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“Is the Measurement of
Systolic Function same as Ejection Fraction (%EF)?”
Systolic function and Ejection Fraction (%EF) are
correlated but EF does not provide a specific measurement of the level
of ischemia, as does the isovolumic contraction. Current clinical
evaluation is done utilizing the %EF but it measures the compound effect
of heart contraction, amount of blood in the ventricle and pressure
against which the heart pumps.
Since the most important part of the heart cycle (the
principal driving force) is the isovolumic contraction, any measurement
to determine systolic function should rely heavily on the measurement
of its energy or amplitude (strength of cardiac muscle).
The ejection fraction depends on the afterload that
involves the resistance of valves and head pressure (blood pressure)
whereas the isovolumic contraction occurs before the valves are open
and therefore unaffected by the resistance due to valves and head
pressure and provides a true measurement of contractile force (the
strength of the heart muscle). The echocardiogram cannot measure this
most important phase of the cardiac cycle where the maximum energy by
the heart muscle is expended.
“Is
Contractility the same as Ejection Fraction?”
The terms low EF, systolic dysfunction, and reduced
contractility are all used synonymously and by and large, a low EF does
not denote anything about myocardial systolic function or
contractility; it principally reflects the degree of ventricular
dilatation.
There are a variety of hemodynamic variables confounding
the EF value, cavity size , chronic pressure overload , and the lack of
the measurement of the right ventricular EF. As well as abnormal valve
function. The main reason that contractility can not be derived from
performance measurements is that there is a huge expenditure of
internal energy as is testified by the low efficiency ( approximately
14%) of the heart. This energy is dissipated as heat after the
isovolumic contraction and therefore can’t be measured by any
performance method.
“Can Heart Movement be a Measure of
Contractility?”
The heart does move and rotate in the chest as a result
of its contraction and recoil upon ejection of blood. This movement is
an effect of the heart’s forceful contraction but not a direct
measurement of contractility. Contractile force is best measured by
acceleration measurements not displacement.
Heart motion may be small and yet have a large impact
force release. The three coin experiment illustrates this as the middle
coin moves little but releases a large amount of energy.
Tension generation during the isovolumic phase generates
a force during the buildup and again at its very abrupt end. The latter
is the result of the fact that blood is not very compressible. The
other factor is that the internal structures of the heart resist
deformation.
The illustration of internal component action is the
hammer without the bounce. This hammer illustrates the large internal
inertial forces without any indication of movement on its external
surface.
“Do Tissue Doppler Imaging and High Frame
Ultrasound Measure Contractility?”
In principle, TDI and HFU will be able to image the local
movement of the myocardium and calculate velocity and therefore
regional acceleration. Several academic papers have already
demonstrated that this technique can be performed in a controlled
setting. These measurements are made on the cardiac features such as
the mitral ring or the atrio-ventricular plane or even on the
myocardium itself using Doppler imaging.
To get accurate results the probe has to be positioned
either perpendicular or in parallel to the long axis of the heart to
compensate for off angle measurements. A sufficiently skilled
sonographer with enough time should be able to generate a full view of
regional lengthening, take measurements off this view and calculate regional
acceleration. Algorithms will have to be developed to view this
regional acceleration on a whole heart map as is done currently for
myocardial perfusion studies.
“What are the Implications of the Flow model of
Heart Failure (Cardiac Output) versus Biomechanical Model?”
The heart is a pump therefore it was obvious that amount
of flow it generates should be used as measure of how well this pump is
functioning. The amount of flow as measured in Litres per Minute has
been taken as an indicator of reduced function and the likely onset of
heart failure.
But the heart is also a motor that builds torque, exerts
force and drives the pump. How should the health of this aspect of the
heart’s function be measured? The Biomechanical Model of heart
failure has been proposed as a means to better understand this aspect
of the heart and its functional state.
The Biomechanical Model measures the health of the heart
by its capacity to exert force. If the heart is able to exert force on
the volume of blood it contains then it is healthy and if it is unable
to do so then it is unhealthy. This model encompasses all aspects of
the heart as a motor and complements the Flow Model of heart failure.
For instance, one
individual may have reduced flow due to severe aortic stenosis while
another may have a similar flow state due to reduced contractile
reserve as a result of coronary artery occlusion. These individuals
have equivalent heart health according to the Flow Model but have very
different heart health state according to Biomechanical Model.
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