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(Circulation Research. 2006;98:443.)
© 2006 American Heart Association, Inc.

Editorials

Hypertrophic Cardiomyopathy

Exercise and Eat Right

Elizabeth M. McNally

From the Departments of Medicine and Human Genetics, Institute for Cardiovascular Research, University of Chicago, Ill.

Correspondence to Elizabeth M. McNally, University of Chicago, Departments of Medicine and Human Genetics, Institute for Cardiovascular Research, 5841 S. Maryland Ave MC6088, Chicago, IL 60637. E-mail emcnally@medicine.bsd.uchicago.edu

See related article, pages 540–548

Key Words: hypertrophic cardiomyopathy • exercise • soy • casein • NFAT

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Hypertrophic cardiomyopathy is a common disorder¹ that arises from mutations in genes encoding the proteins of the sarcomere. Although 9 different sarcomere genes have been implicated, point mutations in the gene encoding the ß heavy chain of myosin (Myh7) or myosin binding protein C (MyBPC3) are responsible for more than half of genetically confirmed cases of HCM.² Clinical management of HCM revolves around 2 significant issues: (1) reducing heart failure symptoms, if present, and (2) preventing sudden cardiac death.³ The underlying pathological process in HCM is one of cellular hypertrophy that affects cardiomyocytes and is associated with myofibrillar disarray. Hypertrophy of the ventricular chambers is variable in HCM and may target the intraventricular septum leading to outflow gradient. HCM may also target the ventricular apex or hypertrophy may be concentric. Hypertrophy itself can increase the risk of sudden death by promoting subendocardial ischemia.^4,5 The mechanisms that underlie the risk and incidence of sudden death in HCM are likely heterogeneous,⁶ and therefore, sudden death remains difficult to predict and manage.

In humans, HCM is variable in its presentation. The precise genetic mutation that underlies HCM offers some predictive value.² For example, some mutations lead to an earlier or later onset of disease, whereas some are highly pathologic inducing a rapid onset of hypertrophy (first or second decade) or risk of highly penetrant sudden cardiac death. As a generalization, with notable exceptions, mutations in Myh7 tend to be earlier onset and more pathologic than HCM associated with MyBPC3 . . . [Full Text of this Article]