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A multicenter study has described and validated a new strategy for guiding ablation procedures in patients with complex tachycardias. Ablation procedures use energy—usually heat or cold—to eliminate small areas of heart tissue that cause pathological cardiac arrhythmias, thereby restoring normal heart rhythm.
Ventricular tachycardia is a potentially life threatening cardiac arrhythmia. On the ECG, ventricular tachycardia can be defined as three or more ventricular ectopic beats occurring in a sequence at a rate more than 100 per minute. Another rare form of ventricular tachycardia is bidirectional ventricular tachycardia.
A 64-year-old male with recurrent ventricular tachycardia (VT) was referred for repeat ablation. He had undergone three prior VT ablation procedures elsewhere. Reports from his previous VT ablation procedures suggested low endocardial voltage at the basal inferior/inferoseptal left ventricle.
Mapping data in post-myocardialinfarction (MI) patients describe ventricular tachycardia (VT) re-entry circuits of slow VT, that are typically related to transmural scars. Fast VTs with cycle lengths close to the refractory period may be related to functional re-entry in the scar border zone (BZ).
Three or more ventricular beats in a row at a rate above 100 per minute is termed ventricular tachycardia. Ventricular tachycardia lasting more 30 seconds or requiring termination earlier due to hemodynamic compromise is called sustained ventricular tachycardia. Either case, the treatment is ablation of the right bundle.
Different imaging modalities have been used to image and display scar tissue accelerating substrate identification and streamlining mapping and ablation of ventricular tachycardias (VTs). Integration of CMR data has been used to identify an area of interest for mapping and ablation of VT in patients with prior infarctions2.
The activation signal, or signature, defined as the cumulative number of recording sites that have activated per millisecond, was utilized to segment each re-entrant ventricular tachycardia (VT) circuit into inner and outer circuit pathways, and as an estimate of best ablation lesion location to prevent VT. sites activating/ms).
Troponin T peaked at 38,398 ng/L ( = a very large myocardialinfarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ).
A 34 yo woman with a history of HTN, h/o SVT s/p ablation 2006, and 5 months post-partum presented with intermittent central chest pain and SOB. ng/mL This single initial troponin at this level, in the context of chest pain, is high enough to be diagnostic of acute myocardialinfarction. This was sent by a colleague.
Background:Patients with adult congenital heart disease (ACHD) form a unique subset of patients with complex ventricular tachycardia (VT).Objective:To The primary composite outcome was recurrent monomorphic VT, and repeat ablation.Results:Out of 508 procedures for ventricular tachycardiaablation, 37 were performed in ACHD patients.
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