Long-Term Arrhythmic and Nonarrhythmic Outcomes of Lamin A/C Mutation Carriers.

Implications of Genetic Testing in Dilated Cardiomyopathy. Clinical Presentation, Long-Term Follow-Up, and Outcomes of 1001 Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Patients and Family Members.

Sudden cardiac death risk prediction in arrhythmogenic right ventricular cardiomyopathy: A practical approach to navigating the challenges of prediction models. The author declare no conflict of interest. This single-gene mutation is responsible for causing ACM in several countries in Europe and North America.

Furthermore, the deletion of three nucleotides in the PLN is typical for the arginine 14 in the protein (PLNR14Del) at high risk of ventricular arrhythmias in the young carriers. PLN is a 52 amino acid protein that binds to SERCA2a and inhibits its function. With the time being, these perturbations were confirmed as arrhythmogenic right ventricle cardiomyopathy in part due to genetic mutations in desmosomal and/or non-desmosomal proteins (especially LMNA, TTN, SCN5A, RBM20, and PLN. ACM defines, since its inception of families with sudden cardiac death, ventricular arrhythmias, and right ventricle malfunction followed by RV dysplasia and atrial fibrillation. Currently, 40% of the population worldwide has been suffering from all forms of genetic cardiomyopathies mediated heart failure, in these patients left ventricular ejection fraction is not adequately tracked. Arrhythmogenic cardiomyopathy (ACM) is an inherited multifaceted cardiac disease that causes sudden cardiac death, especially in young adults and athletes.

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