Key result
Concentric left ventricular hypertrophy in aortic valve stenosis normalizes wall stress, allowing high systolic pressures to be consistent with normal afterload and ejection fraction.
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Discusses the pathophysiological mechanisms of angina in patients with aortic stenosis who have normal coronary arteries, focusing on left ventricular hypertrophy and wall stress.
ypertrophy 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 (pressureϫradius/ 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.
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Gould et al. (2003) conducted an editorial in Aortic Stenosis. Concentric left ventricular hypertrophy in aortic valve stenosis normalizes wall stress, allowing high systolic pressures to be consistent with normal afterload and ejection fraction.
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