Tissue Doppler
Imaging
Tissue
Doppler Imaging (TDI) is a novel use of ultrasound to image the motion of
tissue with Doppler echocardiography. Doppler echocardiography records and
displays the velocities of the moving targets. When Doppler echocardiography is
used to measure blood flow velocity, erythrocytes are the targets. Their normal
velocities range from 10 cm/s in the venous circulation to 150 cm/s in the
arterial circulation. However, the velocities of myocardial tissue are much
lower (1-20 cm/s), but their amplitudes are greater than those produced by
blood. Therefore, Doppler ultrasounds instruments have been modified to record
the low velocities of myocardial tissue and to reject the high velocities
generated by blood flow. TDI requires a high frame rate. A special function key
needs to be selected to activate TDI. After TDI has been selected, the
subsequent operation is identical to that used to perform regular pulsed wave
Doppler echocardiography, except that the TDI gain needs to be lowered from the
regular gain setting used for blood flow Doppler recordings and the velocity
scale needs to be adjusted to a lower aliasing velocity (about 20-30 cm/s or
even lower) to optimize TDI signals.
TDI
can be displayed in the color mode, just as in colour imaging of blood flow.
Tissue velocities are colour coded by autocorrelation: red for tissue moving
toward the tranducer and blue for tissue moving away from the tranducer.
Movement and velocities of cardiac structures are regulated by the underlying
systolic function and diastolic function of the heart.
Assestment Of Myocardial
Relaxation
Early
diastolic velocity (Ea or E’) of the miral annulus measured with TDI is a good
indicator of LV myocardial relaxation. This is one of the most important
components of myocardial diastolic function, the others being LV compliances
and filling pressure. Longitudinal motion of the mitral annulus can be
appreciated visually from the the parasternal long axis and apical four chamber
views, but TDI records and demonstrates the velocity of the longitudinal motion
in numerical value. In the normal heart with normal myocardial relaxation, E’
increases with an increasing transmitral gradient, increasing preload, exercise
and dobutamine infusion. However when myocardial relaxation is impaired because
of aging or a disease process, E’ is affected less or even unchanged by preload
or transmitral gradient.
Velocities
of longitudinal mitral anulus motion are best obtained from apical views.
Although various locations of the mitral anulus can be interrogated with TDI,
the two most frequently used locations are the septal and lateral mitral anulus.
Usually, E’ from the lateral is higher (normal>15cm/s) than that from the
medial anulus (normal>10cm/s). Regional myocardial dysfunction or valvular
surgery involving the mitral annulus may effect mitral annulus velocities. A
localized disease process, such as lateral myocardial infarction, can result in
mitral annulus velocities being lower at the lateral annulus than at the septal
annulus. Late diastolic velocity (Aa or A’) of the mitral annulus at the time
of atrial contraction increases during early diastolic dysfunction, as is the
case for the mitral inflow A wave, but decreases as atrial function
deteriorates. A’ has been correlated with left atrial (LA) function.
Estimation Of Left Ventricular Filling
Pressure
LV diastolic filling pressures can be
estimated reliably with 2D and Doppler echocardiography. The deceleration time
(DT) of mitral inflow early diastolic velocity (E) has a good inverse
correlation with the pulmonary capillary wedge pressure (PCWP) when the LV ejection fraction
(LVEF) is less than 35 %. A DT of less than 130 miliseconds usually indicated a
PCWP greater than 20 mmHg. However, mitral inflow DT alone is not highly
accurate in patients who have relatively normal LVEF or atrial fibrillation.
Because Ea is reduced in patients with impaired relaxation and is affected less
by preload than mitral inflow E, the ratio (E/Ea) between mitral inflow early
diastolic velocity and mitral annulus early diastolic velocity increases as
PCWP increases.
Investigation
at Baylor College and in Mayo Clinic have demonstrated
that PCWP is higher than 20 mmHg when E/Ea is more than 10 at lateral annulus
or 15 at medial annulus. This ratio works well even in patients who have fused
miral inflow signals, preserved LVEF and atrial fibrillations. The only
exception is patients with constrictive pericarditis, in whom Ea, especially
from the medial annulus, is increased (≥8 cm/s) and E/Ea is reduced with high
filling pressures. Because PCWP can be estimated reliably with E/Ea, estimation
of PCWP with exercise is feasible which is helpful in assessing patients who
have exertional dyspnea.
Evaluation Of Regional
And Global Systolic Function
The
extent of systolic movement of the mitral annulus correlates with LV systolic function and
stroke volume. Normally, the systolic velocity (Sa or S’) of the mitral annulus
is more than 6 cm/s. Although TDI of the mitral annulus reflects the global
systolic and diastolic function of the LV,
segmental or regional function can be assessed by performing TDI of various LV segments by placing
the sample volume (2-5 mm) in the region of interest. The size of the sample
volume depends on the location and intensity of the signal and is usually
between 2-5 mm. Futher clinical experience with this variable will determine if
Sa (or S’) can replace other more commonly used systolic variables.
Tissue Velocity Gradient
TDI
can measure the difference in velocities of adjacent myocardial tissues
(velocity gradient), and this can be used to assess the viability and
deformation (strain) of the myocardium. The velocity of the endocardium is
normally higher than that of the epicardium, thus producing a tissue velocity
gradient. In akinetic but viable or nontransmurally infracted myocardium, the
myocardial velocity gradient persists, but there is no velocity gradient in
scarred or transmurally infarcted myocardium. Because days to weeks are needed
for myocardial contractility to recover after successful reperfusion of an
occluded coronary artery, measurements of the tissue velocity gradient can be
useful in patients with an acute myocardial infarction. To record or display
the myocardial velocity gradient, the direction of myocardial contractility
needs to be aligned in parallel with the direction of the ultrasound beam.
Therefore, imaging views are limited to the parasternal windows to image
anterior or posterior walls.
Cardiac Time Interval
Cardiac
time interval are regulated precisely by the mechanics and functions of the
myocytes; hence, these intervals are good measure of cardiac function. TDI is
well suited for determining the timing of myocardial events. The precise timing
of these events is helpful in understanding the mechanism of myocardial
relaxation and myocardial suction during early diastolic filling. In healthy
heart, in which efficient myocardial relaxation is used effectively to suck
blood from LA into the LV
during early diastole, the time of onset of mitral inflow (E) coincides with
what of myocardial early diastolic motion (relaxation) of the mitral annlus
(Ea). However, in hearts with delayed myocardial relaxation and increased
filling pressure, diastolic filling (onset of the E wave) depends more on the
increased LA pressure and occurs earlier than the onset of the early diastolic
motion of the mitral annulus. Therefore, the time interval between the onset of
the mitral E velocity and that of the mitral annulus diastolic motion (Ea)
increases, and this increased interval has been proposed as a new variables to
assess LV
filling pressure.
A
limitation of measuring cardiac time intervals by pulsed wave Doppler
echocardiography is nonstimultaneity because different cardiac cycles are
usually needed to measure various intervals which in turn are used together.
One solution is to have the capability of obtaining multiple pulsed wave
Doppler recordings simultaneously. Another creative means to measure cardiac
intervals from a single cardiac cycle is to use tisuue Doppler anatomic colour
M-Mode from the anterior mitral leaflets. From this technique, isovolumic
contraction time, isovolumic relaxation time, and LV ejection time can be measured reliably
from a single cardiac cycle.
Mechanical
dyssynchrony is measured by time intervals between peak ejection systolic
velocities or peak strain of multiple myocardial segments.
Evaluation Of Thick
Walls
The
ventricular walls become thick for several reasons including LV hypertrophy, hypertrophic cardiomyopathy,
infiltrative cardiomyopathy, restrictive cardiomyopathy and the athletics
heart. These entities can usually be differentiated on the basis of clinical
and laboratory findings, but differentiating then can occasionally be
difficult. The evaluation of myocardial relaxation with TDI is able to
distinguish between a thick athletics normal heart and other disease
conditions. Mitral annulus motion is well preserved in the athletic heart
because myocardial relaxation is preserved, but it is reduced in all other
conditions that have impaired myocardial relaxation.
Prognostication
Because
E/Ea can estimate LV
filling pressures and patients with increased filling pressure have higher
rates of morbidity and mortality, it is expected that a high E/Ea predicts a
poor outcome. E/Ea more than 15 was found to be associated with increased
mortality of patients with acute myocardial infarction. By itself, Ea is also a
good predictor for clinical outcome. In various clinical conditions, patients
who have an Ea less than 5 cm/s are more likely to have much higher mortality
than those with an Ea more 5 cm/s.
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