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[Asymmetric septum hypertrophy in the pressure-overloaded heart]
1Institut für Pathologie der Universität Zürich.
Insights
Asymmetric septal hypertrophy is not typically observed in hypertension or aortic stenosis, contrary to echocardiographic findings. Autopsy studies suggest this feature is more indicative of hypertrophic cardiomyopathy.
Area of Science:
- Cardiovascular Pathology
- Cardiac Imaging
- Surgical Anatomy
Context:
- Echocardiography suggests asymmetric septal hypertrophy in hypertensive and aortic stenosis patients.
- Surgical intervention for aortic stenosis may involve resecting a basal ventricular septum muscular hump.
- Autopsy findings contrast with echocardiography, associating asymmetric septal hypertrophy primarily with hypertrophic cardiomyopathy.
Purpose:
- To investigate the prevalence of accentuated septal hypertrophy in hearts with hypertension and aortic stenosis.
- To reconcile discrepancies between echocardiographic and autopsy observations regarding septal hypertrophy.
Summary:
- Autopsy examination of 10 hearts with aortic stenosis and 12 with hypertension revealed no evidence of accentuated septal hypertrophy.
- Prominent crista supraventricularis was observed, potentially explaining echocardiographic findings of a thickened septum.
- Concentric hypertrophy adequately explains muscular humps causing left ventricular outflow tract obstruction, with functional relevance limited to below the aortic valve.
Impact:
- Challenges the echocardiographic diagnosis of asymmetric septal hypertrophy in hypertension and aortic stenosis.
- Suggests that the term asymmetric septal hypertrophy may be inadequate for describing septal thickening in these conditions.
- Highlights the importance of correlating imaging findings with pathological examination for accurate diagnosis.
Abstract:
According to echocardiographic observations, the hypertrophic left ventricle in hypertension and in aortic stenosis is inclined to asymmetric septal hypertrophy. The heart surgeon, after removal of the stenosed aortic valve, is not so rarely forced to resect an additional muscular hump of the basal ventricular septum. These findings contrast with our experiences from autopsy examinations; we see asymmetric septal hypertrophy only in hypertrophic cardiomyopathy (or coronary heart disease). The aim of this study was to demonstrate or refute this impression by measurements of the relevant parameters. In ten hearts with aortic stenosis and in 12 hearts of hypertensive patients there was no evidence of accentuated septal hypertrophy. In some hearts we found a prominent crista supraventricularis, which could explain the echocardiographic feature of a thickened ventricular septum. The muscular hump stenosing the left ventricular outflow tract can easily be explained by concentric hypertrophy. The thickness of the septum corresponded to that of the free wall, but only below the aortic valve did the hypertrophy become functionally relevant. There is no doubt that in certain cases this muscular hump has to be removed. The term asymmetric septal hypertrophy, however, is inadequate.