A Case-based Approach to Pacemakers, ICDs and Cardiac Resynchronisation: Questions for Examination Review and Clinical Practice. Editors: Paul A. Friedman, Melissa A. Rott, Anita Wokhlu, Samuel J. Asirvatham, David L. Hayes. Cardiotext Publishing, LLC

Unknow

Ablation of Ventricular Arrhythmias in GUCH: The Surgical Scar and the Second Substrate

Patients with grown-up congenital heart (GUCH) disease pose a few unique problems for the cardiac electrophysiologist due to the myocardial substrate with high propensity for arrhythmias. Arrhythmias are the main reason for hospital admission in these patients and, unfortunately, in a significant proportion of these patients, these arrhythmic events could be life-threatening [1]. Furthermore, the onset of arrhythmias may herald the hemodynamic decompensation in a sizable segment of the population with already compromised functional status. The abnormal circulation, in turn, may amplify the hemodynamic effect of arrhythmias in these patients with unrepaired or partially repaired abnormal cardiac anatomy. Previous studies into the natural history of patients with GUCH have been helpful in identifying the likely risk factors for arrhythmogenesis, and the associated risk of sudden cardiac death (SCD) in them [2-4]. Clinical variables like older age at repair, ventricular dysfunction, and need of ventriculotomy at repair are known to adversely affect the survival in patients with GUCH [2-4]. In majority, the increased arrhythmogenecity, at cellular level, is mediated by the co-existing myocardial fibrosis. Ventricular fibrosis suggested by cardiovascular magnetic resonance is known to be an important marker of poor survival in adults with repaired tetralog

Mapping for the Target Sites of Ablation in Post-infarction Ventricular Tachycardia- Is Sinus Rhythm Sufficient?

The long road to success with radiofrequency ablation for scar-related ventricular tachycardia (VT) has taken the electrophysiologists down many unexpected paths in the last two decades. During this period, the progress in defining the pathological circuits involved in genesis of this complex tachyarrhythmia has undoubtedly improved the ablation outcome. However, empiricism still prevails as to how optimally map the ablation targets of this arrhythmia commonly encountered in clinical practice

Ventricular Arrhythmias in Hypertrophic Cardiomyopathy- Can We Ever Predict Them?

Hypertrophic cardiomyopathy (HCM) is characterized by gross cardiac and myocyte hypertrophy, myocyte disarray, and interstitial fibrosis. This condition is relatively common, with a prevalence of about 1:500 in the general population. Most patients with HCM are either asymptomatic or have only minimal symptoms. In general, HCM is a relatively benign disease with an annual mortality rate of slightly less than 1% in unselected HCM populations [1,2]. However, sudden cardiac death (SCD) may be the first manifestation of the disease. Approximately 60% to 70% of all patients with HCM die suddenly [3], and the fatal event is generally assumed, though not proven so far, due to ventricular arrhythmias

Clinical Characteristics To Guide The Extent Of Ablation In Paroxysmal AF Patients: Discovering An Old Science

Anthony G. Brooks, Narayanan Namboodiri, and Prashanthan Sander

Mahaim Fiber Accelerated Automaticity and Clues to a Mahaim Fiber Being Morphologically an Ectopic or a Split AV Node

Mahaim Fiber tachycardia characteristically causes a wide QRS tachycardia with left bundle branch morphology and left axis deviation, especially in young patients, having no structural heart disease. Mahaim fiber automaticity further cements the proposition of Mahaim fiber, due to its Atrioventricular (AV) node like property, being called as an ectopic AV node

Flecainide challenge test: Predictors of unmasking of type 1 Brugada ECG pattern among those with non-type 1 Brugada ECG pattern

AbstractBackgroundMany subjects in community have non-type 1 Brugada pattern ECG with atypical symptoms, relevance of which is not clear. Provocative tests to unmask type 1 Brugada pattern in these patients would help in diagnosing Brugada Syndrome. However sensitivity and specificity of provocating drugs are variable.MethodsWe studied 29 patients referred to our institute with clinical presentation suggestive but not diagnostic of Brugada or with non-Type 1 Brugada pattern ECG. Flecainide Challenge Test (FCT) was done in these patients (IV Flecainide test in 4 patients and Oral Flecainide in 25 patients). Resting 12-lead ECG with standard precordial leads and ECG with precordial leads placed 1 Intercostal space above were performed after flecainide administration every 5 min for first 30 min and every 30 min thereafter until ECG became normal or upto 6 h. The positivity was defined as inducible Type 1 Brugada pattern in atleast 2 right sided leads.ResultMedian age was 35(range = 5–65) years. In 16 (55%) patients the Type 1 Brugada pattern was unmasked. There were no episodes of major AV block, atrial or ventricular tachyarrhythmia. Three groups were considered for analysis: Group 1(n = 9) – FCT Positive among patients with non-type 1 Brugada ECG pattern, Group 2(n = 4) – FCT Negative among the patients with non-type 1 Brugada ECG pattern, and Group 3(n = 7) – FCT Positive among patients with no spontaneous Brugada ECG pattern. Binary logistic regression analysis found that family h/o SCD was predictive of FCT positivity in Group 1 (Odd’s ratio 21, 95% Confidence interval 1.04 to 698.83, p = 0.004).ConclusionOral flecainide is useful and safe for unmasking of Type I Brugada pattern. In our study, among the many variables studied, family history of sudden cardiac death was the only predictor of flecainide test positivity among those with non-Type 1 Brugada pattern