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A 68-year-old woman was transferred to the emergency room with paroxysmal nocturnal dyspnea. She had comorbidities with obesity, hypertension, and glucose intolerance and had been treated with calcium channel and angiotensin-II receptor blockers. On admission, her oxygen saturation was 90%, blood pressure 186/102 mmHg, and heart rate 102 bpm with regular rhythm. The point-of-care echocardiography revealed mildly reduced left ventricular (LV) systolic function with concentric hypertrophy, while LV ejection fraction was visually estimated to be 50%. The left atrium and inferior vena cava were dilated. Physical examination confirmed jugular venous dilatation and edema in bilateral lower extremities. Laboratory tests showed that estimated glomerular filtration rate was 36 mL/min/1.73 m 2 and B-type natriuretic peptide level was 360 pg/mL. Her symptoms and signs of heart failure were controlled by adding loop diuretics, whereas Doppler echocardiography showed that E wave velocity was 84 cm/sec, A wave velocity was 40 cm/sec, E/e′ 21, and left atrial volume index was 42 mL/m 2 , indicating that LV filling pressure remained to be elevated.
This is a typical case with heart failure with preserved ejection fraction (HFpEF). Enlarged left atrial (LA) size is an important characteristic of HFpEF besides signs of impaired diastolic function. Because the number of patients with HFpEF is increasing, routine measurement of LA size is mandatory when scanning a patient with heart failure symptoms.
The left atrium is the most posteriorly positioned among all cardiac chambers. The four pulmonary veins (right superior, right inferior, left superior, left inferior) enter from the posterior part of the left atrium. The left atrium also has a continuum of mitral leaflets in conjunction with the left ventricle. In front of the left atrium, the ascending aorta exists, and the tracheal bifurcation, the esophagus, the descending aorta, and the vertebra column coexist behind. The walls of the left atrium consist of thin musculature with nonuniform features and include the left atrial (LA) appendage with pectinate muscles. In one cardiac cycle, the LA dimension changes mainly at anteroposterior and superoinferior directions, producing the phasic LA volumetric changes. The left atrium has three functions (see Chapter 4 ), including reservoir, conduit, and booster pump, and can be a buffer chamber to modulate left ventricular (LV) filling. During ventricular systole, the left atrium actively relaxes and passively dilates through the descent of cardiac base. The LA reservoir capacity thus enables to sufficiently collect the pulmonary venous inflow and then functions as a conduit, allowing the passage of stored blood from the left atrium and the left ventricle. During LV late diastole, the left atrium acts as a booster pump. The LA booster function contributes to one-third of the LV filling and plays an important role in maintaining normal cardiac output through the Frank-Starling mechanism.
The left atrium gradually enlarges due to a burden of elevated LV filling pressure and diastolic dysfunction. Thus the LA size is widely recognized as a novel marker of cardiovascular risks in the general population and various cardiovascular diseases. The LA function can be assessed using transthoracic echocardiography (TTE) from phasic changes of LA volumes, transmitral flow and mitral annular velocities, and atrial deformation indices. The estimation of LA functional parameters in addition to LA size leads to a better understanding of LA mechanics as well as risk stratification of cardiovascular outcomes.
To measure the LA size, TTE is recommended by the American Society of Echocardiography. Transesophageal echocardiography (TEE) should not be used for the measurement of the LA size because the entire left atrium frequently cannot be included within the image plane with TEE.
M mode echocardiography was the first TTE application used to assess LA size. The LA internal dimensions should be measured at LV end systole when the LA chamber reaches its maximal dimension, from the parasternal long axis view perpendicular to the aortic root long axis. After the cursor is set at the level of the aortic sinuses, the anteroposterior diameter can be calculated by trailing the leading edge of the posterior aortic wall to the leading edge of the posterior LA wall.
When the M mode cursor is not perpendicular to LA posterior wall, two-dimensional (2-D) guided linear measurement should be performed to measure LA anteroposterior diameter. Despite its lower temporal resolution, 2-D guidance provides the optimal orientation for obtaining the anteroposterior linear dimension of the left atrium. While the anteroposterior diameter is the most reproducible measurement, the left atrium also expands in the superoinferior direction through LV long axis shortening. Thus M mode or 2-D guided linear methods for determination of LA size underestimate LA volume due to geometric assumption. Consequently the inconsistencies are pronounced among patients with LA remodeling.
Instead of linear dimensions, LA area can be planimetered from the apical views. The measurements of LA area overcome the inaccuracy of the M mode method because LA enlargement is not uniform. While recording images for the measurements of optimal LA area, care should be taken to avoid foreshortening of the left atrium.
LA volume can be used as a biomarker of the burden and chronicity of LV diastolic dysfunction. LA volume can be estimated using the biplane calculation of the LA area-length from apical four-chamber and two-chamber views. The area-length method is based on the assumption of an ellipsoidal LA shape. Accordingly, the biplane disk summation algorithm, similar to its application for measurements of LV volume, should be used for the standard of the LA volumetric assessment. Mathematically, the measurements of the LA volume can be performed by adding the volumes of a series of elliptic cylinders of known height ( h ):
where D 1 and D 2 are orthogonal minor and major transverse axes of each cylinder ( Fig. 12.1 ). When the left atrium maximally expands just before mitral valve opening, the LA volume should be measured on the optimal frame ensuring alignment along the true long axis of the left atrium. The tracings of LA endocardial border should exclude the area under mitral annular plane, the pulmonary veins, and the LA appendages. The upper normal indexed maximal LA volume of 34 mL/m 2 is recommended to use in a risk-based approach for determination of cutoffs between a normal and an enlarged left atrium. The measurements of the LA volume using B mode echocardiography are still limited in accuracy due to the asymmetrical process of LA remodeling. 2-D echocardiographic methods significantly underestimate the LA volume compared with computed tomography (CT).
Three-dimensional (3-D) echocardiography is not based on geometric assumption, providing more accurate measurement of the LA volume and greater prognostic ability than a 2-D approach. The 3-D technique enables to accurately display a maximized LA plane without LA foreshortening in the apical four-chamber and two-chamber views in which LA and LV axes do not lie in the same plane. Despite these advantages, 3-D echocardiography has limitations to analyze the LA volume in a clinical practice because of low spatiotemporal resolution, lack of standardized methodology, and limited normative data compared with the 2-D method. Another limitation may be the time and training required to obtain accurate and reproducible 3-D volumetric data. A recent advance of automated cardiac chamber quantification technique allows simultaneous quantification of LA and LV volumes with a short acquisition time ( Fig. 12.2 ).
The left atrium acts to modulate LV filling and performance through three functions: (1) booster (active contraction), (2) reservoir (active relaxation and passive dilatation), and (3) conduit (passive emptying). The instantaneous changes in LA pressure and volume during a cardiac cycle can facilitate to understand the LA functions ( Fig. 12.3 ). The LA pre-A volume (LAV pre-A ) can be measured at the beginning of the electrocardiogram (ECG) P wave when the left atrium is completely relaxed. The left atrium acts as a contractile chamber to produce an A wave in the LA pressure tracing, while the LA volume is minimized (LAV min ). The A wave is interrupted by the C wave, which is a transmitted wave by closure of the mitral valve. During LV isovolumic contraction, the left atrium intrinsically relaxes to enhance LA early filling. Thus the x descent, which is the first nadir of LA pressure, correlates with LA early filling, resulting in a rapid increase of LA volume. The change of slope in the upsloping curve of the LA volume indicates a transition between the LA early and late reservoir phases. The late reservoir phase is determined by the LV long axis shortening of the cardiac base and LA chamber stiffness. At the late reservoir phase, the pulmonary venous blood progressively flows into the left atrium, causing the V wave, while the LA volume is maximized (LAV max ). With mitral valve opening, the blood rapidly drains into the left ventricle, and the LA volume decreases (passive emptying), causing the y descent. During LV diastole, LA conduit function is mainly influenced by LV diastolic properties.
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