Objectives: The goals of this study were to determine regional systolic function of the septum and to relate it to regional wall thickness and wall stress.
Background: Wall thickening, a parameter of systolic function, is determined by wall thickness and wall stress. In patients with hypertrophic obstructive cardiomyopathy (HOCM), hypertrophic nonobstructive cardiomyopathy (HNCM), and hypertensive heart disease (HHD), regional systolic function of normal and hypertrophic septal regions has been incompletely characterized by 2-dimensional echocardiography. Thus, multiplane transesophageal echocardiography with 3-dimensional reconstruction of the septum was used.
Methods and results: In 49 patients (15 controls, 11 with HOCM, 8 with HNCM, and 15 with HHD) 4 parallel (2 basal and 2 apical) equidistant short-axis cross sections from base to apex were obtained from the reconstructed septum. In each short-axis cross section, 6 wall-thickness measurements were made in 15 degrees intervals at end diastole and end systole, for a total of 48 measurements in each patient. Fractional thickening was calculated as wall thickening divided by end-diastolic wall thickness. Wall thickness of the basal cross sections was significantly thicker (P < .001) in HOCM and HNCM than in HHD. However, circumferential wall thickness was more evenly distributed in HNCM and HHD when compared with HOCM. In the basal cross sections, fractional thickening was similarly reduced in all hearts, though basal wall stress was significantly different in all groups (P < .001). In the apical cross sections, wall thickness was similar in all diseased hearts, but fractional thickening was better (P < .001) and wall stress lower (P < .001) in HNCM than in HOCM and HHD.
Conclusions: In septal regions without or with only mild hypertrophy, regional systolic function is preserved and appears to be determined by hemodynamic factors such as wall stress. However, in regions with moderate to severe hypertrophy, systolic function is markedly and uniformly impaired in all groups, which seems not to be caused by differences in wall thickness and wall stress but by the degree of the myocardial disease process.