Skip to main content
Article thumbnail
Location of Repository

Left ventricular regional wall curvedness and wall stress in patients with ischemic dilated cardiomyopathy

By Liang Zhong, Yi Su, Si-Yong Yeo, Ru-San Tan, Dhanjoo N. Ghista and Ghassan Kassab


Geometric remodeling of the left ventricle (LV) after myocardial infarction is associated with changes in myocardial wall stress. The objective of this study was to determine the regional curvatures and wall stress based on three-dimensional (3-D) reconstructions of the LV using MRI. Ten patients with ischemic dilated cardiomyopathy (IDCM) and 10 normal subjects underwent MRI scan. The IDCM patients also underwent delayed gadolinium-enhancement imaging to delineate the extent of myocardial infarct. Regional curvedness, local radii of curvature, and wall thickness were calculated. The percent curvedness change between end diastole and end systole was also calculated. In normal heart, a short- and long-axis two-dimensional analysis showed a 41 ± 11% and 45 ± 12% increase of the mean of peak systolic wall stress between basal and apical sections, respectively. However, 3-D analysis showed no significant difference in peak systolic wall stress from basal and apical sections (P = 0.298, ANOVA). LV shape differed between IDCM patients and normal subjects in several ways: LV shape was more spherical (sphericity index = 0.62 ± 0.08 vs. 0.52 ± 0.06, P < 0.05), curvedness at end diastole (mean for 16 segments = 0.034 ± 0.0056 vs. 0.040 ± 0.0071 mm−1, P < 0.001) and end systole (mean for 16 segments = 0.037 ± 0.0068 vs. 0.067 ± 0.020 mm−1, P < 0.001) was affected by infarction, and peak systolic wall stress was significantly increased at each segment in IDCM patients. The 3-D quantification of regional wall stress by cardiac MRI provides more precise evaluation of cardiac mechanics. Identification of regional curvedness and wall stresses helps delineate the mechanisms of LV remodeling in IDCM and may help guide therapeutic LV restoration

Topics: Translational Physiology
Publisher: American Physiological Society
OAI identifier:
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)
  • Suggested articles

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.