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Left Atrial Function: Basic Physiology
Case Study
DL is a 75-year-old white male with a history of hypertension who presented with a 6-month history of reduced exercise tolerance, dyspnea on exertion, and occasional palpitations. The patient was scheduled for an exercise test but was noted to be in atrial fibrillation (AF). His physical examination was normal except for a blood pressure of 150/98 mmHg and an irregularly irregular pulse at 73 bpm. He underwent an unsuccessful cardioversion and was referred for cryoablation of his arrhythmia. The preablation transesophageal echocardiogram revealed normal left ventricular (LV) size and systolic function, restrictive LV filling, biatrial enlargement, mild mitral regurgitation, and normal sinus rhythm ( Fig. 4.1 A). There was spontaneous echo contrast in the left atrial (LA) appendage, but no thrombus (see Fig. 4.1 B). Transmitral, pulmonary venous, and LA appendage velocities ( Fig. 4.2 A–C) were consistent with LA systolic failure. A transthoracic echocardiogram 6 weeks later showed a pseudonormal transmitral filling pattern with a return of atrial systolic activity (see Fig. 4.2 D), leading to the diagnosis of atrial stunning. Symptomatically, the patient was improved.
Atrial stunning is a transient (minutes to weeks) mechanical dysfunction of the body and appendage of the atrium that is reported to occur with all methods of cardioversion (including spontaneous) of AF and flutter. Postulated mechanisms include tachycardia-induced atrial cardiomyopathy and abnormal calcium homeostasis.
Introduction
A resurgence of interest in atrial function has enhanced our understanding of the atrial contributions to cardiovascular (CV) performance in health and disease. The reasons responsible for this renaissance are multifactorial and include (1) the recognition that atrial function is an important, at times critical, determinant of LV filling; (2) the increasing number of drugs, devices, ablative procedures, and surgery available for the treatment of AF ; (3) the considerable interest in dual and three-chamber pacemakers that maintain atrioventricular and biventricular synchrony, respectively ; (4) the growing number of transcatheter procedures for mitral valve repair, atrial septal defect closure, and LA appendage occlusion ; (5) the pathophysiologic and clinical relevance of chamber-specific structural, electrical, and ionic remodeling ; (6) the availability of newer techniques to accurately measure atrial size and function ; (7) the clinical impact of atrial stiffness and stunning, particularly post cardioversion and ablation ; and (8) the increasing data that support the use of atrial size and function to assist in risk stratification and the prediction of CV outcomes. Despite this attention, quantifying atrial function is difficult, in part because the atria are geometrically complex.
Anatomic and Histologic Considerations
Because of the obliquity of the atrial septum, the right atrium projects anteriorly, inferiorly, and to the right of the left atrium (LA). The broad, triangular, muscular right atrial 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 LA appendage is longer, narrower, and more tortuous 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, have fewer T tubules, and have more abundant Golgi apparatus in the atrium than ventricle. Rates of contraction and relaxation, and 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).
Atrial interstitium contains cellular and extracellular components. The cellular elements are comprised of fibroblasts/myofibroblasts, adipocytes, and undifferentiated mesenchymal cells. The extracellular components include primarily collagen (mostly type I) fibers, which form the largest part of the myocardial skeleton, and proteoglycans, matrix vesicles, and lipidic debris.
While there are important differences between left and right atrial structure and function at various organizational hierarchies, 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 three decades.
Pathophysiology
Atrial Function in Health
The primary mechanical function of the left atrium is to modulate LV filling and CV performance; this task is accomplished by its interrelated roles as a reservoir for pulmonary venous flow during ventricular systole, as a conduit for pulmonary venous flow during early ventricular diastole, and as a booster pump that increases ventricular filling during late ventricular diastole. There is a critical interplay between these cardiac cycle-dependent atrial functions and ventricular performance. For example, while reservoir function is most strictly defined by the atrial compliance (or its inverse, stiffness), it is influenced by systolic ventricular function and atrial contraction and relaxation. Conduit function is affected by atrial compliance during ventricular diastole but is closely related to LV relaxation and stiffness. Finally, atrial booster pump function is largely due to the magnitude and timing of atrial contractility but is also determined by the degree of venous return (atrial preload), LV end-diastolic pressures (atrial afterload), and LV systolic reserve.
Although atrial function can be evaluated with a number of imaging modalities, including echocardiography, cardiac computed tomography (CCT), cardiac magnetic resonance imaging (cardiac MRI), angiography, and sonomicrometry, echocardiography is arguably best suited for this task because of its availability, safety, versatility, and ability to image in real time with high temporal and spatial resolution. LA function is assessed using volumetric analysis (maximum, minimum, and pre-A wave LA volumes and their derived functions [total, passive, and active emptying fractions and expansion index]); transmitral, pulmonary venous, and LA appendage flow analysis; and deformational imaging (strain and strain rate).
Left Atrial Booster Pump Function
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 ; (3) atrial shortening using methods such as two-dimensional (2D) and three-dimensional (3D) echocardiography, CCT, cardiac MRI, angiography, and sonomicrometry ; (4) by estimating the kinetic energy and force generated with atrial contraction ; and (5) strain and strain rates during atrial systole, which represent the magnitude and rate of myocardial deformation, respectively, that are measured using either echocardiographic (color tissue Doppler imaging or 2D speckle tracking) techniques or cardiac MRI (feature tracking or tagged MRI) ( Figs. 4.3 and 4.4 ). LA appendage pump function is assessed by late emptying spectral and tissue Doppler velocities. 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, and (as noted) the magnitude of venous return, LV end-diastolic pressures, 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.
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