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(Circulation. 2003;107:3121.)
© 2003 American Heart Association, Inc.

Editorials

Why Angina in Aortic Stenosis With Normal Coronary Arteriograms?

K. Lance Gould, MD; Blase A. Carabello, MD

From the Department of Medicine, Houston Veterans Affairs Medical Center, Baylor College of Medicine (B.A.C.), and Department of Internal Medicine, Division of Cardiology, The University of Texas–Houston Medical School (K.L.G.).

Correspondence to Blase A. Carabello, MD, Chief, Medical Service (111), Houston Veterans Affairs Medical Center, 2002 Holcombe Blvd, Houston, TX 77030. E-mail blaseanthony.carabello@med.va.gov

Key Words: Editorials • stenosis • angina • myocardium • hypertrophy

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

Hypertrophy is considered one of the major mechanisms of the myocardium for adapting to hemodynamic overload. More muscle mass provides more contractile elements for generating the extra work required by the overload. In pressure overload of aortic valve stenosis, concentric left ventricular hypertrophy (LVH) normalizes wall stress, a key determinant of ejection performance.¹ Afterload is often expressed as wall stress (pressurexradius/thickness). As the pressure term in the numerator increases, it is offset by an increase in the thickness term of the denominator. In this way, the high systolic pressure required to drive blood through even a very stenotic aortic valve can be consistent with normal afterload and normal ejection fraction.

See p 3170

Unfortunately, hypertrophy not only provides benefits but also has many pathological consequences. One of these is myocardial ischemia and the attendant angina reported by patients with aortic stenosis despite normal epicardial coronary arteries. The onset of angina greatly increases the risk of sudden death compared with the risk in asymptomatic patients with aortic valve stenosis.^2,3

Angina occurs when myocardial oxygen demand exceeds supply. Demand is proportional to heart rate and wall stress, and the latter can be elevated in cases of aortic stenosis when hypertrophy is inadequate to normalize stress.¹ After aortic valve replacement, there is marked regression of hypertrophy that may occur over the next several months to years,⁴ but angina is relieved immediately. Relief of angina immediately after surgery is probably due to the combination of sudden decreased oxygen demand after removal of . . . [Full Text of this Article]

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Functional Changes in Coronary Microcirculation After Valve Replacement in Patients With Aortic Stenosis

Kim Rajappan, Ornella E. Rimoldi, Paolo G. Camici, Nicholas G. Bellenger, Dudley J. Pennell, and Desmond J. Sheridan
Circulation 2003 107: 3170-3175. [Abstract] [Full Text]

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