Background: The Gorlin equation is the reference method for the assessment of aortic valve area in aortic stenosis and is calculated using a constant, called the coefficient of contraction, which is empirically assumed to be 1. This coefficient is the ratio of effective aortic area to anatomic aortic area, and a value of 1 indicates that both are the same. The purpose of this study was to estimate the actual coefficient of contraction in patients with aortic stenosis and to evaluate its impact on aortic area as calculated by the Gorlin equation. Methods: We studied 17 patients with moderate to severe aortic stenosis. Effective aortic area was calculated using the continuity equation. Anatomic aortic area was obtained by planimetry with transesophageal echocardiography. Aortic valve area by the Gorlin equation was calculated from echocardiography data. The coefficient of contraction was derived as above. Results: The coefficient of contraction was inversely related to the pressure recovery. Effective area was correlated with anatomic area (r = 0.86, P < 0.01) but there was a high mean difference (0.22 ± 0.14 cm 2 ). Aortic area by the Gorlin equation was not correlated with anatomic area, but the correlation became significant when the Gorlin equation was corrected for coefficient of contraction and pressure recovery. Conclusions: Using a coefficient of contraction of 1 in the Gorlin equation gives a poor correlation with anatomic area. Using the calculated coefficient of contraction for each patient and the mean gradient for pressure recovery improves the correlation with anatomic area. These facts could be taken in account when Gorlin equation is considered as the reference method.
Muscle fiber disarray (MFD) has been described as the histologic feature of hypertrophic cardiomyopathy (HC), but it was also found in normal and other abnormal conditions. Its distribution related to the topography of the myocardium has not been described. In this paper, the incidence of MFD in hearts free from HC, the frequency of the histologic disorganization and the affected muscles involved were studied at autopsy. 29 hearts with acute myocardial infarction and 1 with suppurated myocarditis were employed. Macroslides containing the point of maximum septal enlargement were selected for histological examination. The areas of MFD were measured by a polar planimeter and correlated with the involved wall, the total slice area, parietal widths and involved muscles. 27 patients (90%) presented with MFD; hypertrophic ventricular walls were observed in 10, 8 of which had MFD. The remaining 20 patients with nonhypertrophic ventricular walls had MFD in 19 instances. There was septal posterior involvement in 26 cases (p < 0.0005). 12 patients (44.4%) had only one wall involved. Only 1 patient presented more than 5 % of MFD in regard to the total area. The septal wall was the most affected (p < 0.0005). The most commonly affected muscle was the deep-sinospiral, either alone or combined with other muscles (p < 0.01). Greater MFD was found (23/30) in patients with septum/posterior wall ratio < 1.3 cm. It is concluded that MFD may affect up to 10% of the septum in patients free from HC, and that secondary hypertrophy is not a prerequisite for MFD. The splitting of the superficial and deep fibers as observed at the anterior and posterior septum and the change of the course of two nearby muscular groups may explain these findings. Thus, a high probability exists of finding MFD at the septal and right ventricular level in patients who do not have HC and are studied by endomyocardial biopsy.
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