Tissue Doppler velocity profile of the mitral annulus. A further tool available to estimate the determinants of LV DF is tissue Doppler sampling of the mitral annulus (the cardiac base), which reflects LV longitudinal function. The main purpose of this analysis is to estimate LV relaxation. Unlike the transmitral and pulmonary venous flow profiles, we sample the velocity of a tissue (the mitral annulus), so we no longer measure local differences in pressure. The main determinants of the peak e’ velocity are LV relaxation (t), minimum LV pressure, and LV preload (16).
Sampling methodology. The sample volume is positioned at the level of the atrio-ventricular junction (lateral and medial), at the intermediate point between the most “ventricular” (towards the LV apex) and the most “atrial” (towards the pulmonary veins) position reached by the annulus in its systolic-diastolic longitudinal excursion.
Figure 13a. Mitral annulus tissue Doppler normal flow velocity profiles: medial (A) and lateral (B) annulus. There are 2 systolic peak waves (s’1 and s’2): in normal subjects the first is higher. There is a consensus to measure the highest wave.
Figure 13b. Mitral annulus tissue Doppler flow velocity profiles in a patient with aortic stenosis and normal LV ejection fraction (upper panels) and a patient with dilated cardiomyopathy, moderate reduction of LV ejection fraction ( 41 %), and mildly increased filling pressures (lower panels).
Measurements. The tissue Doppler velocity profile recognizes several peaks: two positive systolic peaks in the ejection phase (which correlate broadly with LV longitudinal systolic function), and two negative early (e’) and late (a’) diastolic peaks (Figure 13a). There are also two other minor positive and/or negative peaks in the isovolumic contraction and relaxation phases of uncertain significance) LV relaxation is estimated by averaging the lateral and medial e’: the cutoffs for abnormal values are shown in Table 3. Annular lateral velocities are always higher (in the absence of lateral wall ischemia or constrictive pericarditis) because the lateral mitral annulus has a greater spatial excursion (due to the translational movement of the heart)
Pathophysiology. The average peak e’ approximates (with a positive relation) LV relaxation (16, 17). This measurement is particularly important since LV relaxation is the first diastolic property to be impaired in most LV heart diseases (Figures 3-5). The reduction of peak e’ is proportional to the prolongation of LV relaxation. Thus e’, together with the modification of the transmitral E wave (peak E velocity and deceleration time), allows us to estimate the impairment of LV relaxation. Since e’ is less dependent on loading conditions and not related to LV chamber stiffness, its measurement allows us to easily distinguish a normal transmitral flow profile (normal LV filling pressures) from a “pseudo-normal” (increased LV filling pressures). Of note, e’ may independently increase following a significant increase in LV preload (i.e, moderate to severe mitral regurgitation).