1. What data in particular will be shared?
   Response - All of the individual participant data collected during the trial, after de-identification.
   


2. What additional supporting information will be shared?
   Response -  Study Protocol
   Response -  Statistical Analysis Plan
   Response - Informed Consent Form
   Response - Clinical Study Report
   Response -  Analytic Code
   
   
3. Who will be able to view these files?
   Response - Researchers whose proposed use of the data has been approved by an independent review committee identified for this purpose.
   


4. For what types of analyses will this data be available?
   Response - To achieve aims in the approved proposal.
   


5. By what mechanism will data be made available?
   Response - Proposals should be directed to [drdaljeetsaggu@gamil.com].
   


6. For how long will this data be available start date provided 01-08-2025 and end date provided 01-04-2030?
   Response - Beginning 9 months and ending 36 months following article publication.
   


7. Any URL or additional information regarding plan/policy for sharing IPD? 
   Additional Information - Nil

Arrythmogenic cardiomyopathy (ACM) is an inherited cardiomyopathy characterized by frequent ventricular arrhythmias and an increased risk of sudden cardiac death (SCD)1 The disease is inherited as an autosomal dominant trait with incomplete penetrance and variable expressivity2. Diagnosis of ACM is made by a complex set of Task Force criteria (TFC), which include electrocardiographic, arrhythmia, imaging, histological, and family history criteria 3. The revision of ACM diagnostic criteria in 2010 increased the specificity of the diagnosis, but it still lacks sensitivity, especially in the early stages of the disease (3,4). Genotype/phenotype studies have shown that ACM, which was initially described as an isolated or predominant RV disease, exhibits frequent left ventricular (LV) involvement. This involvement may be present or predominant at early stages in some mutation carriers, expanding the clinical spectrum of the disease to a larger group of scar-related cardiomyopathies or arrhythmic cardiomyopathies according to the suggestion of some authors (5).

Limitations of the 2010 Task force criteria include the absence of specific criteria for left ventricle (LV) involvement and the limited role of cardiac magnetic resonance (CMR) as the use of the late gadolinium enhancement technique for tissue characterization was not considered. In 2020, new diagnostic criteria (“the Padua criteria”) were proposed. The main element of novelty compared to the 2010 Task force criteria is the central role of CMR, which has become mandatory to characterize the ACM phenotype and to exclude other diagnoses The traditional organization in six categories of major/minor criteria was maintained. The criteria for identifying the right ventricular involvement were modified and a specific set of criteria for identifying LV involvement was created. Depending on the combination of criteria for right and LV involvement, a diagnosis of classic (right dominant) ACM, biventricular ACM or left dominant ACM is then made (6,7)

The main anatomopathological feature of ACM is the replacement of myocytes by fibrous or fibro adipose tissue in the RV free wall. Lesions extend from the epicardium to the endocardium and predominantly involve the area between the anterior part of the pulmonary infundibulum, the apex, and the infero-posterior wall (the so-called “triangle of dysplasia”). Myocyte loss and fibrous replacement are most often segmental and usually do not involve the interventricular septum. LV histological involvement is frequently reported in autopsy cases or explanted hearts, even in the absence of macroscopic LV involvement (8).

The diagnostic yield of endo myocardial biopsies is relatively low and largely depends on the location and number of targeted sites because of the patchy nature of fibrous replacement and the subepicardial location of lesions. Endo myocardial biopsies are generally non-contributively on the right side of the interventricular septum (4).