Final answer:
Familial idiopathic Dilated Cardiomyopathy is often a result of genetic mutations such as those found in the LDL receptor or ApoB genes, which lead to abnormal cell communication and can cause the heart to enlarge and weaken.
Step-by-step explanation:
Familial idiopathic Dilated Cardiomyopathy is often genetic, or truly familial as a result of a mutation. This can involve mutations in genes such as the LDL receptor gene on chromosome 19 or the ApoB gene.
These mutations can lead to abnormal cell communication and contribute to the development of cardiac hypertrophy or the pathological enlargement of the heart. In Dilated Cardiomyopathy, the heart's ventricles enlarge and weaken, which reduces the heart's ability to pump blood effectively, leading to heart failure and other complications.
Abnormal cell communication is essential in understanding heart conditions, as seen in research related to NSML where the PTPN11 mutation affects cardiac hypertrophy by disrupting communication between the myocardium and endocardium. Such insights into cellular interactions and mutations provide a better understanding of not only rare conditions like NSML but also more common heart disorders.
The structure of the heart with components like the inferior vena cava, interatrial band, interatrial septum, and intercalated discs play vital roles in maintaining the healthy function of the heart. Any anomalies due to familial genetic mutations can alter the normal functioning leading to Dilated Cardiomyopathy or other related heart diseases.