2 edition of method of controlling the left ventricular wall stress of the human heart found in the catalog.
method of controlling the left ventricular wall stress of the human heart
Written in English
|Statement||by Soheil Sohrab.|
|The Physical Object|
|Pagination||, 71 leaves, bound :|
|Number of Pages||71|
Dilated cardiomyopathy is a heart disease characterized by both left ventricular dilatation and left ventricular systolic dysfunction, leading to cardiac remodeling and ultimately heart failure. We. Thus, when the heart is viewed from the anterior aspect, most of the left ventricle is hidden by the right ventricle. Furthermore, the left ventricular outlet overlaps the inlet. Normally, the left ventricular free wall is thickest at the cardiac base and it gradually becomes thinner towards the apex.
The heart becomes enlarged, or hypertrophic, due to intense cardiovascular workouts, creating an increase in stroke volume, an enlarged left ventricle (and right ventricle), and a decrease in resting pulse along with irregular rhythms. The wall of the left ventricle increases in . As systolic function declines, the end-systolic dimension increases further, left ventricular wall stress increases, and left ventricular function is further compromised by the excessive ventricular afterload. At this point, the decline of ventricular function is progressive and can be quite rapid.
The heart has a three-layered heart wall composed of connective tissue, endothelium, and cardiac muscle. It is the muscular middle layer known as myocardium that enables the heart to contract. Due to the force needed to pump blood to the body, ventricles have thicker walls than do atria. The left ventricle wall is the thickest of the heart walls. Although global left ventricular function can be well quantified, analysis of regional wall motion has been limited mainly for lack of a satisfactory method of measuring segmental motion. Radiographic cine left ventriculography has been used for evaluating left ventricular function.
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Measurement of left ventricular wall thickness and mass by echocardiography. Circulation. Mar; 45 (3)– SANDLER H, DODGE HT. LEFT VENTRICULAR TENSION AND STRESS IN MAN. Circ Res. Aug; – Hood WP, Jr, Rackley CE, Rolett EL. Wall stress in the normal and hypertrophied human left ventricle.
Am J by: A method of controlling the left ventricular wall stress of the human heart Public Deposited. In this thesis a method is presented for maintaining the left ventricular wall stress of the human heart at a constant level during the systole (active portion of the heart's cycle). This constant stress level makes it possible to take isotonic Author: Soheil Sohrab.
Am Heart J. Oct; – Eber LM, Greenberg HM, Cooke JM, Gorlin R. Dynamic changes in left ventricular free wall thickness in the human heart. Circulation. Apr; 39 (4)– Gaasch WH, Battle WE, Oboler AA, Banas JS, Jr, Levine HJ.
Left ventricular stress and compliance in by: Objectives This study sought to determine the prevalence of reduced contractility and uncompensated wall stress in patients with aortic stenosis (AS) with preserved or reduced left ventricular ejection fraction (LVEF) and their impact on survival.
Background LVEF in AS is determined not only by contractility but also by loading conditions. Methods Patients with first diagnosis (time 0) of Cited by: 8. Summary. A methodological study of the requirements for reliable determination of the left ventricular end-diastolic pressure-volume relationship, wall stress and wall elasticity was performed using angiocardiographic measurement of the inner volume and wall thickness, as well as simultaneous measurement of left ventricular pressure on closed-chest by: 7.
A set of stress differential equations of equilibrium is presented for a thick prolate spheroid which is the assumed shape for the left ventricle.
An analysis for the stresses in the ventricular wall indicates that maximum stresses occur at the inner layers and decrease to a minimum at the epicardial surface, a result that is partially validated by experiment. tributions through the wall thickness, a result which cannot be predicted by La- place's law.
However, their assumptions with regard to the deformation behavior ofthe left ventricle are restrctive. Atheory, to be valid for thick shell structures, must include the effects of transverse normal stress (radial stress) and transverse shear deformationwhichalways accompaniesbendingstresses.
Left ventricular hypertrophy is a condition where the muscle wall becomes thickened (hypertrophied). The left ventricle is the strongest and most muscular chamber of the heart, as it is. The EKG machine then records your heart's rhythm, frequency of beats and electrical conduction.
What an EKG reveals: Whether you've had a heart attack If the left ventricle is thickened (enlarged heart muscle wall) If the heart rhythm is abnormal (noting any arrhythmias such as atrial fibrillation, or AFib).
A set of stress differential equations of equilibrium is presented for a thick prolate spheroid which is the assumed shape for the left ventricle. An analysis for the stresses in the ventricular wall indicates that maximum stresses occur at the inner layers and decrease to a minimum at the epicardial surface, a result that is partially.
Ventricular pressure is a measure of blood pressure within the ventricles of the heart. Left. During most of the cardiac cycle, ventricular pressure is less than the pressure in the aorta, but during systole, the ventricular pressure rapidly increases, and the two pressures become equal to each other (represented by the junction of the blue and red lines on the diagram on this page), the.
two-dimensional and M-mode ES wall stress (7 and 11 %), while variability of the ES pressure–area product was less than 5 %. Discussion We have estimated the ES pressure–area product of the left ventricle as an indicator of LV wall stress changes.
Changes in M-mode derived ES wall stress were in accordance with the ES pressure-area product. The human muscle fibers oriented at different angles throughout the ventricle wall in the form of sheets that are separated by a complex structure of cleavage surfaces (see Figure 3) –.
The myofibers could be fully described by two inclination projection angles; the helix angle (β) and the transverse angle (η) in the two perpendicular planes. A method is described for calculating tension and stress acting within the wall of the left ventricle during the cardiac cycle.
This method is based upon ventricular pressure observations and measurements of left ventricular dimensions and wall thickness made from biplane angiocardiograms. 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. wall stress D = LVDd, h = (IVSd + LVPWJ/2 and P = resting systolic BP. The dimensions of the left ven-tricle were taken from end diastole, on the assumption that there would have been no significant change in these dimensions from end diastole to peak stress, as peak systolic wall stress.
Ventricular dysfunction in heart failure. The major role of the ventricles in pumping blood to the lungs and body means that even a slight decrease in ventricular efficiency can have a significant impact on heart function.
If the left ventricle encounters either absolute or relative functional insufficiency (called left ventricular heart failure, or left-sided heart failure), a series of.
ventricular wall stress since Woods' publication late in the last century (Woods, ). There are many reasons for this interest in wall stress: (1) Myocar-dial wall stress is one of the primary determinants of myocardial oxygen consumption (Samoff et al., ).
(2) In diseases characterized by abnormal. Apoptosis (programmed cell death) is a potentially important cause of cell loss in several cardiac pathological conditions, including acute myocardial infarction, 1 ischemia-reperfusion damage, 2 and cardiomyopathies.3, 4 The loss of cardiomyocytes in dilated cardiomyopathy has been linked to the progressive decline in left ventricular function and congestive heart failure.
5 Recent studies. Chamber-stress equations relate wall stresses to pressure and wall dimensions. Such equations play a central role in the analysis and understanding of heart-chamber function.
Over the past three decades, several stress equations giving radically different results have been derived, used, and/or espoused. THE LEFT VENTRICULAR WALL 1. The generalized form of Laplace's law was applied to the data in this study to calculate the forces acting within the left ventricular wall.
This law, when applied to the heart, states that the forces within the left ventricular wall are functions of intraluminal pressure and the size and shape of the chamber.An Inverse Finite Element Method for Determining the Tissue Compressibility of Human Left Ventricular Wall during the Cardiac Available via license: CC BY Content may be subject to.
This prospective observational study will compare the physiologic responses between exercise stress echocardiography and dobutamine stress echocardiography on left ventricular volume and wall stress. Exercise and dobutamine stress testing are two widely employed diagnostic modalities that are often used, interchangeably, to detect inducible.