The left atrium: an old 'barometer' which can reveal great secrets.

Abstract

In patients with heart failure (HF), left atrial (LA) function plays a central role in maintaining optimal cardiac output despite impaired left ventricular (LV) relaxation and reduced LV compliance. 1 It has been demonstrated that the Frank-Starling mechanism is also operative in the left atrium and that LA output increases as atrial diameter increases, which contributes to maintain a normal stroke volume. In a non-compliant left ventricle, as the left atrium is exposed to the pressures of the left ventricle during diastole, LA pressure rises to maintain adequate LV filling. The resulting increase in LA wall tension, through myocyte stretch, induces myolysis, fibrosis, and apoptosis, and leads to progressive LA enlargement, which tends to prevent passive transmission of pressure to the pulmonary circulation. 2,3 Clinically, LA enlargement is most commonly expressed by the maximum LA volume obtained at end-systole when LA chamber is at its greatest dimension. It should be noted that left atrium is not a symmetrically shaped three-dimensional (3D) structure, and that LA enlargement is not a uniform process. Therefore, measurement of the left atrium by M-mode echocardiography is likely to be an insensitive assessment of any change in size of the left atrium. Conversely, LA volume by two-dimensional (2D)/3D echocardiography provides a more accurate and reproducible estimate of the size of the left atrium. 4 Because a large number of individuals with LV dysfunction are in a pre-clinical phase of the disease, 5 increased LV filling pressures (E/e ' ) could only be expressed during exercise. The causes of increased E/ewith exercise are not well characterized. In a group of patients with a resting a E/e ' 1 3i n12% of the population) were those with larger LA volumes at rest. A LA volume index >33 mL/m 2 ,a cut-off already shown associated with increased risk of developing symptomatic HF, 7 predicted abnormal exercise LV filling pressures with a high sensitivity (91%) and a good specificity (78%), while a LA volume index <26 ml/m 2 was a marker of normal exercise echocar- diogram. Therefore, abnormal exercise LV filling pressures could be suspected in patients with enlarged left atria. The LA volume is thus a good expression of the cumulative/chronic exposure to abnormal LV filling pressures over time. Whether LA volume could be used to identify patients in whom an exercise echocardiography should be ordered needs to be further addressed. Increased LA volume may be accompanied/preceded by a pro- gressive impairment in LA function and both may occur before symptom development and may adversely affect prognosis. 8 Dys- function of the left atrium could be an early sign of LA pathological process. Left atrial function has three components: reservoir, conduit and active contractile functions. Reservoir function occurs during LV systole, the conduit function results from the blood transiting from the pulmonary veins into the left atrium during early diastole and finally, the active contractile function arrives in late diastole to increase LV filling. Left atrial function has been initially described by volumetric method in several diseases. 9 In recent years, tissue Doppler-derived strain imaging has also been documented to adequately assess regional and global LA function in normal subjects, in increased afterload states and in HF. Two-dimensional speckle tracking-derived strain, an angle inde- pendent tool, overcomes the main drawbacks of tissue Doppler imaging and thus provides more accurate quantification of LA function. 10 Compared with normal subjects, the different components of LA function—reservoir, conduit and active contractile functions—have been shown to be altered in various cardiovascu- lar diseases. 9,11 Left ventricular systolic and diastolic dysfunction, elevated filling pressure, LV hypertrophy, mitral regurgitation, and intrinsic atrial myopathy are all potential contributors to ongoing LA remodelling/dysfunction. 12 In a group of patients with HF, preserved LV ejection fraction and elevated N-terminal pro-brain natriuretic peptide (NT-proBNP) derived from the PARAMOUNT trial (The Prospective comparison of ARNI with ARB on Manage- ment Of heart failUre with preserved ejectioN fraction), Santos et al. 13 also reported an impairment of LA reservoir and pump (active contractile) function compared with controls. Interestingly, reduction in LA reservoir function (LA positive strain during LV systole), as assessed by 2D speckle tracking, occurred regardless of LA size (LA volume) or history of atrial fibrillation. Therefore, volumetric methods and strain imaging are not interchangeable approaches to assessment of LA function. Impairment in LA func- tion may thus precede/promote LA dilatation, which in turn may