Our study showed that for persistent AF ablation, a specified substrate modification guided by nonlinear phase mapping could eliminate localized re-entry and non-pulmonary focal sources after pulmonary vein isolation.

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BackgroundThe aim of this study was to investigate the different substrate characteristics of repetitive premature ventricular complexed (PVC) trigger sites by the non-contact mapping (NCM).MethodsThirty-five consecutive patients, including 14 with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC) and 21 with idiopathic right ventricular outflow tract tachycardia (RVOT VT), were enrolled for electrophysiological study and catheter ablation guided by the NCM. Substrate and electrogram (Eg) characteristics of the earliest activation (EA) and breakout (BO) sites of PVCs were investigated, and these were confirmed by successful PVC elimination.ResultsOverall 35 dominant focal PVCs were identified. PVCs arose from the focal origins with preferential conduction, breakout, and spread to the whole right ventricle. The conduction time and distance from EA to BO site were both longer in the ARVC than the RVOT group. The conduction velocity was similar between the 2 groups. The negative deflection of local unipolar Eg at the EA site (EA slope3,5,10ms values) was steeper in the RVOT, compared to ARVC patients. The PVCs of ARVC occurred in the diseased substrate in the ARVC patients. More radiofrequency applications were required to eliminate the triggers in ARVC patients.Conclusions/InterpretationThe substrate characteristics of PVC trigger may help to differentiate between idiopathic RVOT VT and ARVC. The slowing and slurred QS unipolar electrograms and longer distance from EA to BO in RVOT endocardium suggest that the triggers of ARVC may originate from mid- or sub-epicardial myocardium. More extensive ablation to the trigger site was required in order to create deeper lesions for a successful outcome.

A 44-year-old man with structurally normal heart underwent catheter ablation of left ventricular summit tachycardia. The initial mapping revealed the origin of tachycardia at the junction of great cardiac vein and anterior interventricular vein. During ablation the exit site shifted to the nearby regions, which was recognized by subtle changes of 12-lead ECG. Mapping and ablating at different exit sites rendered the tachycardia noninducible.

My first days of learning about ECG was during the summer of second year at the medical school. I went through the graduation test with very little knowledge about ECG. I started learning ECG by comparing the ECG tracings with the echocardiographic results. However, the echo could not help in case of arrhythmia. So I spent my time reading the “Marriott's Practical Electrocardiography” – kind of textbook of ECG. It was so boring and I quickly gave up the goal of finishing the book. Then I changed to another strategy. Every time I saw an arrhythmic case, I went back home reading a whole chapter about some entity. This strategy proved to be effective. Gradually my skill of interpreting an ECG was built up. From the point of reading an ECG superficially and making a quick diagnosis (which is erroneous most of the time), I became very tedious in finding subtle abnormal signs. When you work really hard, life always has some rewards. I had been selected to study abroad about cardiac electrophysiology. Nowadays, being the Head of Cardiac Electrophysiology department in my hospital, my daily work is to deal with challenging arrhythmic cases. Interpreting elusive ECG tracings is always a passion for me.