dysplasia

The confirmed presence of fibrous tissue in addition to the marked fatty infiltration on histology suggested the possible diagnosis of ARVD.

ARVD, known as one of the common causes of SCD during a sports activity, has not been found in our study.

The largest and most statistically significant decrease of SCD from a specific cause was a decrease in death from ARVD to 0.

Sarcoidosis Subepicardial progressing inwards, basal Amyloidosis Diffuse, subendocardial to epicardial, altered T1 kinetics Anderson-Fabry disease Mid myocardial, basal inferolateral wall, symmetrically hypertrophied myocardium, normal or increased function Myocarditis Subepicardial progressing inwards, inferolateral/lateral/anteroseptal walls, focal wall-motion abnormalities Chronic myocarditis Mid myocardial, linear ARVD RV-free wall-septum, wall-motion abnormalities, fatty replacement Endomyocardial fibrosis Diffuse subendocardial, adherent thrombus Noncompaction Enhancement of noncompacted myocardium Chagas disease Subepicardial, LV apex, inferolateral wall Muscular dystrophies Inferolateral wall

Patient's demographics, extraction indications and results Underlying Size of Case Age, Type of heart locking number years Gender arrhythmia disease stylet 1 39 M VT ARVD LLD #2 2 37 F VT Sudden LLD #2 cardiac death 3 49 M VT Ischemic LLD #1 CMP 4 52 M VT Ischemic LLD #2 CMP Size of Implantation Case laser, duration.

A known family history of hypertrophic cardiomyopathy, LQTS, cardiomyopathy or ARVD warrants further work-up.

Zareba was in charge of ECG core lab for the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) and currently runs the ECG core lab for the North American ARVD Registry (22 enrolling centers) as well as for the MADIT-CRT (100 enrolling centers).