INTRODUCTION
A resurgence of interest in atrial function has enhanced our understanding of the atrial contributions to cardiovascular performance in health and disease (see Chapter 13 ). The reasons for this “renaissance” are multifactorial and include (1) the recognition that atrial function is an important, at times critical, determinant of left ventricular (LV) filling, (2) the increasing number of drugs, devices, ablative procedures, and surgeries available for the treatment of atrial fibrillation, (3) the considerable interest in dual- and three-chamber pacemakers that maintain atrioventricular and biventricular synchrony, respectively, (4) the pathophysiological and clinical relevance of chamber-specific structural, electrical, and ionic remodeling, (5) the clinical impact of atrial distensibility and stunning, particularly postcardioversion, and (6) the important prognostic role of atrial function in heart failure.
Despite this attention, quantifying atrial function is difficult, in part because the atria are geometrically complex. Because of the obliquity of the atrial septum, the right atrium projects anteriorly, inferiorly, and to the right of the left atrium. The broad, triangular, muscular right atrial (RA) appendage protrudes anteriorly, the superior vena cava opens into the dome of the right atrium, and the inferior vena cava opens into its inferior and posterior portion. The body of the left atrium is smaller and thicker than the right atrium. The chamber has been modeled as a sphere, cube, or ellipse. The left atrial (LA) appendage is longer and narrower than the right appendage and contains all the pectinate muscles of the left atrium. The four pulmonary veins, upper and lower from each lung (the left pair frequently opening via a common channel), enter the posterior aspect of the left atrium.
The atrial walls consist of two muscular layers, the fascicles of which both originate and terminate at an atrioventricular ring and follow nearly perpendicular courses. Fascicles in the inner layer ascend vertically through a pectinate muscle, change depth and course circumferentially in the outer layer, encircle the atrium, dive into the inner layer, and descend vertically within a pectinate muscle. While some fascicles are intrinsic to one atrium, others are shared. The muscular terminations of the veins are also composed of two layers, the inner longitudinal and the outer circular.
Ultrastructurally, atrial myocardium differs significantly from ventricular myocardium. For example, myocytes are smaller in diameter and have fewer T-tubules and more abundant Golgi apparatus in the atrium than in the ventricle. Rates of contraction and relaxation and of conduction velocity and anisotropy differ, as do their respective biophysical underpinnings (i.e., myosin isoform composition and qualitative and quantitative differences in a wide assortment of ion transporters, channels, and gap junctional proteins).
While there are important differences between left and right atrial structures and functions at various organizational hierarchies, the function of the left atrium at the organ level will be used in this chapter to illustrate the atrial contributions to ventricular filling. The discussion is drawn largely from studies our group has performed over the past 15 years.
PATHOPHYSIOLOGY
Atrial Function in Health
Left Atrial Booster Pump Function
The principal role of the left atrium is to modulate LV filling and cardiovascular performance through the interplay of atrial reservoir, conduit, and booster pump functions. Typically, the importance of the atrial booster pump function (i.e., the augmented ventricular filling resulting from active atrial contraction) has been estimated by measurements of (1) cardiac output and LV diastolic volume both with and without effective atrial systole, (2) relative LV filling (e.g., early to late [E/A] filling ratios) using steady-state Doppler echocardiographic transmitral flow or radionuclide angiography, and (3) atrial shortening using methods such as two-dimensional echocardiography, angiography, and sonomicrometry. Booster pump function is also evaluated echocardiographically by estimating the kinetic energy and force generated with atrial contraction. However, measurements of atrial systolic function and the importance of the atrial booster pump are dependent on a multiplicity of factors, including the timing of atrial systole, vagal stimulation, the magnitude of venous return (i.e., atrial preload), LV end diastolic pressures (i.e., atrial afterload), and LV systolic reserve. Not surprisingly, despite considerable study, the magnitude and relative importance of the atrial contribution to LV filling and cardiac output remain controversial. Analogous to end systolic elastance measurements in the left ventricle (where end systolic elastance is calculated as the slope of the ventricular end systolic pressure-volume [P-V] relation), a load-independent index of atrial contraction based on the instantaneous atrial P-V relation has the potential to explain and minimize the discrepancies and confusion that exist in the literature. Accordingly, understanding and deriving atrial elastance require a consideration of the relation between instantaneous atrial pressure and volume.
Pressure-Volume Relations of the Atrium
A time-independent representation of the atrial events during the cardiac cycle can be obtained by plotting instantaneous atrial pressure and volume ( Fig. 4-1 ). During ventricular systole, atrial relaxation and descent of the ventricular base lower atrial pressure (the “x” descent) and assist in atrial filling; the latter results in a “v” wave on the atrial pressure tracing. Thus, during ventricular systole, the atrium operates as a reservoir, storing systemic and pulmonary venous return. When the atrioventricular valves open, blood stored in the atria empties into the ventricles, and atrial pressure falls (the “y” descent), during which time the atria act as conduits for venous blood flow into the ventricles. Atrial contraction, denoted by an “a” wave on the atrial pressure tracing, actively assists ventricular filling. The resultant P-V loop inscribes a “figure-eight” that consists of a clockwise “V” loop due to atrial filling and passive emptying, and a counterclockwise “A” loop due to active atrial contraction.
Although Alexander et al. described instantaneous LA P-V relations by a time-varying elastance in the isolated left atrium using computer-simulated LA loading conditions, assessment of atrial systolic elastance in vivo was hampered by the lack of an accurate measurement of LA volume with an adequate sampling frequency. Therefore, as a critical initial step, we demonstrated that cast-validated LA volumes could be estimated accurately with high temporal resolution sonomicrometry using two nearly orthogonal atrial dimensions. The left atrium was assumed to be a general ellipsoid of revolution:
LA volume = π / 6 ( SAX ) 2 ( LAX ) ,
E ( t ) = P ( t ) / [ V ( t ) – V ( o ) ] ,
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