Color M-mode Doppler - Clinical Tree

Introduction

Pulsed-wave Doppler velocities of mitral inflow are the most commonly used indices of diastolic function. Their application is nevertheless limited by their load dependency. Flow propagation (Vp) using color M mode Doppler has been proposed as a complementary technique to evaluate left ventricular (LV) relaxation.

Color M mode Doppler echocardiography provides a spatiotemporal map of blood distribution within the heart, with a typical temporal resolution of 5 msec, a spatial resolution of 300 microns, and a velocity resolution of 3 cm/sec. By aligning the cursor parallel to the streamlines of flow we can observe the propagation of flow from the mitral valve to the apex ( Fig. 11.1 ). Assessment of diastolic flow propagation has offered novel information about LV filling dynamics and has been applied in a variety of clinical conditions. Since the initial description of Jacobs and later Brun, computer simulation, in vitro modeling, animal, and clinical studies have improved our understanding of the determinants of Vp but also have shown the complexity of this index. The Vp appears to be relatively independent of loading conditions and therefore may overcome one of the main limitations of Doppler-based techniques.

Fig. 11.1, Color M-mode of mitral inflow obtained from the apical window.

In this chapter we will review the current understanding of how flow propagates from the base to apex of the left ventricle, its major determinants, how to properly obtain a color M mode (CMM) tracing, and clinical situations where this technique may be applied. We will also describe its application in the calculation of intraventricular pressure gradients.

Case Study

A 53-year-old female patient presents with shortness of breath putting on shoes and climbing one flight of stairs. She reports a fullness in the epigastric area. There is no lower extremity edema. Normal coronaries.

Echo shows dilated left atrium, mild respiratory variation, but septal bounce. This color M-mode was obtained showing rapid flow propagation from base to apex ( Fig. 11.2 ).

Fig. 11.2, This color M-mode was obtained showing rapid flow propagation from base to apex.

Background

It is now well recognized that in early diastole there are small but significant intraventricular mitral-to-apex pressure gradients that are generated. These intraventricular pressure gradients (IVPG) are related to elastic recoil and represent one of the driving forces of the blood entering the left ventricle (ventricular suction). As a result, when the mitral valve opens, a column of blood accelerates from the atrium toward the ventricular apex. In normal ventricles, flow propagates very rapidly ( Fig. 11.3 A) while in dilated, poorly contracted ventricles it occurs rather slowly (see Fig. 11.3 B).

Fig. 11.3, Example of a young normal individual (A) and a patient with delayed relaxation (B). Note the difference in color M mode (CMM) Vp slope between the two.

Mitral inflow flow propagation displayed by CMM has a complex pattern. The earliest CMM velocities often occur during isovolumic relaxation. After the mitral valve opens there is a rapid initial component (phase I) often followed by a slower component (phase II). Finally the last component in late diastole is associated with atrial contraction (see Fig. 11.1 ).

Computer and in vitro modeling have helped to understand the complex phenomenon of flow propagation. During phase I, blood moves almost simultaneously in the whole left ventricle behaving as an incompressible fluid column (columnar flow). Phase II is a flow wave thought to be caused by propagation of a ring vortex formed at the ventricular base. Advances in imaging techniques have expanded our understanding of vortex formation and propagation ( Figs. 11.4 and 11.5 ). It has been suggested that vortex formation may contribute to increased efficiency of LV filling. The formation of a vortex is affected by the size and eccentricity of the mitral orifice as well as the geometry and size of the left ventricle. In small, tubular ventricles there is predominant columnar flow with no space from the mitral leaflets to the ventricular wall for vortex formation. In dilated ventricles with decreased ratio of mitral valve orifice to ventricular diameter there would be predominant vortex formation and propagation (see Fig. 11.4 ). In dilated cardiomyopathy vortices move flow toward the LV outflow tract in diastole with little loss in energy and without significant increase in pressure. By in vitro modeling, the ratio of flow velocity to vortex propagation is around 2:1.

Fig. 11.4, Streamlines and color map of the vorticity field showing vortex formation in a normal subject (A) and in a patient with dilated cardiomyopathy (B). Note a larger vortex displaced to the apex in the patient with dilated cardiomyopathy.

Fig. 11.5, Echocardiographic techniques for vortex visualization.

Obtaining and Measuring Flow Propagation

CMM flow propagation is usually measured from the apical four-chamber view. The M mode cursor is carefully aligned with direction of flow, maximizing the distance from mitral tips to apex. At least 4 cm of CMM depth should be obtained and displayed at 100 cm/sec sweep speed. In the initial description by Brun, CMM flow propagation was measured as the slope of color-noncolor interface. The use of the slope of the color-noncolor interface is limited by its interference with isovolumic flow. Since then, several other methods have been proposed, and this constitutes one of the main limitations of this technique and makes it difficult to compare studies among different authors. The slope of the first aliasing velocity has also been used by several authors, setting the aliasing velocity at a percentage (40–70%) of the maximal inflow velocity (see Fig. 11.3 ). An aliasing velocity of 40% of the peak E wave velocity appears to be more reproducible and better reflect the velocity of propagation. There is no consensus guidelines whether phase I or phase II should be measured. Garcia et al. proposed the use of phase II when present.

Stugaard et al. used a computer algorithm to detect the maximal velocities along the center of the flow propagation wave and measured the time delay between the velocity at mitral tips and apex. This method is attractive for it appears to be more objective, but it is not widely available. An automated way to measure the slope of Vp has been described.

Normal values of Vp depend on the methodology used. The slope of first aliasing (40%–50% of peak E velocity) values less than 45 cm/sec are considered abnormal. The interobserver variability of Vp measurements has been reported to be around 12% but can be as high as 20%.

More recently Stewart et al. proposed a semiautomated method taking into account the change of the slope of the curvilinear isovelocity contours. Using statistical point-change analysis, the authors defined the deceleration point. Thus the contour was divided at the deceleration point into the initial propagation and the terminal propagation. Finally a new parameter, the strength of early filling (Vs), was calculated as the product of the distance from the position of the mitral annulus to the deceleration point and the initial Vp ( Fig. 11.6 ). The authors showed that in a validation study of 160 patients, Vs was more accurate than Vp to assess diastolic dysfunction (as defined by reduced diastolic intraventricular pressure gradient, elevated pulmonary capillary wedge pressure (PCWP), or elevated B-type natriuretic peptide). In diastolic dysfunction, the initial velocity was slower and the deceleration point occurred closer to the mitral annulus than with normal filling. Although promising to better describe flow propagation properties, further studies are needed in other laboratories to test the feasibility and usefulness of this method.

Fig. 11.6, Flow velocity propagation and deceleration point. L1 is the distance between annulus and deceleration point.

Late (A Wave) CMM Flow Propagation

Most of the studies have focused on the propagation of early mitral inflow. There are limited data about the importance and clinical significance of the propagation of flow during atrial contraction (Vpa). One study that includes 75 healthy adult subjects age 18 to 79 years revealed a large range of values of Vpa from 26 to 179 cm/sec. Vpa was mainly dependent on age, gender, and LV mass.

There is a fundamental difference between the early and late flow propagation. During early propagation blood is pulled into the ventricle, while during late propagation it is pushed (atrial contraction). A ratio of early to late flow propagation has been reported in patients with pseudonormal filling pattern, although the advantage of this over early Vp alone or E/Vp is unclear. Further studies are required to explore the importance and clinical significance of late diastolic flow propagation.

CMM Intraventricular Pressure Gradients

Given the complexity of CMM inflow pattern and the variability of measurements of flow propagation, a more objective analysis of LV filling is desirable.

It is well known that the presence of regional pressure differences in the left ventricle is related to LV relaxation and suction. Ling et al. demonstrated in a canine model the presence of regional diastolic IVPG between the base and apex of the left ventricle. These gradients resulted in the active filling of the left ventricle. Courtois et al. validated these findings and later demonstrated reduction in IVPG during myocardial ischemia in an animal model. These IVPG relate to elastic recoil and apical untwisting. Greenberg and Thomas used the Euler equation to calculate local pressure gradients:

\frac{\partial p}{\partial s} = - ρ (\frac{\partial v}{\partial t} + v \frac{\partial v}{\partial s})

$\frac{\partial p}{\partial s} = - ρ (\frac{\partial v}{\partial t} + v \frac{\partial v}{\partial s})$

where p, s, t, and v are pressure, distance, time, and velocity, respectively. Integrating the Euler equation from the LV base to apex IVPG can be estimated

Δ P_{IV} (t) = \int_{base}^{apex} \frac{\partial p}{\partial s} d s

$Δ P_{IV} (t) = \int_{base}^{apex} \frac{\partial p}{\partial s} d s$

where ΔP _IV (t) represents IVPG.

This methodology has been reproduced by others and opens the possibility of evaluating diastole in a more fundamental way by measuring one of the driving forces of early filling.

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