+Genetic basis Gene Locus Type MYH7 14q12 CMH1 () TNNT2 1q32 CMH2 () TPM1 15q22.1 CMH3 () MYBPC3 11p11.2 CMH4 () ? ? CMH5 PRKAG2 7q36 CMH6 () TNNI3 19q13.4 CMH7 () MYL3 3p CMH8 () TTN 2q24.3 CMH9 () MYL2 12q23-q24 CMH10 () ACTC1 15q14 CMH11 () CSRP3 11p15.1 CMH12 () Familial<unk>  is inherited as an autosomal dominant trait and is attributed to mutations in one of a number of genes that encode for the sarcomere proteins. Currently, about 50–60% of people with a high index of clinical suspicion for<unk> M will have a mutation identified in at least one of nine sarcomeric genes. Approximately 40% of these mutations occur in the β-myosin heavy chain gene on chromosome 14 q11.2-3, and approximately 40% involve the cardiac myosin-binding protein C gene. Since<unk> M is typically an autosomal dominant trait, children of a single<unk> M parent have 50% chance of inheriting the disease-causing mutation. Whenever such a mutation is identified, family-specific genetic testing can be used to identify relatives at-risk for the disease, although clinical severity and age of onset cannot be predicted. An insertion/deletion polymorphism in the gene encoding for angiotensin converting enzyme (ACE) alters the clinical phenotype of the disease. The D/D (deletion/deletion) genotype of ACE is associated with more marked hypertrophy of the left ventricle and may be associated with higher risk of adverse outcomes. Some mutations could have more harmful potential compared to others (β-myosin heavy chain). For example, troponin T mutations were originally associated with a 50% mortality before the age of 40. However, a more recent and larger study found a similar risk to other sarcomeric protein mutations. The age at disease onset of<unk> M with MYH7 is earlier and leads to more severe symptoms. Moreover, mutations on troponin C can alter Ca+2 sensibility on force development in cardiac muscle, these mutations are named after the amino acid that was changed after the location in which it happened, such as A8V, A31S, C84Y and D145E.
Hypertrophic cardiomyopathy
Aortic stenosis
Noncompaction cardiomyopathy
Hypertensive heart disease
Amyloid cardiomyopathy
Athletic heart syndrome
Restrictive cardiomyopathy
Fabry disease