our hypothesis is that in beat 2, the activation spreads via His bundle, left bundle, and then transseptally conducts to the right ventricle before going via the pathway back to the atrium. This is responsible for the longer stimulation to atrial activation time. The patient has incomplete right bundle branch block in the basal electrocardiogram, consistent with our hypothesis. The accessory pathway was mapped to 7 o’clock of the tricuspid annulus and unfortunately mapping catheter was not available at the time of para-Hisian pacing to demonstrate the true earliest atrial activation. In short with simultaneous His bundle and myocardial capture producing broader QRS, the retrograde conduction is faster via the right accessory pathway, whereas with pure Hisian capture with left bundle branch activation and transseptal conduction, it takes longer time for retrograde activation to the atria. In this index case, narrow to broad paced QRS morphologies were not demonstrated during para-Hisian pacing. The accessory pathway was mapped to 7 o’clock of the tricuspid annulus and successfully ablated. We too agree that the index case highlights how a conventional pacingmaneuver could produce complex responseswith intriguing electrophysiological phenomena and different interpretations.

Response of Narrow QRS Tachycardia to Late Coupled PVC: What Is the Mechanism?: Arrhythmia Rounds

A 45-year-old gentleman was referred for radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead electrocardiogram (ECG) was normal during sinus rhythm. The electrophysiological study showed an atriohisian (AH) interval of 84 ms and hisioventricular (HV) interval of 37 ms during sinus rhythm. Ventricular pacing showed concentric activation of the atrium with nondecremental conduction. Atrial pacing reproducibly induced regular narrow QRS tachycardia. A late coupled premature ventricular extra delivered during tachycardia demonstrated an interesting phenomenon (Fig. 1). What is the likely mechanism?