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December NaN, 1999


Author Affiliations

Phil B.FontanarosaMD, Interim CoeditorIndividualAuthorMargaret A.WinkerMD, Deputy EditorIndividualAuthorStephenLurieMD PhD, Fishbein FellowIndividualAuthor

JAMA. 1999;282(24):2302-2303. doi:10-1001/pubs.JAMA-ISSN-0098-7484-282-24-jbk1222

In Reply: In response to Dr Maron and colleagues, I value the role of echocardiography in establishing the diagnosis and severity of HCM. ("ECG" in Table 3 of my article is an unfortunate typographical error and should be "ECHO"). However, as discussed in the article, some individuals who inherit a genetic disease known to cause HCM have normal echocardiograms. Certain mutations that are characterized by mild or subclinical hypertrophy may be associated with a high incidence of sudden death.1 Hence, the caution that HCM is occasionally difficult to distinguish from physiologic hypertrophy by echocardiography is correct. In addition to outflow gradient, cardiac catheterization provides information concerning filling pressures and cardiac output, hemodynamic indices that are critical in ascertaining whether a therapy has not only reduced left ventricular outflow obstruction but also improved indices of left ventricular systolic and diastolic function.

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