Apparent asymmetric septal hypertrophy due to angled interventricular septum

doi:10.1016/0002-9149(80)90005-3

The American Journal of Cardiology

Volume 46, Issue 3, September 1980, Pages 386-392

https://doi.org/10.1016/0002-9149(80)90005-3 Get rights and content

Abstract

A distinct geometric pattern is described in patients whose M mode echocardiogram falsely indicates asymmetric septal hypertrophy. Sixty-four patients were referred because of clinically suspected idiopathic hypertropic subaortic stenosis. Thirty-six of these patients had M mode echocardiograms showing asymmetric septal hypertrophy (septal/free wall ratio 1.3 or greater). On two dimensional study, only 16 of the 36 had this finding; each of the remaining 20 had a normal interventricular septum. The apparent asymmetric septal hypertrophy on M mode echocardiography was due to anterior angulation of the septum: The thickness of the septum was exaggerated because of its oblique orientation with respect to the path of the single dimensional echocardiographic beam. This anterior direction of the septum was indicated by measuring the angle between the mid line axis of the aortic root and that of the septum. In patients with apparent asymmetric septal hypertrophy this angle was lower (97 ° ± 2.6 ° [mean ± standard error of the mean]than in patients with true asymmetric septal hypertrophy (124 ° ± 2.9 °, p <0.001) or in normal subjects (128 ° ± 1.9 °, p <0.001).

M mode echocardiograms were similar in the groups with apparent and true asymmetric septal hypertrophy with respect to septal velocity and percent thickening. The two groups were likewise similar with respect to clinical features (chest pain, palpitation, systolic murmur). The group with true asymmetric septal hypertrophy had a larger proportion of electrocardiographic abnormalities. Because of limitations in technique, M mode echocardiography may allow overdiagnosis of asymmetric septal hypertrophy in certain patients. When a more secure diagnosis of this abnormality is necessary, two dimensional echocardiography is helpful.

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The lack of inclusion of that outflow tract plane can be considered a study limitation. Previous studies in humans have recognized an overestimation and variation of the IVS measurements depending on the different angle and location of the transducer [18–20]. In humans, it has been described that FTs can be difficult to distinguish from the LV endocardium possibly leading to artifactual measurements of both septal thickness and LV dimension [13–16].
False tendons (FTs) are string-like structures in the left ventricle. A FT might produce focal thickening at its insertion region of the left ventricle, which could be mistaken for focal hypertrophic cardiomyopathy.
To perform a prospective, echocardiographic follow-up examination of feline FTs and compare the wall thickness at the FT insertion region and a normal region without FTs at both examinations.
One hundred twenty-eight cats with one or multiple FTs without other cardiac abnormalities or systemic disease.
Measurements of the interventricular septum at end-diastole at a region with and without FT insertion were performed using two-dimensional echocardiography at both examinations and compared statistically using a Student's t-test.
The follow-up interval ranged from 5 to 110 months (mean, 33 months). Myocardial wall segments with FT insertions were significantly thicker compared with neighboring wall regions in the long axis, but not in the short-axis views obtained. Comparing the wall thickness of follow-up examinations with the initial examination, revealed a significant growth of both FT and non-FT segments. However, differences in growth between the FT region and region without FTs were not statistically different.
Many normal cats have FTs, associated with focal thickening compared with neighboring regions. This thickening can increase over time, proportionate to growth in other (non-FT) segments. The association of such thickening with an FT and the absence of disproportionate growth in this segment over time suggests that these segments are simply thicker related to FT insertion.
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The present study was designed to determine the aorto-septal angle (AoSA) in Boxer dogs with or without subaortic stenosis (SAS) by using two-dimensional echocardiography. Forty-five Boxer dogs were prospectively included in the study. The AoSA was steeper in the group with SAS than in healthy Boxers with a mean difference of 10°. According to the proposed regression model, the AoSA is associated with SAS in Boxers, particularly because it becomes steeper as SAS severity increases. Several studies in humans demonstrate that small changes in the AoSA produce important changes in septal shear stress, which in turn causes proliferation of the endocardial cells resulting in subaortic obstruction. A definite conclusion about the role of the AoSA on the formation and/or progression of subvalvular lesions in Boxers cannot be drawn from the data analysed due to the transversal nature of the observations.
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The length of first order chordae tendineae was measured from the tip of the papillary muscle to their insertion into the free edges of the mitral valve leaflets at end-diastole (Fig. 1D). The septo-aortic angle (IVS-to-aortic root angle) was measured as the angle between the mid line axis of the septum and that of the aortic root as illustrated in Fig. 2B from an end-diastolic frame.33,37 The inter-papillary muscle distance was determined as demonstrated in Fig. 2C from an end-diastolic image.
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106 cats (28 controls and 78 with HCM) had transthoracic two-dimensional and Doppler echocardiography performed with quantification of 33 variables. Three groups of cats (control [Group-1], HCM without obstruction [Group-2], and HCM with obstruction [Group-3]) were identified and compared by analysis of variance, χ² analysis, and correlation analysis.
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Abnormalities of the mitral valve are common in cats with HCM suggesting a possible role in the pathogenesis of dynamic outflow tract obstruction.
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Distance of the lesion from the hinge point of the right coronary cusp of the AoV was measured in systole and diastole from the parasternal long-axis view as described by Kleinert and Geva (14). Other measurements included: length of the membrane or FMR, measured from the parasternal long-axis view as the distance from the septal insertion to the free edge of the obstructive lesion; AoV annulus diameter zscore; aortoseptal angle, measured as described by Kleinert and Geva (14) and Fowles et al. (15); and distance between the aortic and mitral valves in diastole. Degree of override of the aorta was graded qualitatively as normal when less than one-third of the annulus was intercepted by an extrapolation of the ventricular septum long axis, as mild when one-third to two-thirds of the annulus was intercepted, and as marked when more than two-thirds was intercepted.
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Recurrence of DSS has been reported to range from 0% to 55% of patients. Factors associated with recurrence have not been adequately defined.
Patients were included if they had a diagnosis of DSS, normal segmental cardiac anatomy, previous resection of DSS, and at least 36 months’ follow-up. Demographic, surgical, and echocardiographic data were analyzed. Primary outcome was repeat resection of DSS in patients after successful primary resection.
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^☆: This study was supported in part by Grant HL-21278 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.

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Clinical studyApparent asymmetric septal hypertrophy due to angled interventricular septum☆

Abstract

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Chest

Chest

Am J Cardiol

Ultrasound location of left ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy

Circulation

Ultrasound in the diagnosis and evaluation of therapy of idiopathic hypertrophic subaortic stenosis

Circulation

Asymmetric septal hypertrophy. Echocardiographic identification of the pathognomonic anatomic abnormality of IHSS

Circulation

Asymmetric septal hypertrophy (ASH): the unifying link in the IHSS disease spectrum. Observations regarding its pathogenesis, pathophysiology, and course

Circulation

Familial prevalence and genetic transmission of idiopathic hypertrophic subaortic stenosis

N Engl J Med

Clinical study
Apparent asymmetric septal hypertrophy due to angled interventricular septum☆