Programmed ventricular stimulation in structural heart disease: Implications of patterns of ventricular arrhythmias induced to long-term outcomes.

INTRODUCTION: Currently available data gives some credence to utility of VT induction studies in patients with stable ischemic cardiomyopathy, there are some unresolved questions as to define sensitive threshold for low-risk and the prognostic relevance of ill sustained or non-specific tachycardia on induction study. We evaluated potential ability of VT inducibility to predict likelihood of SHD (Structural heart disease) patients for subsequent arrhythmic or adverse cardiac events. MATERIAL AND METHODS: All consecutive patients with syncope/documented arrhythmia who had VT induction done were included and patients with VT storm, ACS,uncontrolled HF were excluded. We studied in 4 groups-monomorphic VT, sustained polymorphicVT, ill sustainedVT/VF and no VT/VF induced. The primary-endpoints were - Sudden death, all-cause mortality and secondary-endpoints were - MACE (AICD shock, death,HF, recurrence of VT). We screened 411 patients and included 169 within inducible (n = 79) and non-inducible group (n = 90). RESULTS: There were a higher number of patients with coronary artery disease, LV dysfunction, patients on amiodarone in inducible group and no difference in usage of beta-blockers. Recurrence of VT, composite of MACE was significantly higher in inducible group (p < 0.05). Mortality was not different in 3 groups compared with no VT/VF group. We found that monomorphic VT group had significantly higher MACE as compared to others and also predicted recurrence of VT and AICD shock and showed a trend towards significance for prediction of mortality. Inducible patients on AICD had mortality similar to non-inducible group. CONCLUSION: Induction of monomorphicVT/polymorphicVT with ≤3extrastimuli is associated with a higher number of MACE events on follow up. Induction of monomorphicVT predicts recurrence of VT/ICD shock.

Rheumatic Mitral Stenosis with Incidental Wolff-Parkinson-White Syndrome: A Rare Association. Treated by Percutaneous Transmitral Commissurotomy and Radiofrequency Ablation.

The combination of Wolff-Parkinson-White (WPW) syndrome and rheumatic mitral stenosis (MS) is rare in clinical practice. The management of this condition primarily depends on the clinical picture. We describe a 26-year-old male patient with no significant previous medical history and who came for a routine medical assessment before entrance to a police academy service. He was found to have rheumatic MS and WPW.

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?

Long-term effects of cardiac resynchronization therapy on electrical remodeling in heart failure-A prospective study.

INTRODUCTION: Effects of cardiac resynchronization therapy (CRT) on arrhythmogenicity and sudden death have not been fully ascertained. CRT has been shown to increase transmural dispersion of repolarization (TDR) immediately on implantation, which may favorably remodel on long-term follow-up. However, such a hypothesis has not been prospectively evaluated. METHODS AND RESULTS: We included 35 consecutive patients who underwent CRT implantation between September 2013 and August 2014 (mean age 56.8 ± 11.09 years; 71.43% males). QT and Tpeak-Tend (Tp-e) intervals were measured during endocardial (RVendoP), epicardial (LVepiP), and biventricular pacing (BiVP) at CRT implantation and 1-year follow-up. Compared to RVendoP (130.41 ± 16.75 ms), Tp-e was significantly prolonged during BiVP (142.06 ± 21.98 ms; P < 0.001) and LVepiP (183.45 ± 27.87 ms; P < 0.001) at baseline. There was a significant decrease in Tp-e during BiVP on follow-up (117.93 ± 15.03 ms; P < 0.001). High responders had significantly lower Tp-e at 1 year compared to low responders (113.16 ± 14.3 ms vs 129.59 ± 9.75 ms, P  =  0.004). Tp-e at 1 year had strong negative correlation with reduction in LV end-systolic volumes (r  =  - 0.51; P  =  0.003). Seven patients with sustained ventricular arrhythmias during follow-up had significantly longer baseline Tp-e compared to those without arrhythmias (158.19 ± 17.59 ms vs 139.72 ± 20.94 ms, P  =  0.043). A baseline Tp-e value of ≥ 148 ms had a specificity of 75% and sensitivity of 71% to predict ventricular arrhythmias. CONCLUSIONS: Baseline TDR is greater during BiVP and LV epiP compared with RVendoP in patients with heart failure. However, BiVP causes a significant reduction in TDR reflective of reverse electrical remodeling on long-term follow-up.

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

BACKGROUND: 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. CASE REPORT: Three patients who had rheumatic mitral valve disease with past history of surgical-/catheter-based intervention and having no significant residual disease had symptomatic atrial flutter despite optimal medical management. An electrophysiological study confirmed an LA focal/micro-reentrant mechanism in all. There was patchy scarring of the LA, and successful RFA of these arrhythmias could be achieved. CONCLUSION: The focal nature of the scar in these patients may suggest that the rheumatic involvement of the atrium or the hemodynamic consequence of the vulvar lesion causes nonuniform insult to the atrial tissue and limited scar. At least in some patients with limited scarring, early RFA may help in the maintenance of sinus rhythm.

Narrow QRS Tachycardia in a Patient with Tachycardiomyopathy: What Is the Mechanism?

A 50-year-old female presented with incessant palpitation of 2 weeks duration. She was hemodynamically stable and there was no evidence of heart failure. A transthoracic echocardiogram showed mild left ventricular (LV) dysfunction with LV ejection fraction of 45%. Electrocardiogram (12 lead and rhythm strip) was taken during the palpitation. What is the mechanism?

Bundle branch reentry: A rare mechanism of ventricular tachycardia in endomyocardial fibrosis, without ventricular dilation.

INTRODUCTION: Bundle branch reentry as a mechanism of ventricular tachycardia (VT) in endomyocardial fibrosis (EMF) is not described. CASE REPORT: A 52-year-old woman with left ventricular (LV) EMF had VT needing cardioversion. She had mitral regurgitation and left bundle branch block, but no LV dilation or heart failure. During electrophysiological study, clinical VT could be easily induced, and it was confirmed to be bundle branch reentrant VT (BBRVT). She was treated with ablation of the right bundle branch. CONCLUSION: BBRVT can occur in EMF even without cardiac dilatation. Its recognition is important, as radiofrequency ablation can be curative.