Dilated cardiomyopathy

In approximately 50% of patients, CMD has a genetic cause, and in approximately 25% it is caused by mutations in the gene for titin, an important cardiac protein, which can be analyzed with NGS genetic analysis. In other patients, it is caused by mutations in genes that produce sarcomeric proteins (e.g., myosin, myosin-binding protein C, troponin), which in this case are responsible for dilation rather than hypertrophy. Some patients have mutations in lamin A/C, desmoplakin, or ion channels, all of which are more likely to develop complications such as life-threatening arrhythmias (tachycardia and/or ventricular fibrillation).

When other family members of the patient have had or have cardiomyopathy, heart failure, or even sudden death at a young age, CMD is likely genetically caused. In these patients, genetic testing is essential to identify the mutation and the causative gene, allowing for more targeted and effective therapy.

A form of CMD is also often present in patients who have genetic “neuromuscular” diseases, such as dystrophies (for example Duchenne muscular dystrophy).

Heart infections (myocarditis) almost always caused by viruses, but also by bacteria
chemotherapy and / or radiotherapy to treat cancer
exposure to toxic substances, such as alcohol abuse
fast and prolonged supraventricular / ventricular arrhythmias ("tachycardiomyopathy")
from food deficiency, (e.g. in patients with "anorexia" or during a famine)
after childbirth ("postpartum")
autoimmune diseases (e.g. rheumatoid arthritis, etc)