Echocardiographic Assessment of Atrial Function: From Basic Mechanics to Specific Cardiac Diseases

Abstract

The left and right atria serve as buffer chambers to control the flow of venous blood for ventricular filling. If an atrium is absent, blood does not flow effectively into the ventricle, leading to venous blood retention and low cardiac output. The importance of atrial function has become increasingly recognized, because left atrial (LA) function contributes to cardiac performance, and loss of LA function is associated with heart failure. LA volume change has been used for LA function assessment in experimental and clinical studies. In conjunction with LA pressure, the LA pressure-volume relationship provides a better understanding of LA mechanics. LA strain measurement by speckle tracking echocardiography was introduced to evaluate three components of LA function as a (booster) pump, reservoir and conduit. Furthermore, increasing evidence supports the theory that LA reservoir strain has prognostic utility in various cardiac diseases. In this review, we summarize LA contribution to maintain cardiac performance by evaluating LA function with echocardiography according to our experiences and previous reports. Furthermore, we discuss LA dysfunction in challenging cardiac diseases of cardiac amyloidosis and adult congenital heart disease.

Keywords: adult congenital heart disease; atrial fibrillation; cardiac amyloidosis; heart failure; left atrial function; left atrial strain; pressure–volume loop.

Conflict of interest statement

The authors declare no conflict of interest regarding to this review article.

Figures

Figure 1

Left atrial pressure–volume loop curve. (A) Normal left atrial pressure–volume loop consisting of A- and V-loops. The A-loop is produced by LA contraction (booster pump function) and relaxation (early reservoir function), while the V-loop is produced by LA dilatation (late reservoir function) and emptying (conduit function). LA pressure includes the x-trough and v-wave pressures, and the slope connecting the two pressure points (dotted line) on the loop is defined as the LA stiffness index. (B) During afterload increase. When systolic blood pressure increases from 120 to 180 mmHg for instance, left ventricular (LV) systolic and diastolic function worsen due to afterload increase. The A-loop area immediately enlarges to pressure-overloaded LV dysfunction, resulting in the maintenance of stroke volume without a critical elevation in LA pressure. (C) Atrial fibrillation occurrence. Atrial fibrillation promotes atrial myopathy, resulting in LA dilatation, functional impairment and perhaps elevated mean LA pressure. The A-loop disappears during atrial fibrillation, and it mainly depends on ventricular function to maintain cardiac performance. (D) Left atrial stiffening. The pressure–volume loop in a case of cardiac amyloidosis. Abnormal amyloid proteins deposit into the myocardial wall, including the left atrium. LA, left atrial; LV, left ventricular.

Figure 2

Calculation of left atrial strain. LA strain can be analyzed from a non-foreshortened apical four-chamber view. The zero-strain reference is set at end-diastole according to the recommendation by Badano et al. [17], enabling one to obtain LA strain value even in patients with atrial fibrillation. LA reservoir strain (LASr) is calculated as difference between end-diastole and onset of early LV filling, while LA pump strain (LASp) as difference between onset of atrial contraction and onset of late LV filling. LA, left atrial, LV, left ventricular.

Figure 3

Calculation of left atrial dispersion. LA dispersion is defined as the standard deviation of the time to peak positive strain corrected by the R-R interval (%). White arrows indicate contraction durations defined as the time from the R wave on the electrocardiogram to the maximal time of positive deformation in each LA segment. LA, left atrial.

Figure 4

Visual assessment (grading) of left atrial reservoir function. (A) A case of hypertrophic cardiomyopathy. (B,C) Two cases of cardiac amyloidosis. The upper panel in each case is a frame when the LA size is minimized, while the lower panel is a frame when the LA size is maximized. In a patient with hypertrophic cardiomyopathy, the LA dilatation grade (Inoue grade) was preserved (A). In contrast, two patients with cardiac amyloidosis showed abnormal (B) and restricted (C) LA dilatation, indicating LA stiffening. LA, left atrial.

Figure 5

Atrial function in atrial septal defect and Fontan palliation. (A) TEE showing a right-to-left (R-L) shunt from a residual leak after ASD device closure with RA dysfunction. (B) Four-chamber views of end-systole (RAA max) and end-diastole (RAA min). The decreased RA fractional area change (FAC) suggests RA dysfunction. (C) Illustration of the Fontan circulation and the process of impairment of systemic ventricular relaxation after Fontan palliation. (D) Transmitral Doppler early diastolic (E-wave) and late diastolic (A-wave) velocities in a control subject, and the SV peak E-wave and A-wave inflow velocities in a patient with Fontan palliation (EC-TCPC). (E) Representative atrial strain curves in a patient with Fontan palliation (EC-TCPC) and a control subject. Peak negative (red arrow) and positive (white arrow) atrial strain are noted. TEE, transesophageal echocardiography; ASD, atrial septal defect; RA, right atrial; RAA, right atrial area; EC-TCPC, extracardiac total cavopulmonary connection.