A clinical appraisal of left atrial function

Abstract

The left atrium modulates left ventricular filling through three components: a phase of reservoir or expansion during systole, a conduit phase during diastole, and an active contractile component (when sinus rhythm is present) during late diastole. This active contractile component of the left atrium has an important role in patients with ventricular dysfunction as a 'booster pump' to augment ventricular volume. Augmented left atrial booster function is one of the mechanisms compensating for decreased early filling in patients with reduced left ventricular compliance, whereas a loss of atrial contraction, as a result of atrial fibrillation or ventricular pacing, reduces cardiac output by approximately 15-20% [1,2] .During exercise left atrial reservoir and booster functions are augmented, whereas conduit function is not; increased reservoir function may play an important role in accelerating left ventricular filling by helping to maintain an enhanced atrioventricular pressure gradient during diastole and also by increasing left atrial booster function through an increase in preload [3] . An isolated decrease in left atrial compliance is associated with relative increases in the conduit function of the left atrium. The ability to optimally redistribute left ventricular filling among reservoir, conduit and boosterpump functions is a potentially important adaptation that may occur in the left atrium in response to changing haemodynamics [4] . Frank-Starling mechanismThe stretch of the atrium was controlled by intra-atrial pressure. The Frank-Starling behaviour of the atrium was manifested as a biphasic increase of the contraction force after increasing the stretch level. The development of the contraction force after step increase of the stretch (intra-atrial pressure from 1 to 3 mmHg) was accompanied by an increase in the amplitude of the calcium transients and a decrease in the time constant of Ca 2+ transient decay. The stretch-activated channel activation led to gradual augmentation of Ca 2+ transients, which modulated the action potentials through increased Na + /Ca 2+ -exchanger inward current. The role of troponin C affinity change was to modulate the Ca 2+ transients, stabilize the diastolic [Ca 2+] i, and presumably to produce the immediate increase of the contraction force after stretch seen in experiments. The same mechanism that caused the normal physiological responses to stretch could also generate arrhythmogenic afterpotentials at high stretch levels in the model [15] .With a stepwise decrease in the pacing rate from 110 beats . min 1 to 70 beats . min 1 , the left atrial dimension increases just before atrial contraction and left atrial systolic shortening increases as well. However, the calculated left ventricular filling volume during atrial systole decreases. The pulmonary venous flow during atrial systole is directed toward the left atrium, and the left atrial influx volume from pulmonary venous flow decreases. With a decrease in the pacing rate, the left atrial Frank-Starling mechanism operates....

<b>Value of Left Atrial Function in Predicting Exercise Capacity in Heart Failure With Moderate to Severe Left Ventricular Systolic Dysfunction</b>

“…21) The LA modulates LV diastolic filling and increases cardiac performance. 22) During exercise, the LA reservoir and active pumping function are augmented, nevertheless, its conduit facilities remain unchanged. 9) To maintain LV filling at an optimum level during hemodynamic changes, the LA reservoir, conduit, and pumping function should work in harmony.…”

Loss of atrial contractility is primary cause of atrial dilatation during first days of atrial fibrillation

“…In contrast, in anesthetized dogs (15) and pigs (4) atrial compliance was found to decrease during the transition from sinus rhythm (SR) to AF. Because during AF fibrillatory contractions continuously spread over the atrial myocardium, the compliance of the fibrillating atrium is generally lower than the diastolic atrial compliance during SR (11). However, the long-term effect of a loss of atrial contractility due to AF on compliance and size of fibrillating atria has not been studied yet.…”

Effects of levosimendan versus dobutamine on left atrial function in decompensated heart failure

“…We showed that both levosimendan and dobutamine increased AEF, which expresses LA systolic function and is analogous to LV ejection fraction (25,26). However, levosimendan, but not dobutamine, improves PEF, which reflects the passive emptying of the LA into the LV during early diastole.…”