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(Circulation. 2008;117:429-439.)
© 2008 American Heart Association, Inc.

Contemporary Reviews in Cardiovascular Medicine

Management of Symptoms in Hypertrophic Cardiomyopathy

Michael A. Fifer, MD; Gus J. Vlahakes, MD

From the Cardiology Division, Department of Medicine (M.A.F.), and Cardiac Surgical Division, Department of Surgery (G.J.V.), Massachusetts General Hospital and Harvard Medical School, Boston, Mass.

Correspondence to Michael A. Fifer, MD, Cardiology Division, Massachusetts General Hospital, 55 Fruit St, Gray/Bigelow Bldg, Suite 800, Mailstop 843, Boston, MA 02114-2696. E-mail mfifer@partners.org

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

	Introduction

 
In 1957, Brock¹ made the distinction between congenital subaortic stenosis characterized by a fibrous ridge and "functional subvalvar stenosis" resulting from "muscular hypertrophy," describing 3 patients with the latter. Brock initially attributed the hypertrophy and resultant outflow obstruction to systemic hypertension, a conclusion he withdrew in a 1959 publication.² Between these 2 publications, Teare³ described asymmetrical septal hypertrophy in 8 autopsies (from a series of 16 000!). Remarkably, he identified myocyte disarray, proclivity for sudden death during exertion, and occurrence of stroke in association with atrial fibrillation as features of the disease. Quantitative definition of asymmetrical septal hypertrophy as septal to posterior wall thickness ratio 1.3 was introduced in 1961.⁴ The discovery that the left ventricular outflow tract (LVOT) gradient was created by systolic anterior motion (SAM) of the mitral valve was made from analysis of cineangiograms a year later.⁵

Soon thereafter, it was recognized that diverse patterns of hypertrophy existed. In the early 1970s, investigators came to realize that, even among patients with asymmetrical septal hypertrophy, obstruction to left ventricular (LV) outflow at rest was present in only a minority.⁶ The recognition that an impediment to LV inflow (eg, diastolic dysfunction) might be at least as important as any obstruction to outflow came with the observation that LV end-diastolic pressure (LVEDP) was elevated while LV end-diastolic volume (LVEDV) was normal or low in many patients with hypertrophic cardiomyopathy (HCM).⁷ The genetic basis of the disease was demonstrated in 1990.⁸

Half a century after the descriptions of Brock and Teare, . . . [Full Text of this Article]

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