Mechanical Stress And Hypertrophy
Author(s)
A. K. Macpherson, S. Neti, P. A. Macpherson, S. R. Houser,
M. Hari & J. Marzillier
Abstract
There is accumulating evidence that mechanical stress on the left ventricle is a
significant trigger for left ventricular hypertrophy. It has been known for
sometime that mechanical stress activates a number of protein kinases and
reprogramming of gene expression in the myocardium. A recent study has shown
that there is a link between mechanical stress and the activation of angiotensin II
(Ang II) receptors. Ang II has been known for a long time to initiate
hypertrophy. Providing clinicians with stress maps of a patient’s heart would be
useful aid in diagnosis. Based on a patient’s echo cardiogram the left ventricular
(LV) characteristics of chamber wall velocity and position as a function of time
and myocardium thickness are obtained. In addition Doppler measurements of
velocity through the mitral valve are also extracted from the echo cardiogram. A
simulation program is used to solve the equations of fluid flow in the LV during
both diastole and systole. The velocity through the mitral valve is compared with
the Doppler measurements as a check on the accuracy of the calculations. The
flow velocities are used to calculate the shear stress on the myocardium as a
function of time. It was found that the maximum stress occurs during the
opening of the mitral valve near the valve. The regions of peak stress occur at
different locations of the myocardium and septal wall over a heart cycle. It is not
known if the average stress over a heart beat or the maximum shear stress that
triggers the gene changes. There are large peaks in the stress and extended
periods of low level stress which could play a significant role in the development
of hypertrophy. Some initial tests on rabbits have shown that there is a variation
in the development of certain biomarkers as a function of location.
Keywords: hypertrophy, stress, biomarkers, Angiotensin II.
Keywords
hypertrophy, stress, biomarkers, Angiotensin II.
Related Book
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