The frequency of familial dilated cardiomyopathy in a series of patients with idiopathic dilated cardiomyopathy

Article Abstract:

An examination of 315 relatives of 59 patients with dilated cardiomyopathy found that 12 of the patients had at least one relative who also had the disease. Eighteen relatives had impaired heart function, and 8 had never been diagnosed with heart disease prior to the study. Dilated cardiomyopathy, characterized by enlargement of one or both heart ventricles and subsequent impairment of heart function, usually occurs sporadically. But in 20% of these patients, the disease appears to be hereditary. Otherwise, there were few differences between these patients and those whose relatives did not have dilated cardiomyopathy.

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Pathogenesis of inherited forms of dilated cardiomyopathy

Article Abstract:

Research continues to elucidate the cause of dilated cardiomyopathy. Dilated cardiomyopathy is a heart disease caused by an enlarged heart. This eventually leads to heart failure. Dilated cardiomyopathy can be caused by mutations in the genes for proteins such as dystrophin, alpha-cardiac actin, emerin, and lamin. A 1999 report describes several families with a mutation in the gene for lamin. Although they had dilated cardiomyopathy, they did not have any skeletal muscle abnormalities. Lamin occurs in the membrane surrounding the cell nucleus and it is not clear how this mutation causes heart disease.

Editorial

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The genetics of dilated cardiomyopathy - emerging clues to the puzzle

Article Abstract:

Animal studies are revealing the genetic basis of dilated cardiomyopathy. This heart disease is characterized by an enlarged heart that cannot pump blood properly. This leads to congestive heart failure. One gene defect linked to dilated cardiomyopathy is a mutation in genes that code for structural proteins like the LIM muscle protein and the protein dystrophin. These proteins maintain the integrity of the heart muscle cell. A second gene defect occurs in genes that code for transcription factors, which are proteins that turn on other genes.

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