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(Circulation. 2005;112:936-938.)
© 2005 American Heart Association, Inc.

Editorial

The Transition From Hypertrophy to Failure

How Certain Are We?

Mark H. Drazner, MD, MSc

From the Donald W. Reynolds Cardiovascular Clinical Research Center, Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Tex.

Correspondence to Dr Mark Drazner, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9047. E-mail Mark.Drazner@utsouthwestern.edu

Key Words: Editorials • hypertension • hypertrophy • heart failure • remodeling

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

Hypertensive heart disease is a major contributor to cardiovascular morbidity and mortality, especially in African Americans, in whom LV hypertrophy is 2 to 3-fold more common in the general population as compared with whites.¹ In the classic paradigm of hypertensive heart disease, concentric hypertrophy (a nondilated, thick-walled left ventricle typically with a normal left ventricular ejection fraction [LVEF]) is a common precursor to LV failure (an increased LV volume with reduced LVEF).² Although molecular triggers of this transition from concentric hypertrophy to failure have been the subject of intense investigation, there are no previous large, longitudinal cohort studies in humans demonstrating that this progression occurs frequently. The transition from concentric LV hypertrophy to failure has been well demonstrated in animal models including the spontaneously hypertensive rat,³ or after aortic banding⁴ or transgenic manipulation,⁵ and also in humans with aortic stenosis⁶ or familial hypertrophic cardiomyopathy.⁷ Whether this paradigm faithfully represents the natural history of hypertensive heart disease is not yet known (Figure). An alternative paradigm is that the LV response to elevated blood pressure is either hypertrophy or failure, with transition between the 2 uncommon in the absence of an interval cardiac injury.

View larger version (21K): [in this window] [in a new window]   Potential pathways in progression of hypertensive heart disease. Hypertension can lead to concentric left ventricular hypertrophy (LVH), characterized by nondilated, thick-walled left ventricle (arrow, top left). After "transition to failure," the LV is dilated with reduced LVEF. Coronary artery disease often via MI is a common contributor to this transition (first horizontal arrow). Whether concentric LVH . . . [Full Text of this Article]

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