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Left Atrial Function in Heart Failure With Reduced Ejection Fraction.

Echocardiography in patients with heart failure and reduced ejection fraction (HFrEF) remain the cornerstone of the initial diagnosis, selection of therapies, and risk stratification.1 Fundamentally, the left ventricle (LV) in this patient group can only maintain adequate stroke volume and sufficient cardiac output at the expense of detrimental ventricular remodeling. Further, LV filling pressure will usually be elevated at rest and especially during periods of increased physical activity contributing importantly to the cardinal symptoms of dyspnea and exercise intolerance.2 Echocardiography gives us a range of easily obtainable indications of abnormal filling3; shortened mitral valve early inflow indicating restrictive LV filling, E/eʹ ratio in the range above 15 suggesting elevated resting filling pressure and left atrial (LA) volume distension above 40 mL/m2 indicating a more chronic state of increased preload.4 During the past 10 years 2-dimensional speckle tracking has refined the quantification of myocardial dysfunction. The added prognostic value of measuring global longitudinal strain (GLS) has been consistently demonstrated across the spectrum of cardiovascular disease. Perhaps most convincingly in conditions such as severe aortic stenosis or cardiac amyloid deposition, where LVEF measurements in the normal range does not fully inform the clinician about the magnitude of myocardial dysfunction.5,6 More recently the application of 2-dimensional strain to the LA has been reported in many studies. Analogous to the concept of LV GLS where systolic deformation of the base toward the apex is quantified, peak atrial longitudinal strain (PALS) captures the maximum elongation of the LA during LV systole.7,8 The LA wall thickness ranges from 3.5 to 6.5 mm as compared with the normal myocardial thickness of 10 to 11 mm. Further as the LA is anchored to the great veins, the major determinant of LA expansion is the systolic contraction with downward displacement of the LV base toward the apex. Thus, any condition with adverse effect on the LV longitudinal myocardial function will also inherently reduce PALS. Strain being a measure of deformation is of course dependent on the baseline length and LA dilatation, all other factors being equal, must therefore also result in reduced PALS. The mean value of PALS in healthy controls is 42%8 and for GLS around −21% corresponding to the LV to LA length ratio in healthy people. Thus LV and LA deformation in healthy individuals is tightly coupled which is in accordance with the nearly constant volume pump law of the whole heart.9 Given these considerations, the potential challenges of applying PALS as an isolated metric of LA function are significant. Severe LA wall remodeling in the absence of LV longitudinal fiber dysfunction could result in depressed PALS because of isolated constrained LA compliance. Similarly, isolated LA dilatation with or without reduced LA compliance and normal LV long axis deformation should also © 2018 American Heart Association, Inc. Circulation: Cardiovascular Imaging