It was subsequently documented 2 that cavity obliteration can be seen in states other than hypertrophic cardiomyopathy. Left ventricular cavity obliteration (LVCO), defined as obliteration of the apex in systole on angiography, was first described 1 in 1965 and proposed as the cause of the intraventricular pressure gradient accompanying hypertrophic cardiomyopathy. Spectral profiles of severe AS, HOCM, and LVCO can be differentiated by the peak/mean gradient ratio. The magnitude of ICG is quantitatively associated with the extent and duration of LVCO.
Most patients with LVCO without HOCM or severe LVH have an ICG < 36 mm Hg. The spectral profile of patients with AS, HOCM, and LVCO is differentiated by the peak/mean gradient ratios of 2 or less, 2–3, and 3 or greater, respectively, in >90% of patients. Higher ICG is associated with a greater extent and more prolonged apposition of LV walls, and smaller left ventricular cavity size. To clarify the cause and characteristics of the ICG in patients with LVCO in patients without HOCM, we assessed the extent and duration of cavity obliteration, and for differentiation, we compared the spectral profiles with patients with HOCM and severe aortic stenosis (AS). The distinction has clinical relevance, because treating the intracavitary gradient (ICG) of LVCO as if it were a SAM-associated gradient associated with HOCM would be inappropriate and possibly harmful. They both have a similar “dagger” profile, are obtained from the cardiac apex, are associated with a hyperdynamic left ventricle, and the gradients are worsened by Valsalva. Nevertheless, the two gradients, though different in origin and significance, share similar characteristics. Left ventricular cavity obliteration (LVCO) was first described as the cause of the gradient but subsequently systolic anterior motion (SAM) of the mitral valve has been established as the cause. Controversy surrounds the cause of the pressure gradient in patients with hypertrophic obstructive cardiomyopathy (HOCM).
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