Ectopic atrial rhythm after superior septal approach to the mitral valve - an often under-reported entity.

Purpose: Very few reports elaborate on the changes in P wave following superior septal approach to the mitral valve. We aimed to describe the changes in the P wave axis and other electrocardiographic changes following this approach among patients preoperatively in sinus rhythm. Methods: We did a retrospective review of medical records among all our patients undergoing superior septal approach for mitral valve surgery from September 2014 to September 2019. Electrocardiograms during hospital stay and until 6-month follow-up were analyzed. A deviation in P wave axis from the normal range of + 30 to + 60° was classified as ectopic atrial rhythm. Results: In the study population of 47 patients (age 16-75 years, 51.3 ± 13.6 years; M:F ratio 3.7:1), who were in normal sinus rhythm preoperatively, 34 patients (72.3%) had a visible P wave on electrocardiogram (ECG) at discharge. Among them, the P wave axes of 17 patients (36.2%) were within normal range (normal sinus rhythm), whereas 17 patients (36.2%) had ectopic atrial rhythm at discharge. The most frequent abnormal P wave axis was between 0 and - 30° (12 patients). At 6 months, 8 patients (17.0%) had a persistent ectopic atrial rhythm. These patients underwent a Holter test at 6 months and were followed up for symptomatic bradycardia for 3 years. None of the patients with ectopic atrial rhythm required pacemaker insertion. Conclusion: Persistence of ectopic atrial rhythm at 6 months is common (17%) after superior septal approach. Documentation of P wave axis after this approach will help avoid missing it. These patients may be kept on follow-up to look for symptomatic bradycardia.

Narrow QRS Tachycardia: What Is the Mechanism?

A 45-year-old man was referred for radiofrequency catheter ablation of narrow QRS tachycardia that terminated with intravenous adenosine. A 12-lead electrocardiogram showed no baseline pre-excitation. The echocardiogram was essentially normal. The electrophysiological study showed a normal atrial-His interval of 110 ms and a His-ventricular interval of 44 ms during sinus rhythm. An anterograde study demonstrated no dual atrioventricular nodal physiology. Atrial pacing protocols easily and reproducibly induced a narrow QRS tachycardia. What is the mechanism of the tachycardia?

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?

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?

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?

Interesting case of narrow QRS tachycardia with atrioventricular dissociation.

A 30-year-old man with no structural heart disease has been evaluated for paroxysmal palpitation with documented regular narrow QRS tachycardia that has not responded to intravenous adenosine. Surface electrocardiogram has not shown any pre-excitation. He has been taken for an electrophysiology study after informed consent. Diagnostic catheters were placed at the coronary sinus, His bundle region, and right ventricle. During catheter manipulation a regular narrow QRS tachycardia with incomplete right bundle branch block morphology and normal QRS axis similar to the clinical tachycardia got induced. No other tachycardia was induced. What is the mechanism of tachycardia?

Arterial Discordance in Cardiac Tamponade.

Ventricular interdependence is a salient hemodynamic feature of cardiac tamponade that manifests as discordance between the left and right ventricles in filling and ejection on hemodynamic assessment. Ventricular interdependence can manifest as arterial discordance at the level of the great arteries.

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?

Response of narrow QRS tachycardia to premature atrial extra. What is the mechanism?

A 60-year-old woman was referred for radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead ECG showed no baseline preexcitation. Echocardiogram was essentially normal. The electrophysiological study showed a normal AH interval of 114 ms and HV interval of 48 ms during sinus rhythm. Anterograde study demonstrated no dual AV nodal physiology. Atrial pacing protocols easily and reproducibly induced narrow QRS tachycardia (Fig. 1A & 1B). Premature atrial extra (PAE) stimuli were delivered during the tachycardia (Fig. 2). What is the mechanism of the tachycardia?