Normal Left Atrial Function
The major contribution of the left atrium (LA) to forward cardiac output is its function as a passive capacitance chamber, not as a contracting pumping chamber like the ventricles. Most of the changes in LA size and volume during a cardiac cycle are passive, and the left atrial muscle contracts only very briefly at the end of ventricular diastole, more like a “twitch” than a smooth prolonged contraction ( Fig. 43.1 ). The mitral valve is fully open when the LA contracts, meaning that the afterload against which the LA contracts is minimum and corresponds to the earliest level of left ventricular diastolic pressure. This is not to imply that left atrial function is unimportant to cardiac hemodynamics, only that its importance is not primarily as a pump.
Volume-time curve of normal left atrial function (red line). Left atrial function is divided into three phases: reservoir phase (yellow), conduit phase (orange), and pump or contraction phase (green). The reservoir phase of left atrial function begins when the mitral valve closes at the beginning of left ventricular systole and the end of left atrial systole. As the left atrium fills with blood from the pulmonary veins, it expands passively (upward slope of curve) until the end of atrial diastole (peak of curve). At that point, the mitral valve opens in response to left ventricular diastole. The LA passively decreases in size because of its blood being sucked into the ventricle during left ventricular diastole (conduit phase). Near the end of the passive conduit phase, the atrial muscle briefly contracts (pump phase) immediately before the beginning of left ventricular systole. LV, Left ventricle.
The physiologic relationship of atrial contraction to forward cardiac output is analogous to that of pushing a child on a swing ( Fig. 43.2 ). Each time the swing reaches its apogee, a small tap on the back is sufficient to keep the swing in motion indefinitely. There is only a very light push (“tap”) on the person on the swing, just as there is a very light push (“tap”) of left atrial blood into the left ventricle during normal sinus rhythm. The critical component of keeping the child swinging is the precise timing of the tap on the back, not the forcefulness of the tap. Likewise, the critical component of optimizing the blood flow through the heart is the atrium’s synchrony with the ventricle, not the strength of atrial contraction.
The left atrium (LA) functions much like a person pushing a swing to keep it in motion. It is not necessary to push a swing hard with each swing cycle to keep it going (upper panel). Rather, a perfectly timed light “tap” on the back of the person swinging is all that is required (lower panel). Similarly, the LA does not create a forceful “kick” that propels blood from the LA into the left ventricle (LV) during a normal cardiac cycle. Rather, the LA provides a perfectly timed light “tap” just before closure of the mitral valve to optimize the delivery of blood from the LA into the LV. The vast majority of LA movement during normal sinus rhythm is passive.
The misperception that a forceful atrial “kick” propels LA blood into the ventricle derives from the appearance of the emptying (“conduit”) phase of the LA during early ventricular diastole. During left ventricular systole, the LA fills passively (reservoir phase) and therefore increases in size. When left ventricular diastole begins and the mitral valve opens, the blood in the LA reservoir is sucked into the left ventricle by contraction of the ventricle’s spiral musculature, so the LA passively and rapidly decreases in size (conduit phase). This dramatic visual movement of the atrium is commonly mistaken for “atrial systole,” which implies forceful contraction of the atrium. However, the entire reservoir phase and the entire conduit phase of atrial function are passive. At the very end of the conduit phase, the left atrial muscle briefly contracts (the “tap”) just before ventricular systole begins again. Thus the actual contractile function of the LA should be viewed as a perfectly timed “atrial tap” rather than as a forceful “atrial kick.”
Normal Left Atrial Appendage Function
The LA appendage (LAA) also participates in all three phases of overall left atrial function ( Fig. 43.3 ). First, the appendage serves as an additional reservoir by passively expanding simultaneously with the body of the LA itself as blood enters the left heart from the pulmonary veins during ventricular systole ( Fig. 43.4 ). Its contribution to the conduit function of the LA is less dramatic because its size usually changes little during the conduit phase ( Fig. 43.5 ). Finally, the LAA contracts simultaneously with the body of the LA at the end of ventricular diastole ( Fig. 43.6 ).
Left panel, Normal volume-time curve of normal left atrial function during sinus rhythm including contributions from both the body of the left atrium (LA) and from the left atrial appendage (LAA). Right panel, Volume-time curves of both the body of the LA (triangles) and the LAA (squares). Note that the LAA contributes to all three phases of overall left atrial function.
Left panel, The reservoir phase of a normal volume-time curve of overall left atrial function is highlighted in pale yellow . Right panel, The reservoir phases of normal volume-time curves of the left atrium (LA) and LAA are highlighted in pale yellow . The additional contribution of the left atrial appendage (LAA) to overall left atrial reservoir function is denoted in bright yellow . This confirms that although the left atrial body is normally the most important capacitance chamber in the left heart, the LAA also functions normally as an additional capacitance chamber.
Left panel, The conduit phase of a normal volume-time curve of overall left atrial function is highlighted in orange . Right panel, The conduit phases of normal volume-time curves of the left atrium (LA) and t atrial appendage (LAA) are highlighted in orange . The impact of the LAA on the conduit phase is less dramatic than it is on the reservoir phase of left atrial function as evidenced by the flattening of the volume-time curve of the LAA during the conduit phase.
Left panel, The pump (contraction) phase of a normal volume-time curve of overall left atrial function is highlighted in green . Right panel, The pump (contraction) phases of normal volume-time curves of the left atrium (LA) and the atrial appendage (LAA) are highlighted in green . Both the LA (red triangles) and the LAA (blue squares) actively contract very briefly after completion of the conduit phase, both serving as synchronized “taps” on the blood just before the mitral valve closes.
Impact of Left Atrial Appendage Exclusion on Left Atrial Function
When catheter and surgical LAA occlusion (LAAO) became more routine for the prevention of strokes, there was concern that occlusion of the LAA would have a negative impact on postocclusion left atrial function. However in 2017, Coisne et al. showed that percutaneous LAA endocardial closure with the Watchman device in a subset of patients in the PROTECT AF trial actually improved left atrial mechanical function by the Frank-Starling mechanism because of a modification of the LA loading conditions. The following year, Dar et al. using two-dimensional speckle-tracking echocardiography to measure left atrial strain (see Chapter 7 ), showed that the left atrial reservoir function, conduit function, and booster function were all increased after epicardial closure of the LAA with a percutaneous LARIAT device (SentreHEART). In addition, these positive changes in LA function after LAA closure resulted in reverse remodeling of the LA (see Chapter 8 ).
Left Atrial Appendage Closure in Patients With Diastolic Dysfunction of the Left Ventricle
The effectiveness of LAA closure in decreasing the incidence of stroke in patients with atrial fibrillation (AF) is now settled science, although a stroke benefit of LAA closure in patients without AF has not been documented definitively (see Chapter 40 ). Nevertheless, documentation of the many benefits of LAA closure and easy access to the LAA during cardiac surgery has promoted the practice among some surgeons of amputating or closing the LAA in virtually all patients undergoing cardiac surgery. However, in addition to the specific detrimental side-effects of amputating or closing the LAA described in Chapters 41 and 42 , patients with significant diastolic dysfunction of the left ventricle can theoretically be permanently harmed by LAA closure. For example, in patients with giant LAAs ( Fig. 43.7 ), the LA is often quite stiff and incapable of passive expansion during the reservoir phase. In such patients, the LAA may be the primary capacitance chamber, rather than the LA itself, and its amputation or closure can result in increased pressure in the LA and the pulmonary vasculature. These patients can become profoundly short of breath after LAAO, and if they do, there is little that can be done to treat it.
Intraoperative photograph of a giant left atrial appendage (LAA). Because such large LAAs are often associated with stiff left atria, the LAA may be a more important capacitance chamber than the left atrium itself (LA). Therefore, one should be wary of amputating such a large LAA until the body of the LA alone has been documented to be sufficiently compliant. Otherwise, left atrial and pulmonary vasculature pressures may increase after LAA amputation, causing detrimental and irreversible cardiopulmonary sequelae. See text for further discussion.
The so-called “stiff LA syndrome” can be caused by infiltrative restrictive cardiomyopathies such as cardiac amyloidosis, cardiac sarcoidosis, and cardiac hemochromatosis, by hypertrophic obstructive cardiomyopathy, and by systemic hypertension. All of these conditions affecting the left heart can cause diastolic dysfunction of the left ventricle, which can lead to loss of compliance in the LA. Amputation or closure of the LAA in these patients can lead to the same detrimental sequelae described earlier and should be done only sparingly if at all. In addition, patients who have undergone extensive radiofrequency catheter ablation for AF can develop a stiff LA that can be problematic for subsequent LAA closure.
One should be particularly mindful of similar problems that can arise from closing the LAA in patients with AF and heart failure with preserved ejection fraction (HFpEF). It has been suggested that the same underlying cardiomyopathy may be causing fibrillation in the atria and HFpEF in the ventricles. It is important to restore atrioventricular synchrony in patients with AF and heart failure with reduced EF (HFrEF) in which the primary problem is left ventricular systolic dysfunction . However, it is especially important to restore sinus rhythm in patients who have HFpEF in whom the primary problem is left ventricular diastolic dysfunction . However, LAAO should not be a part of AF treatment in patients with HFpEF unless it is deemed absolutely essential because the results can be especially detrimental in the presence of left ventricular diastolic dysfunction.
Impact of Left Atrial Appendage Exclusion on the Results of Atrial Fibrillation Ablation
Percutaneous endocardial LAAO devices such as the Watchman (Boston Scientific) and Amulet (Abbott) occlude the LAA, but they do not electrically isolate the LAA myocardium. These devices that occlude the LAA but do not exclude the LAA myocardium have no effect on the results of catheter ablation for AF. The only commercial devices that electrically isolate the LAA are the surgical AtriClip, the percutaneous LARIAT, and stapling devices, all of which are applied at the base of the LAA epicardially ( Fig. 43.8 ).
