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Acknowledgments 245
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246 Cardiac Motion Analysis Based on Optical Flow of Real-Time 3-D Ultrasound Data
CHAPTER 10
Echocardiography: A Tool for LVSD
Identification
Manivannan Jayapalan
10.1 Introduction
The human heart is a hollow, muscular, four-chamber organ that pumps blood
through the blood vessels by repeated rhythmic contractions. Ventricular dysfunc-
tion is the result of a diversity of structural and/or physiologic abnormalities of
myocardial relaxation or contraction that alters the ventricular flow. The cardiac
cycle contains two phases, diastole and systole, and both may be affected by dis-
eases of the heart.Thus, ventricular dysfunction canbe diastolicor systolic, or both.
It is essential to consider the ventricular dysfunction in the left-hand side
because the left ventricle plays an important role in circulating the blood to the
whole body. Systolic dysfunction results from a decrease in global or regional myo-
cardial contractility. The fraction of blood that is expelled in relation to the blood
volume in the heart in diastole is an expression of systolic function and is called the
ejection fraction (EF). During systole, the heart empties and an impairment of con-
tractility causes less blood to be expelled. thus decreasing the stroke volume but
increasing the end-systolic volume as a whole EF that ends in progressive pump fail-
ure. The impaired capacity of the left ventricle to fill and to maintain its stroke vol-
ume without a compensatory increase of atrial filling pressures represents diastolic
dysfunction. Ejection of a lesser volume of blood because of a decrease in contractil-
ity and reduced ventricular filling because of the impairment of myocardial muscles
are shown in the Figure 10.1.
Reduced ability of the left ventricle to eject blood, called left ventricle systolic
dysfunction (LVSD), is a common predecessor of heart failure (HF). The prognosis
for heart failure is poor and the morbidity is high with frequent hospitalizations,
especially among the elderly. The prevalence of HF is increasing and threatens to
become a majorlogistic and economic burden to global health care systems. HF cur-
rently contributes to 30.9% of global mortality and 10.3% of global morbidity [1]
that can be reduced by optimal treatment, requiring objective evaluation of LV
function and cardiac anatomy. Detection and treatment of LVSD is essential to
reduce the incidence of cardiac failure and its consequences. The major cause of
247
LVSD is blockage in the coronary arteries that supply blood to the heart surface,
thus reducing the oxygen supply, which leads to necrosis followed by the impaired
contractility of cardiac muscles [2].
10.1.1 Left Ventricular Systolic Dysfunction
The inability of the LV to eject sufficient blood, referred as systolic dysfunction, is a
complex process involving improper contractions of subendocardial, midwall,
subepicardial, and papillary muscle fibers. In the presence of LVSD, the heart con-
tracts less forcefully and cannot pump out as much of the blood that is returned to it
as it normally does. As a result, more blood remains in the lower chambers of the
heart (ventricles). Blood then accumulates in the veins. The muscle fibers of the
midwall LV are arranged mainly circumferentially, whereas subepicardial,
subendocardial, and papillary fibers are arranged mainly in a longitudinal and/or
oblique fashion. The shortening of these muscle fibers results in a thickening of the
ventricular walls, as well as a movement of the mitral annulus toward the LV apex.
In addition, the oblique fibers produce a twisting movement of the LV. These events
result in a volume reduction of the LV lumen, a reduction of the stroke volume, and,
hence, a reduction in the ejection fraction. The interaction of the LV, the other car-
diac chambers, and the entire vascular system results in decreased cardiac output,
which is the product of stroke volume and heart rate.
248 Echocardiography: A Tool for LVSD Identification
Systolic
dysfunction
Diastolic
dysfunction
Normal
Diastole
(filling)
Systole
(pumping)
The ventricles fill
normally with blood
The enlarged ventricles
fill with blood
The stiff ventricles fill
with less blood than
normal
The ventricles pump
out about 60% of
the blood
The ventricles pump
out less than 40% to 50%
of the blood
The ventricles pump
out about 60% of
the blood, but the
amount may be lower
than normal
Figure 10.1 Left ventricular dysfunction.
10.1.2 Determinants of LV Systolic Performance
The forces acting on the myocardium during filling and contraction are important
determinants of LV systolic performance. These forces are affected by chamber size
and shape and can be described according to the concept of wall stress. The law of
Laplace states that the stress in the walls of a cylinder is directly proportional to the
transmural pressure and the radius of the cylinder and inversely proportional to the
thickness of the cylinder walls. So an increased radius of the LV, that is, dilation,
causes increased stress on the chamber walls, if the transmural pressure and wall
thickness are constant. By increasing the wall thickness (i.e., LV hypertrophy), the
wall stress can be reduced.
The wall stress acting to stretch the noncontracting muscle in diastole can be
viewed as preload. An increase in preload produces an increase in stroke volume by
lengthening the fundamental contractile units—the sarcomeres—in the myocyte (the
length–tension relationship). Frank first described this phenomenon in the frog heart
in 1895, and Starling described it in the mammalian heart in 1914. It is therefore
oftenreferredtoastheFrank-Starlingmechanism. The myocardial wall stress that
builds up during the systolic contraction can be viewed as afterload. In addition to
chamber size and wall thickness, this wall stress depends on the peripheral vascular
resistance, arterial compliance, and intraventricular pressure. An increase in afterload
reduces the myofiber shortening velocity, resulting in a decrease in stroke volume.
Last but definitely not least, contractility is the fundamental quality of cardiac
muscle that determines the systolic performance independent of loading conditions.
Increased contractility produces a greater rate of contraction to reach a greater peak
force. Figure 10.2 shows the left ventricle P-V relationship in a normal heart along
with systolic and diastolic dysfunctions.
10.2 Assessment of Left Ventricular Function—An Overview
Systolic function of the left ventricle represents a complex interaction between
preload, afterload, and contractility. Preload is the force that stretches the
10.2 Assessment of Left Ventricular Function—An Overview 249
Systolic dysfunction
Normal
Diastolic dysfunction
Pressure
Pressure
Pressure
Left ventricular volume Left ventricular volume Left ventricular volume
Figure 10.2 Left ventricle P-V relationship.
myofibrils in diastole. The balance of two opposing forces determines the end-dia-
stolic sarcomere length. These forces are end-diastolic wall stress, which is an esti-
mate of the force stretching the myocardial fibers at end diastole, and the intrinsic
myocardial stiffness or elasticity. These two opposing forces will eventually deter-
mine the left ventricular end-diastolic volume and pressure. Afterload is the force
that resists myofibril shortening in systole and varies throughout systole as blood is
ejected from the ventricles. The left ventricular systolic wall stress is the measure of
the force resisting myofibril shortening in systole in humans and, therefore, repre-
sents afterload. It is directly proportional to the radius of and the pressure inside the
chamber and is inversely proportional to the wall thickness [3].
Contractility is anintrinsic property of themyocardium and generally means the
strength of the shortening of the myofibrils when they contract. Preload, afterload,
and contractility are intimately related in vivo and alterations in any one of these
three parameters will affect the other two. For example, an increase in preload gen-
erally increases contractility according to the Frank-Starling mechanism. However,
an increase in preload may also result in anincrease in afterload because the left ven-
tricular end-diastolic volume will increase.
Therefore, the overall increase in contractility as a result of an increase in
preload is somewhat blunted because the increased afterload (that accompanies an
increase in preload) will decrease contractility. Assessment of ventricular function,
therefore, requires careful consideration of this complex interaction between
preload, afterload, and contractility, and ventricular function is not synonymous
with contractility.
In common usage, left ventricular function usually refers to left ventricular sys-
tolic function. Assessment of left ventricular function remains a vital part of man-
agement of almost all cardiovascular diseases because left ventricular function
carries important diagnostic and prognostic information. The ideal parameter of
ventricular function should be accurate; independent of loading conditions, heart
rate, cardiac chamber shape and size; easily measured; reproducible; and sensitive
only to intrinsic changes of contractile function. Numerous indices of cardiac func-
tion have been proposed and tested. However, none of the currently available indi-
ces fulfills the criteria of the ideal index. In the following sections, the rationale,
benefits, and shortcomings of the commonly used indices are discussed.
10.2.1 Ejection Phase Indices
10.2.1.1 Ejection Fraction and Fractional Shortening
The left ventricular ejection fraction, which is obtained from volume data only, is
the most widely used index of systolic function. It is often quoted as a measure of left
ventricular function in heart failure trials [4–6]. Fractional shortening is the
one-dimensional surrogate of EF and has the advantage of relative simplicity
because its calculation depends only on measurement of a single dimension of the
left ventricle. The velocity of circumferential fiber shortening [7] is the rate of short-
ening of a theoretical myocardial fiber in the circumferential plane at the midpoint
of the long axis of the ventricle. These ejection phase indices can be measured rela-
tively easily from either contrast left ventriculography or noninvasively using
radionuclide ventriculography or echocardiography.
250 Echocardiography: A Tool for LVSD Identification
Except for the velocity of circumferential fiber shortening, both EF and frac-
tional shortening are extremely popular. Their popularity stems from the fact that
these parameters are easily obtainable, quantitative, easy to understand, and repro-
ducible. However, ejection phase indices are very dependent on both preload and
afterload and cannot be considered a reliable index of ventricular contractility,
especially in conditions of altered loading conditions. For example, in patients with
mitral regurgitation, the ejection fraction is increased as a result of the increase in
preload and the decrease in afterload. The increase in EF is not indicative of
increased ventricular function and it can, in effect, mask the development of
ventricular dysfunction.
10.2.1.2 Myocardial Performance Index
Tei et al. [8, 9] advocated the use of a Doppler-derived myocardial performance
index, which isdefined as the sum of the isovolumetric relaxation and isovolumetric
contraction times divided by the ejection time. They studied 100 patients with dif-
ferent degrees of left ventricular dysfunction and 70 normal subjects with Doppler
echocardiography. The researchers found that the mean value of the index was sig-
nificantly different between normal and patients with moderate or severe left ven-
tricular dysfunction (0.39 ± 0.05, 0.59 ± 0.10, and 1.06 ± 0.24, respectively; p <
0.001 for all) with a small degree of overlap [8]. Furthermore, the value of the index
did not appear to be related to heart rate, mean arterial pressure, or the degree of
mitral regurgitation. In a subsequent study, the authors performed simultaneous
cardiac catheterization and Doppler echocardiography in 34 patients [9] and found
good correlations between the Doppler index and simultaneously recorded systolic
peak +dp/dt (r =0.821; p < 0.0001), diastolic peak –dp/dt (r = 0.833; p < 0.001), and
tau (τ, the relaxation time constant; r = 0.680, p < 0.0001).
The Doppler index can be measured easily and is reproducible and appears to
be promising in the assessment of global ventricular function. However, it does not
differentiate between systolic and diastolic function and its use in patients with sig-
nificant mitral regurgitation has not been validated. Moreover, in patients with sig-
nificant mitral regurgitation, the isovolumetric contraction time cannot be
measured accurately. Therefore, the index may have limited applicability in these
patients.
10.2.2 Isovolumetric Indices
The maximum rate of rise of left ventricular systolic pressure (+dp/dt) is the maxi-
mum of the first derivative of ventricular pressure and has been used as an indicator
of contractility. It was first measured by means of a catheter-tip micromanometer.
More recently, dp/dt has been successfully measured noninvasively with the use of
Doppler echocardiography [10]. Using continuous wave Doppler, Bargiggia et al.
found good correlations between catheter-derived and Doppler-derived dp/dt.
Interventions known to increase myocardial contractility, such as exercise, infusion
of adrenaline, and tachycardia also increased left ventricular dp/dt. However, left
ventricular dp/dt is not completely load independent. Studies have shown that left
ventricular dp/dt increased with a moderate increase in preload [11] and showed lit
-
10.2 Assessment of Left Ventricular Function—An Overview 251
tle change with changes in afterload [12]. Whereas changes in dp/dt reflect changes
in contractility in a given individual, its use in comparing one individual with
another is limited, especially when there has been chronic pressure or volume
overload.
10.2.3 Pressure-Volume Analysis
The relationship between left ventricular pressure and volume can be expressed in a
plot of left ventricular pressure versus volume. One cardiac cycle can be represented
by a complete pressure-volume loop (Figure 10.3). In Figure 10.3, segment b is
isovolumetric contraction, segment c is left ventricular ejection, and d is
isovolumetric relaxation.
10.2.3.1 End Systolic Pressure-Volume Relationships (ESPVR)
The fundamental principle underlying ESPVR is that such a relationship is unique
for a given level of contractility and is independent of loading conditions [13]. The
ratio of simultaneous pressure and volume defines the stiffness or the elastance of
the left ventricle. During the cardiac cycle, this ratio increases to a maximum during
systole and decreases to a minimum during diastole. By varying the loading condi-
tions, a series of left ventricular pressure-volume loops can be generated. The line
joining the upper left-hand corners of each individual loop is the end-systolic pres-
sure-volume line, characterized by a slope, the end-systolic elastance (E
es
), an x-axis
intercept, and an extrapolated volume at zero pressure (V
0
) (Figure 10.4).
Therefore, ESPVR is represented by:
()
PEVV
es
=−
0
(10.1)
It is generally agreed that an increase in the slope of the ESPVR line (i.e., an
increase in end-systolic elastance) is indicative of an increase in contractility and
vice versa [13, 14]. Measurement of ESPVR involves simultaneous measurements
of left ventricular pressure and volume. Left ventricular pressures can be measured
with a catheter-tip micromanometer, and measurement of left ventricular volume
252 Echocardiography: A Tool for LVSD Identification
LV pressure (mmHg)
0
0
100
100
200
200
Aortic
valve
closing
Aortic
valve
opening
ESPVR
EDPVR
db
c
a
ESV
EDV
LV volume (ml)
SV
Figure 10.3 A typical left ventricular pressure-volume loop.
can be made by contrast ventriculography, radionuclide techniques [15],
echocardiography [16], or with the use of an impedance catheter [17].
An inflatable balloon inserted into the inferior vena cava near the right atrial
junction usually achieves manipulation of loading conditions. With the use of either
contrast or radionuclide ventriculography to measure volume, alteration of loading
conditions is more commonly achieved by pharmacological means (phenylephrine
to increase afterload and sodium nitroprusside to decrease afterload and preload).
With the use of pharmacological agents, autonomic blockade [18] or temporary
pacing at a slightly higher heart rate [15] may be necessary to eliminate the reflex
changes in heart rate during such manipulations.
Whether the ESPVR is linear has been extensively investigated. A linear ESPVR
has been suggested in isolated hearts [19] and in conscious dogs [20]. It was also
supported by studies involving humans [21]. This linearity is important because,
theoretically, the ESPVR line can be constructed from only two to three pressure-
volume loops [22, 23]. This is especially important for investigators using contrast
ventriculography to measure ventricular volume, because the number of pres-
sure-volume loops that canbe generatedfrom suchmeasurements isusually limited.
Experimental and clinical studies often determined end-systolic elastance over a
limited range of loading conditions and inotropic states and, therefore, may have
failed to demonstrate the nonlinearity of such relationships. However, subsequent
investigators have suggested that the ESPVR is curvilinear at higher afterloads [24]
and that the curvilinearity of ESPVR is also contractility dependent [25]. With
increased contractility (i.e., high-end systolic elastance, E
es
), the ESPVR tended to be
concave to the volume axis. At low contractility, ESPVR tended to be convex to the
volume axis. However, over the range of end-systolic elastance values that are
encountered in normal states of contractility, a curvilinear fit was not statistically
better than a linear fit for the ventricular volumes that could be examined in the ani-
mal model [25]. This curvilinearity has been used to explain why the extrapolated
V
0
is sometimes a negative number [26]. It is important to realize that the linearity
of the ESPVR is a convenience that allows determination of such relationships to be
carried out in simple terms. Although the ESPVR is in fact curvilinear, it does not
alter the fact that such relationships define the systolic performance of the ventricle
at a given state.
End-systolic elastance has also been suggested to be influenced by heart size
[27]. In an animal model of mitral regurgitation, Berko et al. [27] found that the
end-systolic elastance decreased significantly after creation of mitral regurgitation,
10.2 Assessment of Left Ventricular Function—An Overview 253
LV volume (ml)
LV pressure (mmHg)
0
0
20 40
40
60
60
80
120
100
160
Figure 10.4 Determination of ESPVR.