Mohd Farid

Mohd Farid

Saturday, September 29, 2012

The Sonographer Attachment Programme At USA Report : Mayo Clinic: Advanced Echo =Tissue Doppler Imaging=



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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