Assessment of left atrial function. The EAE textbook of ...

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Assessment of left atrial function. The EAE textbook of Echocardiography Chapter · January 2011

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CHAPTER 10

Assessment of left atrial function Río Aguilar-Torres

Contents

Summary

Summary 151 Introduction 151 Left atrial function 152 Assessment of left atrial dimensions 153

The left atrium (LA) plays an important role in cardiovascular performance, not only as a mechanical contributor, elastic reservoir, and a primer for left ventricular filling, but also as a participant in the regulation of intravascular volume through the production of atrial natriuretic peptide. Although LA diameter in the parasternal long-axis view has been routinely employed, LA volume is a more robust marker for predicting events than LA areas or diameters. The assessment of LA performance based on two-dimensional volumetrics, Doppler evaluation of mitral, pulmonary vein flow, and annular tissue Doppler, as well as deformation imaging techniques, may provide incremental information for prognostic purposes and for the evaluation of severity and duration of conditions associated with LA overload. The aims of this chapter are to explain the basics of LA function, and to describe the role of Doppler echocardiography techniques, and how to implement them, for the non-invasive evaluation of LA in clinical practice.

Echocardiographic examining views for left atrial evaluation 153 Left atrial dimensions 153

Assessment of left atrial function 155 Volumetric assessment of left atrial function 155 Doppler assessment of mitral inflow 157 Assessment of pulmonary venous flow 158 Tissue Doppler assessment of mitral annulus velocities 159 Deformation imaging techniques for the assessment of left atrial mechanics and function: left atrial strain and strain rate 160

Conclusions 161 Personal perspective 162 References 163 Further reading 163 Additional DVD and online material 164

Introduction The main mechanical function of the left atrium (LA) is to facilitate and modulate the filling of the left ventricle (LV) with blood returning from the lungs. This is accomplished during LV systole as a reservoir for the inflow volume from pulmonary veins, as a conduit during early LV diastole transferring blood stored in the atrium, and from the pulmonary veins, to the LV, and finally, as a booster pump that enhances LV end-diastolic filling. The LA was the first cardiac chamber to be analysed employing echocardiography. Although LA assessment has been proven to be very useful in many cardiovascular diseases, the assessment of LA function is complex due to a variety of reasons:

10_Galiuto_Ch10.indd 151

◆

For geometrical assumptions, LA shape is not as simple as LV due to the presence of the LA appendage, confluence of pulmonary veins, and the interatrial septum.

◆

As the size of the LA varies during the cardiac cycle, the temporal sampling should be adequate when precise estimations of dimensional changes are required.

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◆

◆

assessment of left atrial function

No other imaging technique, except echocardiography, can be used as a gold-standard for the evaluation of LA dynamic changes. Although cardiac magnetic resonance (CMR) provides adequate spatial resolution, temporal sampling is insufficient for the assessment of fast changes in dimensions, especially when irregular and fast rhythms are present. Assessment of LA pressure (LAP), fundamental for the evaluation of important functional parameters (i.e. compliance, elastance), is invasive and technically difficult. In addition, LAP is only partially determined by intrinsic LA function due to the fact that LV function and volume status have important influences on it.

Doppler echocardiography, including recent developments, like tissue Doppler imaging (TDI), three-dimensional (3D) echocardiography, and myocardial deformation techniques, constitutes the more extensive set of tools for dimensional and functional evaluation of LA providing important parameters for the assessment of therapeutic interventions and for monitoring prognosis in a wide variety of cardiovascular diseases.

Left atrial function During LV systole and isovolumic relaxation, when the mitral valve (MV) is closed, LA works as a distensible reservoir accommodating blood flow from the pulmonary veins and storing elastic energy generated by systolic descent of the mitral annular plane, in the form of pressure. During early LV diastole, the elastic energy is returned facilitating early LV filling. Then the LA behaves as a conduit that starts with MV opening and terminates before LA contraction allowing passive emptying during early ventricular diastole and diastasis (see E Chapter 9). Finally, at end-diastole LA is also a muscular pump (booster), which operates depending on its own pre-load according to the Frank– Starling mechanism, which contributes to maintaining adequate LV end-diastolic volume by actively emptying (E Table 10.1). The understanding of each of these functions is crucial to correctly interpret phasic changes in dimensions and the patterns of flow into and out of the LA during the cardiac cycle both in normal hearts and in pathological conditions (E Fig. 10.1).

Table 10.1 LA function: phases PHASE I RESERVOIR

PHASE II CONDUIT

PHASE III PUMP BOOSTER

PERIOD

Mechanical systole, including isovolumic periods (IVC and IVR).

- Early diastole and diastasis.

- Late diastole (atrial contraction) in Sinus Rhythm (SR).

BEGGINING

Mitral Valve Closure (MVC)

- Mitral Valve Opening (MVO)

- ~ End of A Doppler wave

- ~ Beggining of E

- ~ Beggining of QRS (ECG)

- ~ End of T-wave (ECG)

END

MVO.

- ~ Beggining of P-wave. (ECG) - MVC

- ~ Beggining of E VOLUME CHANGE

- ~ Beggining of A-wave

- ~ Beggining of Doppler A-wave.

- ~ End of A-wave.

- ~ End of T-wave (ECG)

- ~ Beggining of P-wave. (ECG)

- ~ Beggining of QRS (ECG)

- INCREASES (Filling)

- DECREASES (Passive emptying)

- DECREASES (Late emptying)

- LA starts at its minimum volume and reaches its Maximal volume at the end of phase I

- Early rapid relatively short descent

- Minimum LA volume at the end of atrial contraction.

- Minimal volume changes in LA during diastasis. - Volume at the end of Phase II corresponds to preload for LA contraction PRESSURE CHANGE

INCREASES

- DECREASES

- INCREASES (in SR)

From low pressure, “x” descent, peaking at “v” wave

- Early rapid descent (“y” descent)

- Peaks at “a” wave

QRS


T

P

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assessment of left atrial dimensions LA FUNCTION PHASE:

II CONDUIT

I RESERVOIR

LA VOLUME

LA PRESSURE

LA Contraction

Diastasis

Early LA emptying

“v” wave

III BOOSTER

“a” wave

153

In fact, the LA is more spherical at ventricular end-systole than at end-diastole because the medial–lateral contribution to dimensional changes is usually of lower magnitude. LA dimensions are usually measured just before MV opening, during LV end-systole, because volume is greatest at this point, the chamber has a more spherical shape, and, thus, a single dimension is more representative of LA cavity volume. Such measurements can be done with either M-mode or two-dimensional (2D) mode from the PLAX view. For each view the transducer should be angled to maximize LA size.

Measurement of LA linear dimension

“x” descent “y” descent

ATRIAL FILLING

ATRIAL EMPTYING

Figure 10.1 Left atrial function. Schema indicating the phases of LA function, volume, and pressure changes over the cardiac cycle.

Assessment of left atrial dimensions Echocardiographic examining views for left atrial evaluation Due to its ovoid shape and the variable angulations that the major axis of LA usually presents in respect to the LV major axis, the longest dimension of the LA may not lie in the longitudinal plane. The recommended planes for better assessment of LA anatomy, shape, and dimensions are: ◆

Parasternal long-axis (PLAX) view.

◆

Parasternal short-axis (PSAX) view.

◆

Apical four-chamber (A4C) view.

◆

Apical two-chamber (A2C) view.

◆

Apical three-chamber (A3C) view.

In PLAX view, the M-mode scan line should be directed orthogonal to aortic root and LA walls. According to European Association of Echocardiography/ American Society of Echocardiography (EAE/ASE) guidelines the convention for M-mode assessment is to measure from the leading edge of the posterior aortic wall to the leading edge of the posterior LA wall. However, to avoid the variable extent of space between the LA and aortic root, the trailing edge of the posterior aortic is recommended. Normal LA anteroposterior dimension ranges from 19–40mm and the LA/aortic root ratio should be equal or less than 1.1/1. This method is the simpler; however, it is neither reproducible nor accurate, and insensitive to changes in LA size (E Fig 10.2).

Measurement of LA volume The measurement of LA volume enables accurate assessment of the asymmetric remodelling of the LA. In addition, LA volume is a more robust marker for predicting events than LA areas or diameters. LA volume reflects the cumulative effects of increased filling pressures over time: due to this reason LA volume has been called the ‘glycosylated haemoglobin of diastolic dysfunction’. Volume is the recommended dimension for the evaluation of LA size and should be determined in all clinical studies in which

As the interatrial septum is orthogonal to ultrasound scan lines in the subcostal long-axis view, this projection is preferred for an adequate assessment of this structure.

Left atrial dimensions Use of a standardized approach for LA size assessment is recommended. The use of a single diameter to assess LA dimension assumes that the chamber expands and contracts symmetrically, maintaining a constant shape and not taking into account that the LA often enlarges asymmetrically. During the cardiac cycle, the LA expands primarily by elongating in the superoinferior and anteroposterior directions, mainly due to the systolic descent of the mitral annular plane (that suctions like a syringe) but also due to the elevation of the aortic roof during the ejective period ( 10.1).


Figure 10.2 Left atrial size measurement. M-mode left atrial linear size.

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atrial distortion would make the information provided by the anteroposterior dimension misleading, and in follow-up studies where quantitative accuracy is important. 2D biplane method In clinical practice, for LA volume measurement 2D biplane methods are recommended because the majority of prior research and clinical studies have used these options. Either the Simpson’s rule (method of discs) or the area–length method is valid (E Table 10.2). After tracing the LA cavity areas, the measurement software package automatically calculates the LA volume in millilitres according to the modified summation of discs method or using the area–length formula (E Fig. 10.3): LA volume (mL) = (0.85 × A4C area × A2C area) / Length (10.1) Table 10.2 Modified biplane methods LA measurement: Modified biplane Simpson’s rule or area–length method How to calculate it: Step 1. Use 2 orthogonal planes of the LA (usually A4C and A2C views) Step 2. Obtain the best image quality, optimizing sector width and place focal zones distally for better lateral resolution in the far-field and increasing gain just to the point on which image drop-outs in the atrial walls have disappeared Step 3. Avoid LA foreshortening to obtain maximal LA size (discrepancies in length measured from the two orthogonal planes should be ≤5mm) Step 4. Select adequate frames for measurement. For maximal LA volume select end-systolic frame (just before mitral valve opening, end of T wave on ECG) Step 5. LA area border planimetry, the inferior border should be the mitral annular plane and endocardial tracing should exclude atrial appendage and pulmonary veins Step 6. Long axis LA: orthogonal to mitral annulus plane from its midpoint to superior margin of LA∗. ∗ As small discrepancies are acceptable, the most common option is to average the two lengths from the 4-chamber and 2-chamber views.

The advantages of Simpson’s method are that it does not require input of a specific length for volume calculation, incorporates small irregularities in each disc, and is theoretically more accurate than the area–length method (being small differences in clinical practice). LA size varies with body size: so, rather than as absolute volumes it is preferable to express ‘body surface area (BSA) indexed LA volume’, in mL/m2 (E Table 10.3) It seems that in people free of cardiovascular disease, indexed LA volume is independent of age from childhood onward. Agerelated LA enlargement could be a reflection of pathological states that often accompany advancing age rather than a consequence of chronologic aging. A LA volume index greater than 34mL/m2 has proven to be a robust, independent, and reproducible predictor of cardiovascular events (atrial fibrillation, heart failure, ischaemic stroke, and death) in large follow-up studies. Real-time 3D echocardiography As real-time 3D echocardiography does not rely on any geometrical assumption, and is not subject to plane positioning errors (which can lead to chamber foreshortening), these

Table 10.3 2D-echocardiographic reference LA volume indexed values in adults Normal LA indexed (BSA) maximum volume:

22 ± 6mL/m2

Normal LA indexed (BSA) minimum volume:

9 ± 4mL/m2

Normal mean total emptying volume:

13.5 ± 4.3mL/m2

Mild LA enlargement (>1 SD from mean normal):

28–33mL/m2

Moderate LA enlargement (>2 SD from mean):

34–40mL/m2

Severe LA enlargement (> 3 SD from mean):

>40mL/m2

∗Established using 2D biplane methods. As a continuous variable, LA volume is best used as such instead of using cut-off values. After correction by BSA, gender has little influence, and reference values and cut-off values are the same for either male or female irrespective of age. SD, standard deviation

Figure 10.3 Calculation of left atrial 2D volume. Biplanar LA volume using A4C and A2C views. Calculations according to A-L formula.


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assessment of left atrial function methods are appealing alternatives for measuring LA volumes. However, a relatively low frame rate might preclude an accurate and reproducible assessment of LA volume change throughout the cardiac cycle and may prove to be the preferred method of LA volume assessment in large studies in the future (E Figs. 10.4 and 10.5; 10.2 and 10.3). E Tables 10.4 and 10.5 summarize causes of LA enlargement and conditions of LA smaller than expected, respectively LA volume measurements should be considered in conjunction with a patient’s age, clinical status, other chambers’ volumes, and Doppler parameters.

155

Assessment of left atrial function Volumetric assessment of left atrial function In addition to LA size, the assessment of LA performance based on the 2D volumetric method may provide incremental information for the evaluation of severity and duration, of conditions associated with LA, of volume or pressure overload, and for predicting events.

Figure 10.4 Real-time 3D imaging of left atrium. Views from the LA roof at the right superior pulmonary vein level. Mitral valve is seen at the bottom of the images in four different phases of the cardiac cycle. Interatrial septum appears at the right-side. ∗ fosa valis; ∗∗ left atrial appendage. A) End-systolic, LA maximal expansion. B) Earlydiastole, beginning of passive emptying. C) Diastasis, immediate before LA contraction (pre-A volume). D) Minimal atrial volume after LA contraction (end of LV diastole).

Figure 10.5 3D echocardiography assessment of left atrial volume. LA volume calculation using 3D echo and automatic tracking of wall. The curve represents changes in volume throughout the cardiac cycle.


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Table 10.4 Causes of LA enlargement Atrial pressure overload: Diastolic dysfunction Mitral valve stenosis Cor triatriatum Stiff LA syndrome: marked decrease in compliance due to wall fibrosis or calcification Atrial volume overload: Atrial fibrillation or flutter Mitral valve regurgitation Left-to-right shunts: Atrial septal defect Ventricular septal defect Patent ductus arteriosus High-output states (usually with generalized four-chamber enlargement): Anaemia Arteriovenous fistulas Athletes in the absence of cardiovascular disease Other causes: Congenital aneurysms of the LA: more frequently confined to the atrial appendage Left juxtaposition of atrial appendages Unroofed coronary sinus Post-surgical abnormalities: Atrial baffles Atrial anastomosis (heart transplant)

Table 10.5 Causes of smaller than expected LA Foreshortened views: are the commonest cause of an apparently small LA Left-to-right shunts with bypass of LA: total or partial anomalous pulmonary venous connection with or without ASD External compression: Enlarged aorta (root aneurysm as in Marfan’s syndrome, chronic aortic dissection) Extracardiac masses or structures (elevation and change in angulation of LA): hiatal hernia LA rotation due to extreme RA dilation Other: hypoplasia of the left heart

mechanism, active LA pumping function improves with greater LA pre-A volumes, only to a certain point, beyond which LA starts to deteriorate. It is recommended to always employ all of these volumes indexed by BSA. LA volumes representing changes throughout the cardiac cycle can be calculated (E Fig 10.6): 1) Reservoir volume, that is considered as filling or expansion volume, is calculated as: LAV AVmax − LAV Vmin

(10.2)

2) Active pumping volume, that is considered as LA stroke volume, is calculated as: LAV AVpre-A

LAV LAV Vmin

(10.3)

Atrial systole also causes contraction at the inner circular muscle layer of the pulmonary vein’s entry into the LA. This sphincter-like effect seems to prevent important flow back during atrial active emptying, if pressure gradients are adequate. In pathological conditions, with elevated LV enddiastolic pressure (LVEDP), as pulmonary veins compliance is greater than LV compliance, the total amount of the retrograde flow into the pulmonary veins will increase. 3) Conduit volume is not easily measured, because, while the MV is open, some blood flows directly from the pulmonary veins. Thus it is estimated as LA passive emptying plus direct blood flow from pulmonary veins to LV and calculated as: LV stroke volume − LA stroke volume

(10.4)

As it can be easily inferred, a reciprocal relation exists between conduit and reservoir and pump booster functions of the LA (E Fig. 10.7)

The basic LA volumes are: ◆

Maximal LA volume (LAVmax): is the volume at end-systole (timed to the moment immediately before MV opening or end of T-wave on electrocardiogram [ECG]).

◆

Minimal LA volume (LAVmin): occurs at MV closure (timed to QRS onset on ECG).

◆

Volume pre-A (LAVpre-a): is the volume immediately before atrial contraction (timed to the onset of the P-wave). This volume represents LA preload before atrial contraction. It has been shown that, according to the Frank–Starling’s


Figure 10.6 Assessment of left atrial function. Schema showing volumetric assessment of LA function.

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157

Figure 10.7 Left atrial volume change during cardiac cycle. Curves, representing simultaneous reciprocal changes in LV areas (top) and LA volumes (bottom) in one cardiac cycle.

The change in total LA volume is not equivalent to the volume entering the LV during ventricular diastole, even in the absence of mitral regurgitation or shunt at the atrial level, because some flow enters the LV directly from pulmonary veins during passive LV filling and also a variable amount of blood flows back to pulmonary veins during atrial contraction phase. When sinus rhythm is present, it has been estimated that, in subjects with normal diastolic function, reservoir, conduit and booster pump functions, relative contributions of the LA to the LV filling is approximately 40%, 35%, and 25%, respectively. As LV diastolic dysfunction progresses, the booster pump and the reservoir functions increase, decreasing conduit function. However, when LV filling pressure is high and diastolic dysfunction is very advanced, LA serves predominantly as a conduit. Both conduit and pump function varies with age. With advanced age, active pumping accounts for less of total emptying. Although many other indices have been described for specific purposes, the main functional parameters that can be derived from volumetric assessment are described in E Table 10.6. Echocardiographic equipment from different vendors allow the use of automatic motion tracking of endocardial border based on diverse algorithms (acoustic quantification, speckle tracking, boundary detectors based on optical flows). The main advantages of these techniques are that are fast, simple, and may provide several indices for LA function assessment derived from LA volume curves. However, when employing automatic tracking, an exquisite verifying is needed, in order to avoid mistakes in traces and timing (selection of end-systolic or enddiastolic frames). As a rule of thumb for automatic tracking systems, the greater the image quality is, the greater the accuracy of automatic tracking (E Fig. 10.8).


Doppler assessment of mitral inflow Doppler analysis of transmitral flow velocities and time intervals may provide fundamental information for the assessment of LA–LV diastolic interaction and function, being considered a mandatory part of each echocardiographic study. In fact, mitral inflow Doppler pattern enables the classification of diastolic dysfunction, according to E/A ratio and DT (see E Chapter 9). These parameters, however, are influenced by many simultaneous haemodynamic variables that make it very difficult to obtain pure information about the functional status and performance of LA (E Table 10.7). Table 10.6 Basic indices of LA function based in volumes Reservoir function: (+Δ, positive volume change) Filling or expansion volume : LAVmax − LAVmin Expansion index: ([LAVmax − LAVmin]/LAVmin) × 100 Diastolic emptying index: ([LAVmax − LAVmin]/LAVmax) × 100 Conduit function: (−Δ, negative volume change) Passive emptying index : ([LAVmax − LAVpre-a]/LAVmax) × 100 Passive emptying percent of total emptying: ([LAVmax − LAVpre-a]/[LAVmax − LAVmin]) × 100 Booster pump function: (−Δ, negative volume change) Active emptying index : ([LAVpre-a − LAVmin]/LAVpre-a) × 100 Active emptying percent of total emptying: ([LAVpre-a − LAVmin]/[LAVmax − LAVmin]) × 100

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Figure 10.8 Automatic endocardial border tracking based on boundary detectors. Upper panel: curves representing changes in LA volume (orange line), volume/time (blue line). Mid panel: changes in diameter. Lower panel: regional contribution of different LA segments to volumetric changes.

Table 10.7 Mitral inflow Doppler analysis determinants for the assessment of LA–LV diastolic interaction E-wave peak velocity and deceleration time (DT)

A-wave∗

LA–LV pressure gradient during early diastole

LA–LV pressure gradient during late diastole

Determinants: LV preload LV relaxation LV elastic recoil (suction) LV compliance Mitral valve orifice area

Determinants: LV compliance (LVEDP) LA contractile function

∗Deceleration time of the A-wave in order to predict high diastolic pressures is low, and in general provides little information about LA function.

function are affected. The LA behaves mainly as a conduit. LA contribution to LV filling decreases (E Fig. 10.9). According to EAE/ASE recommendations for diastolic dysfunction, also the other secondary measurements of diastolic function (A-wave duration, A-wave velocity time integral [VTI], total mitral inflow VTI and atrial filling fraction, that is A-wave VTI/total mitral inflow VTI) may contain LA functional information (see E Chapter 9). Main limitations of transmitral inflow Doppler analysis are: ◆

Tachycardia (merging of waves).

◆

Irregular rhythm (mainly atrial fibrillation).

◆

Mitral valve disease.

Assessment of pulmonary venous flow As diastolic dysfunction progresses, LA volume contributions to LV filling become different: ◆

In cases of abnormal LV relaxation (see E Chapter 9), a reduction in LA conduit volume and an enhancement of reservoir-pump complex take place.

◆

In cases of LVEDP elevation a progressive reduction in LA active contraction occurs. With sustained advanced degrees of diastolic dysfunction, LA contractility and reservoir


The analysis of pulmonary vein flow, especially atrial velocity reversal and duration, is helpful for assessment of LA function and diastolic performance of the LV (see E Chapter 9). The antegrade systolic period represents reservoir function, while the antegrade diastolic period represents conduit function and the atrial reversal wave indicates pump function (E Figs. 10.10–10.12; 10.4). Mechanisms, determinants, and abnormalities of each phase have been summarized in E Tables 10.8 and 10.9.

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159

Figure 10.11 Colour Doppler M-mode for pulmonary vein flow assessment. Colour Doppler M-mode recorded from the pulmonary vein up to the LV in a normal subject. Pulmonary venous flow contribution to LA and LV filling is seen as flows coded in red crossing the LA. Small atrial contribution is represented by a small late A wave across the mitral valve.

Figure 10.9 Abnormal relaxation pattern. Upper panel: pulsed wave Doppler at the mitral inflow. Mid panel: changes in volume and pressure. Lower panel: pulmonary venous flow. The decrease in E velocity and prolonged decay (deceleration time) correlates with changes in D wave at the PV flow.

Figure 10.12 Transoesophageal echo during pulmonary vein ablation procedure for paroxysmal atrial fibrillation. PW Doppler recorded at the left superior pulmonary vein, first beats immediate post-recovery of sinus rhythm. S1, S2, and D waves are clearly seen; however, atrial reversal wave is not seen despite comparison of P wave on the ECG (transient stunning).

Tissue Doppler assessment of mitral annulus velocities

Figure 10.10 Pulmonary venous flow pattern. PW Doppler recorded at the right superior pulmonary vein. Normal LA and LV function.


The two major components of mitral annulus motion diastolic waves, the mitral annular early diastolic (E′) and the late diastolic (A′), can be recorded and evaluated as representative of diastolic LV and LA function (see E Chapter 9). Low E′ peak velocity values are indicative of abnormal LV relaxation even with high LV filling pressures. The lower the A′ peak-velocity, the greater the LVEDP. This parameter is determined mostly by haemodynamic parameters of LA function, such as LA contractility, pre- and afterload (E Fig. 10.13).

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Table 10.8 Pulmonary venous flow analysis mechanisms and determinants for the assessment of LA function Antegrade systolic flow (S wave)

Antegrade diastolic flow (D wave)

Atrial reversal flow (aR wave)

LA expansion during LV systole. RESERVOIR

PV to LA gradient and PV to LV gradient. CONDUIT

Atrial contraction during LA systole. PUMP BOOSTER

This flow can be biphasic: S1: early peak systolic velocity due to atrial relaxation (‘x’ descent on the LA pressure curve). This component is better visualized in the presence of low filling pressures and lower heart rates S2: late systolic peak due to mitral annulus plane displacement

As LA is open to the LV during early diastole, both the peak velocity and the deceleration time of D wave are closely related to transmitral peak E velocity and deceleration time. Timing of peak D wave occurs a short time later than E wave (~50ms)

LA pump function causes both forward flow through the MV and reversed flow into the PV. The LA systolic pressure and the amount of forward flow are influenced by the enddiastolic pressure against which the LA must contract

1. Early systolic-LA relaxation: dependent on the previous LA contraction 2. Late-systolic mitral annular displacement: major determinant of LA filling 3. LA compliance: LA chamber stiffness 4. Right ventricular systole through PV flow 5. Mean LA pressure (LAP)

1. Early diastolic LA–LV pressure gradient 2. LV relaxation 3. LV compliance 4. Pulmonary venous flow 5. Mitral valve apparatus obstruction

1. LV compliance 2. LVEDP 3. LA contractility. 4. LA preload

Table 10.9 Pulmonary venous flow analysis abnormal patterns in LA and LV diastolic dysfunction Antegrade systolic flow (S wave)

Antegrade diastolic flow (D wave)

Atrial reversal flow (aR wave)

1. Abnormal LA relaxation: ↓ S1 wave velocity. Related to the elastic energy stored in previous LA contraction. 2. AV conduction block: S1 due to atrial relaxation follows the P waves of the ECG, including those not conducted to the LV. 3. Atrial fibrillation: ↓ S1 wave velocity (due to atrial relaxation persists although at a reduced velocity) 4. Increase in mean LA pressure (LAP): ↓ S1, disappears if mean LAP is very ↑ 5. LV ischaemia: ↓ S2 as longitudinal LV myocardial shortening 6. Decrease in LA compliance: ↓ S2 as LA chamber stiffness increases: 7. Mitral regurgitation: ↓ S2 progressive decrease with complete reversal if regurgitation is very severe.

1. ↑ 2. ↓ 3. ↑ 4.

1. High LVEDP: ↓ in forward flow into the LV and ↑ in velocity and duration of aR wave lasting 30ms more than antegrade A wave 2. Increase in LA contractility: ↑ in both forward and aR flow velocities.

5. ↑ 6. ↑ 7. ↑

Increase in LA–LV pressure gradient: D wave velocity Prolonged LV relaxation: D wave velocity due to lower LA–LV gradient Decreased LV compliance: D wave as LA pressure increases Mid-diastolic forward flow: In situations with high LV filling pressures. Concomitant with transmitral L wave Pulmonary venous obstruction: D wave velocity > 1m/s (> 2m/s when severe) MV apparatus obstruction: D wave velocity and prolonged decay Obstruction at the atrial level: Masses, membranes (i.e. Cor triatriatum). D wave velocity and prolonged decay

Deformation imaging techniques for the assessment of left atrial mechanics and function: left atrial strain and strain rate Global and segmental deformation analysis for the assessment of LA systolic and diastolic function is possible using deformation parameters obtained with either Doppler myocardial techniques (TD-derived) or with grey-scale derived algorithms (speckle tracking) (10.5) (see E Chapter 6)


Strain and strain rate (SR) can be obtained during ventricular and atrial systole using sample volumes placed in the atrial myocardium. During the reservoir phase, the atrial myocardium is pulled down by the systolic displacement of the LV annular plane. During this phase strain profile quantitates the relative amount of lengthening and stretching of LA walls. LA strain is strongly influenced by LV systolic function but passive atrial tissue properties also play a role.

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conclusions

161

Limitations of deformation techniques for the evaluation of LA function are:

Figure 10.13 Tissue Doppler for left atrial function assessment. Tissue Doppler recorded at the annular level of the interventricular septum. Normal pattern with normal velocities.

LA strain during LA contraction appears to be a measure of LA systolic function, related to LVEDP, while SR better reflects atrial contractility and relaxation (E Figs. 10.14 and 10.15) The advantages of deformation techniques for the evaluation of LA function are: ◆

Excellent temporal resolution, especially using TD.

◆

Possibility of assessing LA strain and SR in atrial fibrillation.

◆

Possibility of allowing global as well as regional assessment of intrinsic myocardial deformation properties (stretch of myocardium related to LA compliance, relaxation, and contractility) that might help to detect functional abnormalities in LA earlier than conventional echocardiographic parameters. However, to better define clinical applications, additional studies are needed.

◆

Angle-dependency of TD-derived deformation parameters, making the analysis of some regions of the LA wall very difficult. In contrast, methods based in grey-scale images provide angle-independent information.

◆

Complexity and time-consuming.

◆

Lower lateral resolution of LA walls located in the far-field in apical projections, in contrast to LV myocardium. Quantitative information is obtained from a relatively low number of stable patterns of speckles.

◆

Difficulty in tracing endocardial and tracking of speckles of LA thin wall.

◆

Possibility of analysing only the longitudinal component of deformation with current technology.

◆

Exclusion for analysis of interatrial septum should be recommended.

◆

Absence of software packages specifically designed for LA deformation evaluation.

Conclusions The assessment of LA function is increasingly being used in various cardiovascular diseases because of its prognostic implications and the ability to detect changes induced by therapies. Quantification of LA size is one of the mandatory items to be included, and should be reported in every echocardiographic study. Indexed volumes are preferred over linear dimension assessment because they better reflect severity and duration of LA pressure or volume overload, and also because it has shown

Figure 10.14 Longitudinal left atrial strain curves obtained with 2D speckle-tracking. Positive peak at end-systole represents maximal elongation caused by LV pull-down at the end of its ejective period.


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Figure 10.15 Algorithm for deformation analysis. la velocity (upper), strain (mid), and strain-rate (bottom) curves obtained using VVI algorithm. It is noticeable how similar the strain curve is to that of volumetric changes.

to be an effective method for the early detection of subclinical abnormalities of LA function. Phasic volumetric changes, and some traditional Doppler parameters, provide important clues, reflecting LA contribution and modulation of LV filling. However, many of these parameters directly affected by atrial function (transmitral A wave, atrial reversal flow at the pulmonary veins, Aa wave by TDI) present

Personal perspective A few years ago, echocardiographic assessment of LA was limited to a little more than the semiquantitative description of its enlargement. Due to its prognostic implications, evaluation of LA has become an important part of every ECG. In addition, echocardiography has provided important physiological information, contributing to better understanding of LA function and its interaction with the LV during the complete cardiac cycle, not only during diastole. Like other cardiac chambers, there is no single parameter to summarize LA function and multiple parameters determine the different phases of LA function.


an important limitation: evaluation in subjects with atrial fibrillation is not possible. Some new appealing techniques, as the recently incorporated deformation parameters, might provide important information about the intrinsic mechanical properties of LA. However, extensive use, development of specific applications, and validation of some measurements are still required before their consolidation in the clinical scenario.

Characterization of LA improves the evaluation of LV dysfunction, providing information about time of evolution (the past), the current haemodynamic situation (the present), and prognosis, regarding cardiovascular events, including death, in follow-up studies (the future). But, even in the absence of LV dysfunction, LA assessment is also of great value for suspecting a constellation of disturbances, categorized as pressure or volume LA overload or primary abnormalities in contractile function, which can be key factors for correct diagnosis of a previously unsuspected cardiac disease. At the clinic, remember that echocardiography is the main method for LA functional assessment, and when at the echo lab, do not forget to assess the LA adequately.

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further reading

References 17 1 Oh JK, Seward JB, Tajik AS (eds). The Echo Manual. 3rd ed. Philadelphia, PA: Lippincott Williams and Wilkins; (2007), pp.120–42. 2 Weyman AE. Principles and Practice of Echocardiography, 2nd ed. Philadelphia, PA: Lea and Febiger; (1994), pp.471–97. 3 Anwar AM, Geleiijnse ML, Soliman OII, Nemes A, Ten Cate FJ. Left atrial Frank-Starling law assessed by real-time, threedimensional echocardiographic left atrial volume changes. Heart (2007); 93:1393–7. 4 Barbier P, Solomon SB, Schiller NB, Glantz SA. Left atrial relaxation and left ventricular systolic function determine left atrial reservoir function. Circulation (1999); 100:427–36. 5 Borg AN, Pearce KA, Williams SG, Ray SG. Left atrial function and deformation in chronic primary mitral regurgitation. Eur J Echocardiogr (2009); 10:833–40. 6 Bukachi F , Waldenström A , Mörner S , Lindqvist P , Henein MY, Kazzam E. Pulmonary venous flow reversal and its relationship to atrial mechanical function in normal subjects – Umea general population heart study. Eur J Echocardiogr (2005); 6:107–16. 7 De Marchi SF, Bondenmüller M, Lai DL, Seiler C. Pulmonary venous flow velocity patterns in 404 Individuals without cardiovascular disease. Heart (2001); 85:23–9. 8 Gentile F, Mantero A, Lippolis A, Ornaghi M, Azzollini M, Barbier P, et al. Pulmonary venous flow velocity patterns in 143 normal subjects aged 20 to 80 years old. An echo 2D colour Doppler cooperative study. Eur Heart J (1997); 18:148–64. 9 Ha JW, Ahn JA, Moon JY, Suh HS, Kang SM, Rim SJ, et al. Triphasic mitral inflow velocity with mid-diastolic flow: the presence of mid-diastolic mitral annular velocity indicates advanced diastolic dysfunction. Eur J Echocardiogr (2006); 7:16–21. 10 Hoit BD, Gabel M. Influence of left ventricular dysfunction on the role of atrial contraction: an echocardiographic-hemodynamic study in dogs. J Am Coll Cardiol (2000); 36: 1713–9. 11 Hoit BD. Assessing atrial mechanical remodelling and its consequences. Circulation (2005); 112:304–6. 12 Kamohara K, Popovi ZB, Daimon M, Martin M, Ootaki Y, Akiyama M, et al. Impact of left atrial appendage exclusion on left atrial function. J Thorac Cardiovasc Surg (2007); 133: 174–81. 13 Marino P, Faggian G, Bertolli P, Mazzucco A, Little W. Early mitral deceleration and left atrial stiffness. Am J Physiol Heart Circ Physiol (2004); 287:H1172–78. 14 Nagueh SF, Sun H, Kopelen HA, Middleton KJ, Khoury DS. Hemodynamic determinants of the mitral annulus diastolic velocities by tissue Doppler. J Am Coll Cardiol (2001); 37: 278–85. 15 Nishimura RA, Martin DA, Hatle LK, Tajik AJ. Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography. Circulation (1990); 81:1488–97. 16 Okamatsu K, Takeuchi M, Nakai H, Nishikage T, Salgo IS, Husson S, et al. Effects of aging on left atrial function assessed by


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two-dimensional speckle tracking echocardiography. J Am Soc Echocardiogr (2009); 22:70–5. Ommen SR, Nishimura RA, Appleton CP, Miller FA, Oh JK, Redfield MM, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures. a comparative simultaneous Dopplercatheterization study. Circulation (2000); 102:1788–94. Ommen SR, Nishimura RA. A Clinical Approach to the assessment of left ventricular diastolic function by Doppler echocardiography: update (2003). Heart (2003); 89(Suppl III):iii18–iii23. Sanfilippo AJ, Abascal V, Sheehan M, Oertel LB, Harringan P, Hughes RA, et al. Atrial enlargement as a consequence of atrial fibrillation: a prospective echocardiographic study. Circulation (1990); 82:792–7. Sirbu C, Herbots L, D’hooge J, Claus P, Marciniak A, Langeland T, et al. Feasibility of strain and strain rate imaging for the assessment of regional left atrial deformation: a study in normal subjects. Eur J Echocardiogr (2006); 7:199–208. Spencer KT, Mor-Avi V, Gorcsan III J, De Maria A, Kimball TR, Monaghan MJ, et al. Effects of aging on left atrial reservoir, conduit, and booster pump function: a multi-institution acoustic qualification study. Heart (2001); 85:272–7. Suga H. Importance of atrial compliance in cardiac performance. Circ Res (1974); 35:39–43. Vianna-Pinton R, Moreno CA, Baxter CM, Lee KS, Tsang TS , Appleton CP . Two-dimensional speckle-tracking echocardiography of the left atrium: feasibility and regional contraction and relaxation differences in normal subjects. J Am Soc Echocardiogr (2009); 22:299–305.

Further reading Abhayaratna WP, Seward JB, Appleton CP, Douglas PS, Oh JK, Tajik J, et al. Left atrial size physiologic determinants and clinical applications. J Am Coll Cardiol (2006); 47:2357–63. Appleton CP, Kovács SJ. The role of left atrial function in diastolic heart failure. Circ Cardiovasc Imaging (2009); 2: 6–9. Evangelista A, Flachskampf F, Lancellotti P, Badano L, Aguilar R, Monaghan M, et al. European Association of Echocardiography recommendations for standardization of performance, digital storage and reporting of echocardiographic studies. Eur J Echocardiogr (2008); 9:438–48. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification. Eur J Echocardiogr (2006); 7:79–108. Nagueh SF, Appleton CP, Gillebert TC, Marino PN, Oh JK, Smiseth OA, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Eur J Echocardiogr (2009); 10:165–93. Stefanadis C, Dernellis J, Toutouzas P. A clinical appraisal on left atrial function. Eur Heart J (2001); 22:22–36. Tsang TSM. Echocardiography in cardiovascular public health: The Feigenbaum Lecture (2008). J Am Soc Echocardior (2009); 22: 649–56.

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CHAPTER 10


Additional DVD and online material 10.1 Left atrial expansion in superoinferior and anteroposterior directions. 10.2 3D echocardiographic image of left atrium and mitral valve.

10.4 Systolic and diastolic period assessed by colour Doppler. 10.5 Assessment of systolic and diastolic LA function using deformation parameters. E For additional multimedia materials please visit the online version of the book (M http:// ——).

10.3 Calculation left atrial volume by 3D echocardiography.

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