Is regional wall stress a stimulus for myocardial hypertrophy in hypertrophic cardiomyopathy?

1988 ◽  
pp. 96-102
Author(s):  
P. K. Blanksma
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Myocardial Hypertrophy ◽  
Wall Stress ◽  
Regional Wall

Disparate difference in preload reserve between myocardial hypertrophy due to essential hypertension and hypertrophic cardiomyopathy

1988 ◽  
Vol 6 (4) ◽  
pp. S138-140 ◽  
Author(s):  
Mikio Mukai ◽  
Mareomi Hamada ◽  
Takumi Sumimoto ◽  
Michihito Sekiya ◽  
Tatsuo Kokubu
Keyword(s):  
Essential Hypertension ◽  
Hypertrophic Cardiomyopathy ◽  
Myocardial Hypertrophy

scholarly journals Genetic relevance and determinants of mitral leaflet size in hypertrophic cardiomyopathy

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Hyemoon Chung ◽  
Yoonjung Kim ◽  
Chul-Hwan Park ◽  
Jong-Youn Kim ◽  
Pil-Ki Min ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Nuclear Dna ◽  
Wall Stress ◽  
Left Ventricular ◽  
Mitral Leaflet ◽  
Systolic Volume ◽  
Left Atrial Wall ◽  
Lv Mass ◽  
End Systolic Volume ◽  
Sarcomeric Genes

Abstract Background Whether mitral leaflet elongation is a primary phenotype of hypertrophic cardiomyopathy (HCM) is controversial. We investigated the genetic relevance and determinants of mitral leaflet size by performing extensive gene analyses in patients with HCM. Methods Anterior mitral leaflet (AML) lengths were measured in HCM patients (n = 211) and age- and sex-matched controls (n = 30) using echocardiography with hemodynamic and chamber geometric assessments. We analyzed 82 nuclear DNA (8 sarcomeric genes, 74 other HCM-associated genes) and mitochondrial DNA. Cardiac magnetic resonance imaging (CMR) was performed in the 132 HCM patients. Results Average indexed AML was significantly longer for HCM than for controls (17.2 ± 2.3 vs. 13.3 ± 1.6 mm/m2, P <  0.001). Average AML length correlated with body surface area (BSA), left ventricular (LV) end-systolic volume (P <  0.001) and LV mass by CMR (P < 0.001). Average indexed AML by BSA of pure-apical HCM was significantly shorter than other typed HCM (16.6 ± 2.0 vs. 17.4 ± 2.4 mm/m2, P = 0.025). Indexed AML was independently correlated with left atrial wall stress. The thin filament mutation group showed larger average AML (31.9 ± 3.8 vs. 29.6 ± 3.8 mm, P = 0.045), but this was not significant with the indexed value. No difference in AML size among subgroups was observed based on the presence of sarcomere protein or mitochondria-related gene variants (P > 0.05). Conclusion AML elongation was a unique finding of HCM. However, the leaflet size was more related to chamber geometry and hypertrophy pattern rather than genetic factors within overt HCM.

Estimation of regional left ventricular wall stresses in intact canine hearts

1998 ◽  
Vol 275 (5) ◽  
pp. H1879-H1885 ◽  
Author(s):  
Abe DeAnda ◽  
Masashi Komeda ◽  
Marc R. Moon ◽  
G. Randall Green ◽  
Ann F. Bolger ◽  
...  
Keyword(s):  
High Speed ◽  
Systolic Function ◽  
Univariate Analysis ◽  
Interventricular Septum ◽  
Wall Stress ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Regional Wall ◽  
Inotropic State ◽  
Lv Systolic Function

Left ventricular (LV) wall stress is an important element in the assessment of LV systolic function; however, a reproducible technique to determine instantaneous local or regional wall stress has not been developed. Fourteen dogs underwent placement of twenty-six myocardial markers into the ventricle and septum. One week later, marker images were obtained using high-speed biplane videofluoroscopy under awake, sedated, atrially paced baseline conditions and after inotropic stimulation (calcium). With a model taking into account LV pressure, regional wall thickness, and meridional and circumferential regional radii of curvature, we computed average midwall stress for each of nine LV sites. Regional end-systolic and maximal LV wall stress were heterogeneous and dependent on latitude (increasing from apex to base, P < 0.001) and specific wall (anterior > lateral and posterior wall stresses; P = 0.002). Multivariate ANOVA demonstrated only a trend ( P = 0.056) toward increased LV stress after calcium infusion; subsequent univariate analysis isolated significant increases in end-systolic LV wall stress with increased inotropic state at all sites except the equatorial regions. The model used in this analysis incorporates local geometric factors and provides a reasonable estimate of regional LV wall stress compared with previous studies. LV wall stress is heterogeneous and dependent on the particular LV site of interest. Variation in wall stress may be caused by anatomic differences and/or extrinsic interactions between LV sites, i.e., influences of the papillary muscles and the interventricular septum.

Evaluation of Analytic Estimates of Ventricular Wall Stress Using the Finite Element Method

2008 ◽  
Author(s):  
Christopher M. Ingrassia ◽  
Shantanu Y. Jani ◽  
Kevin D. Costa
Keyword(s):  
Finite Element ◽  
Circumferential Stress ◽  
Wall Stress ◽  
Cardiac Mechanics ◽  
Ventricular Wall ◽  
The Finite Element Method ◽  
Regional Wall ◽  
Circumferential Wall Stress ◽  
Theoretical Assumptions ◽  
Accurate Quantification

The importance of ventricular wall stress to cardiac function has been well-documented [1, 2], although accurate quantification remains a challenge. In this study, three popular analytic formulas for estimating circumferential wall stress were comprehensively evaluated to identify the conditions for which their use may be appropriate. In particular, the equations of Laplace [3], Mirsky [4], and Janz [5] are commonly used in the fields of cardiology and echocardiography; despite the inaccuracy of key theoretical assumptions, they have been attractive for their simplicity. For validation, we employed specialized finite element methods, developed specifically for cardiac mechanics applications [6], to compute regional wall stress in a series of model chambers having systematically varying geometric and material complexity. We limited our analysis to circumferential stress for consistency with the theoretical equations, and because of its relevance to cardiac mechanics.

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

2009 ◽  
Vol 296 (3) ◽  
pp. H573-H584 ◽  
Author(s):  
Liang Zhong ◽  
Yi Su ◽  
Si-Yong Yeo ◽  
Ru-San Tan ◽  
Dhanjoo N. Ghista ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Myocardial Infarct ◽  
Three Dimensional ◽  
Wall Stress ◽  
Cardiac Mechanics ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Regional Wall ◽  
Significant Difference ◽  
Systolic Wall Stress

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.

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