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Animal models implicate genetic modifiers in HF susceptibility; leaves open their role in human risk prediction.
Congestive heart failure is the eventual outcome of diverse myocardial insults, including postischemic remodeling, primary cardiomyopathies, and infections.1 Even for specific forms of myocardial injury, it remains difficult to predict the development of congestive heart failure. Racial differences in the incidence of congestive heart failure, reduced penetrance in families with familial cardiomyopathy, and strain-specific effects in animal models all suggest that some of the variation in the general population with regard to susceptibility to heart failure is heritable.2 Although early events in the evolution of congestive heart failure are often unknown, the final common pathways are slowly being elucidated. The . . .
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Hajjar et al. (2002) studied this question.
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