Three-dimensional electroanatomical mapping guided right bundle branch pacing in congenitally corrected transposition of great arteries.

AIMS: The ideal pacing strategy has been the Achilles' heel for patients with congenitally corrected transposition of great arteries (ccTGA) with bradycardia. Various pacing modalities were documented in the literature. This article describes a novel pacing strategy and its feasibility in ccTGA with an intact ventricular septum. METHODS AND RESULTS: We prospectively recruited three patients with ccTGA who presented with symptomatic complete heart block to our institute and were evaluated. All patients were planned for conduction system pacing. Those who had more than moderate or severe systemic atrioventricular regurgitation and systemic ventricular dysfunction were planned for conduction system pacing with an additional lead in the coronary sinus (CS) tributary, i.e. bundle branch pacing optimized cardiac resynchronization therapy with the intention to achieve incremental benefit. Since right bundle pacing is not described previously and in view of anatomical complexity in location, three-dimensional (3D) anatomical mapping was done with the EnSite system and later right bundle capture is identified conventionally as that of a left bundle in a normal heart. All three patients have stable lead positions and adequate thresholds at short-term follow-up. CONCLUSION: In this report, we demonstrated the feasibility of permanent physiological pacing of the systemic ventricle by capturing the right bundle with 3D anatomical mapping guidance, which results in physiological activation of the systemic ventricle.

Interesting phenomenon during positioning of the 3830 lead deep inside the septum by rapid rotations. What is the mechanism?

A 66-year-old lady having complete AV block with narrow QRS escape had undergone left bundle branch pacing (LBB) with 4.1-F diameter 3830 Select SecureTM pacing lead (Medtronic Inc., Minneapolis, MN, USA). The pacing lead was placed with the inter-ventricular septum, 2 cm inferior to the distal His region towards the right ventricular apex, by 5 rapid turns. During the rapid turns, an interesting phenomenon was noted [Fig. 1A & B]. What is the mechanism?

Two pacing spikes on the T wave in a single-chamber pacemaker: What is the mechanism?

We report a case of a 54-year-old female, known symptomatic sick sinus syndrome, who had undergone a single-chamber pacemaker (VVI, St. Jude Medical, VERITY ADxXL SC SN 2413520) implantation in 2011. Electrocardiography (ECG) performed on a recent visit to the pacemaker clinic showed intermittent double pacing spikes on top of the T wave (Fig. 1A). What is the mechanism?

Discordant responses to his refractory premature ventricular beats (PVBs) during a regular narrow QRS tachycardia. What is the mechanism.

A 32-year-old lady was evaluated for recurrent episodes of palpitation. During one of the palpitation episodes a regular narrow QRS tachycardia was documented, and it got terminated with the administration of IV adenosine. The baseline 12 lead electrocardiogram (ECG) did not show any manifest preexcitation. There was no evidence of structural heart disease by echocardiogram. Patient underwent an electrophysiology (EP) study after informed consent. Quadripolar catheters were placed at the His region and right ventricular (RV) apex. A decapolar catheter was placed in the coronary sinus (CS) with CS 9, 10 dipoles at CS OS region and CS 1, 2 dipoles at CS distal region. A mapping & ablation catheter was positioned at right atrial (RA) appendage. Baseline atrial and ventricular pacing protocols could not be performed as both atrial and ventricular pacing were easily inducing a regular narrow QRS tachycardia. His refractory premature ventricular beats [PVBs] were delivered from RVRV apex and left ventricular [LV] free wall. Discordant responses were obtained. What is the mechanism?

Regular narrow QRS tachycardia. What is the mechanism?

A 45-years-old lady with no structural heart disease on echocardiogram presented with recurrent episodes of palpitation. There was no baseline preexcitation. Twelve lead surface electrocardiograms (ECG) recorded during one of the episodes are provided. What is the likely mechanism of the tachycardia? [Figure: see text].

Management of a complicated 'pacemaker pocket' site infection.

Pocket site infection after implantation of a pacemaker is a dreaded complication which requires removing the device and reimplanting it at a contralateral site. Difficulties arise when the patient is dependent on pacing and when there are issues with venous access at the contralateral site. We report a patient with pacemaker pocket site infection with congenital complete heart block managed with explantation of the device, semi-permanent pacing during antibiotic treatment, reimplantation of the device at the contralateral site and management of subtotal subclavian vein stenosis noted during reimplantation.

Clinical profile & long-term natural history of symptomatic coronary artery disease in young patients (<30 yr).

Background & objectives: Several studies have shown a high prevalence of cardiovascular risk factors in patients in the age group of 30-74 yr, but there is a paucity of data in young patients below 30 yr. We analyzed the clinical and coronary angiographic profile of patients <30 yr of age with symptomatic coronary artery disease (CAD) and also assessed their intermediate and long-term outcomes. Methods: All patients less than 30 yr of age who presented with symptomatic CAD from 1978 to 2017 in the department of Cardiology of a tertiary care hospital in south India, were studied for coronary risk factors and angiographic and treatment patterns, and the follow up data were collected. Results: The mean age of the 159 patients <30 yr of age was 26.7±3.29 yr. Male preponderance was observed (91.8%), 63.5 per cent patients were smokers and 88.3 per cent were dyslipidaemic. Acute myocardial infarction was the most common mode of presentation. Forty one per cent patients were non-adherent to medications. Risk factor control was inadequate with respect to smoking cessation, alcoholism, physical activity and dietary regulation. The predictors of long-term mortality were multivessel CAD [hazard ratio (HR): 1.927, 95% confidence interval (CI): 1.003-3.701] and reduction in ejection fraction (EF) (10% decrease in EF; HR: 1.349, 95% CI: 1.096-1.662). Overall mortality was 30 per cent at 10 yr and 48 per cent at 20 yr. Interpretation & conclusions: Decreasing EF and multivessel involvement were found to be the strong correlates for long-term mortality in young patients below 30 yr of age with CAD. High long-term mortality rates and poor risk factor control suggest the vast scope for the improvement of outcomes in these patients with aggressive risk factor control.

Response to atrial overdrive pacing during narrow QRS tachycardia. What is the mechanism?

A 35-year old lady with no pre-excitation on surface electrocardiogram underwent EP study for recurrent palpitation and documented adenosine responsive narrow QRS tachycardia. Regular narrow QRS tachycardia was induced with critical AH delay on programmed atrial stimulation. An atrial overdrive pacing (AOD) was performed during the tachycardia (Fig: 1 & 2). What is the response to AOD and what is the mechanism of tachycardia?

Interesting response to ventricular overdrive pacing during regular narrow QRS tachycardia. What is the mechanism?

33 year old gentleman has undergone an electrophysiology study for recurrent paroxysmal palpitation. During one of the episodes of palpitation a regular narrow QRS tachycardia was documented which has terminated with intravenous adenosine. Baseline electrocardiogram did not show any pre-excitation. Atrial-His (AH) and His-Ventricular (HV) intervals were normal at baseline. There was no evidence of dual atrioventricular (AV) nodal physiology. Earliest atrial electrogram during ventricular pacing was recorded at coronary sinus (CS) 9,10 dipoles placed at CS OS region. Narrow QRS tachycardia with cycle length (TCL) of 400 ms and earliest retrograde atrial activation at CS 9,10 dipoles was induced with programmed ventricular stimulation. Ventricular overdrive (VOD) pacing was performed at 30 ms shorter than TCL during the tachycardia (Fig: 1). What is the mechanism of tachycardia?

Response of narrow QRS tachycardia in a patient with surgical closure of atrial septal defect to atrial overdrive pacing: What is the mechanism?

A 57-year old woman who had pericardial patch closure of ostium secundum atrial septal defect (ASD) at the age of 23 years presented with shortness of breath. Her echocardiogram showed no residual ASD, good biventricular function and normal pulmonary artery pressures.

Interesting case of dual tachycardia in a patient with surgical closure of atrial septal defect.

A 34-year-old gentleman, who had undergone pericardial patch closure of ostium secundum atrial septal defect (ASD) at 8 years of age, was evaluated for shortness of breath. Electrocardiogram revealed typical atrial flutter with varying atrioventricular conduction. Echocardiogram showed no residual ASD or pulmonary hypertension and good biventricular function. He was taken for an electrophysiological study with the intention of radiofrequency ablation of the typical flutter.

Classical response of antidromic atriofascicular tachycardia to premature atrial extrastimulus delivered during septal refractoriness.

A 23-year-old gentleman presented with a history of palpitations. The 12-lead electrocardiogram showed no manifest ventricular pre-excitation. Echocardiogram was within normal limits. A retrograde study showed concentric activation of the atrium with decremental conduction. Atrial pacing from right atrial free wall showed progressive pre-excitation. No anterograde nodal duality was documented.

Interesting case of narrow QRS tachycardia. What is the mechanism?

A 67-year-old female presented with history of recurrent palpitations. During one of the episodes of palpitation, a narrow QRS tachycardia was recorded and it was reported to be terminated with intravenous adenosine. The 12-lead electrocardiogram (ECG) showed no manifest ventricular preexcitation. ECG was within normal limits. The patient underwent an electrophysiology study after informed consent. She was taking calcium channel blockers and that was stopped five half-lives prior to the procedure. As catheters were being placed, a narrow QRS tachycardia got induced. During the study, there was development of right bundle branch block during the tachycardia. What is the mechanism of the tachycardia?

Radiofrequency ablation of premature ventricular contractions originating from uncommon sites of right ventricle.

Premature Ventricular Contraction (PVC)/ventricular tachycardia (VT) with left bundle branch block (LBBB) morphology and inferior axis has been described classically to originate from the right ventricular outflow tract (RVOT). Some uncommon sites of idiopathic ventricular arrhythmia (VA) origins have been revealed including tricuspid annulus (TA) and right ventricular (RV) inflow free wall region. We present a series of two cases who have undergone electrophysiological study and successful radiofrequency ablation of frequent monomorphic PVCs with LBBB pattern originating from relatively uncommon sites of RV - TA and RV inflow free wall region.

Wide QRS tachycardia in a patient with pre excitation; what are the pathways involved? Pacing manoeuvres to characterize a unique pathway.

A 30year old patient presented to us with recurrent episodes of palpitation and documented tachycardia. In all his presentations a wide QRS tachycardia was recorded. The baseline ECG showed pre excitation. The 12 lead ECG of the tachycardia and the baseline ECG is shown in Fig. 1A. During EP study the patient had baseline pre excitation and the HV interval was 16 ms. A duo-decapolar halo (HL) catheter was used to map right atrium and a decapolar coronary sinus (CS) catheter was used to map coronary sinus. In addition a His bundle and right ventricular (RV) quadripolar catheters were used. The delta wave morphology was suggestive of a posteroseptal pathway. Ventricular pacing from RV apex showing central decremental conduction with ventriculo-atrial Wenkebach at 290 ms. Ventricular extrastimulation also showed decremental conduction and VA block at S1 S2 of 400,240. The intra cardiac recording of tachycardia and its initiation is shown in Fig. 1B. Pacing from lateral RA (HL 5, 6 electrodes) showed progressive pre excitation with extrastimulation and induction of tachycardia. The QRS morphology was same as the patient's clinical tachycardia and the tachycardia cycle length (TCL) was 304 ms. An atrial entrainment protocol showed entrainment with the same QRS morphology while pacing from right atrium. The VA interval of the first return cycle was the same as the subsequent VA intervals. A ventricular entrainment protocol showed V-A-V response and post pacing interval of 414 ms. An atrial extra systole was given from the mid CS electrodes (CS 5, 6) - the effect is shown in Fig. 3. In sinus rhythm a parahisian pacing manoeuvre was done as shown in Fig. 4A. What is the mechanism of the tachycardia and what are the pathways involved?

Narrow QRS Tachycardia with Transition: What Is the Mechanism?

A 50-year-old woman underwent radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead electrocardiogram was normal during sinus rhythm. The electrophysiological study showed normal atriohisian and hisioventricular intervals during sinus rhythm. Atrial burst pacing reproducibly induced two narrow QRS tachycardias. Figure 1 shows spontaneous switch of tachycardia 1 to tachycardia 2. What are the likely mechanisms of the tachycardia and the transition?