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TRANSCRIPT
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Learning Objectives: 

1) Describe why titin truncating mutations are the main genetic cause of both familial and acquired dilated cardiomyopathies (non-ischemic, non-valvular HFrEF)

2) Indicate why personalized medicine in dilated cardiomyopathies can be obtained by combining phenomics and transcriptomics

3) Appraise and explain why acute myocarditis is the result of a combination of the immune and genetic background of a person, making unhappy few susceptible to exaggerated cardiac inflammation