Key result
Nine-gene systematic screening identifies disease-causing mutations in ~63% of HCM patients.
Why the study?
Hypertrophic cardiomyopathy involves multiple genes and mutations, and the best molecular screening strategy in clinical practice remains to be determined.
What is the distribution of disease-causing mutations across 9 genes in patients with familial or sporadic hypertrophic cardiomyopathy?
Observational (n=197)
What is the distribution of disease-causing mutations across 9 genes in patients with familial or sporadic hypertrophic cardiomyopathy?
Systematic genetic screening in hypertrophic cardiomyopathy reveals that MYBPC3 and MYH7 mutations account for 82% of identified cases, suggesting these should be prioritized in clinical genetic testing.
May support prioritizing MYBPC3/MYH7 in HCM genetic testing; extends observational prevalence data but leaves open broader validation.
BACKGROUND: Hypertrophic cardiomyopathy is an autosomal-dominant disorder in which 10 genes and numerous mutations have been reported. The aim of the present study was to perform a systematic screening of these genes in a large population, to evaluate the distribution of the disease genes, and to determine the best molecular strategy in clinical practice. METHODS AND RESULTS: The entire coding sequences of 9 genes (MYH7, MYBPC3, TNNI3, TNNT2, MYL2, MYL3, TPM1, ACTC, andTNNC1) were analyzed in 197 unrelated index cases with familial or sporadic hypertrophic cardiomyopathy. Disease-causing mutations were identified in 124 index patients ( approximately 63%), and 97 different mutations, including 60 novel ones, were identified. The cardiac myosin-binding protein C (MYBPC3) and beta-myosin heavy chain (MYH7) genes accounted for 82% of families with identified mutations (42% and 40%, respectively). Distribution of the genes varied according to the prognosis (P=0.036). Moreover, a mutation was found in 15 of 25 index cases with "sporadic" hypertrophic cardiomyopathy (60%). Finally, 6 families had patients with more than one mutation, and phenotype analyses suggested a gene dose effect in these compound-heterozygous, double-heterozygous, or homozygous patients. CONCLUSIONS: These results might have implications for genetic diagnosis strategy and, subsequently, for genetic counseling. First, on the basis of this experience, the screening of already known mutations is not helpful. The analysis should start by testing MYBPC3 and MYH7 and then focus on TNNI3, TNNT2, and MYL2. Second, in particularly severe phenotypes, several mutations should be searched. Finally, sporadic cases can be successfully screened.
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Richard et al. (2003) conducted an observational in Hypertrophic cardiomyopathy (n=197). Systematic genetic screening of 9 genes was evaluated on Identification of disease-causing mutations. Systematic screening of 9 genes in 197 index cases with hypertrophic cardiomyopathy identified disease-causing mutations in approximately 63% of patients.
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