The EACVI/ASE/Industry Task Force to standardize deformation imaging prepared this consensus document to standardize definitions and techniques for using two-dimensional (2D) speckle tracking echocardiography (STE) to assess left atrial, right ventricular, and right atrial myocardial deformation. This document is intended for both the technical engineering community and the clinical community at large to provide guidance on selecting the functional parameters to measure and how to measure them using 2D STE.This document aims to represent a significant step forward in the collaboration between the scientific societies and the industry since technical specifications of the software packages designed to post-process echocardiographic datasets have been agreed and shared before their actual development. Hopefully, this will lead to more clinically oriented software packages which will be better tailored to clinical needs and will allow industry to save time and resources in their development.

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To obtain the normal ranges for 2D echocardiographic (2DE) indices of myocardial work (MW) from a large group of healthy volunteers over a wide range of ages and gender.

This article describes the pathophysiology of left atrial mechanical function and discusses both conventional and new echocardiographic parameters used to evaluate left atrial function. The evidence regarding the clinical usefulness of left atrial function assessment is also presented. PATHOPHYSIOLOGY OF LEFT ATRIAL MECHANICAL FUNCTIONAtrial function, in a close interdependence with left ventricular (LV) function, plays a key role in maintaining an optimal cardiac performance. The left atrium (LA) modulates LV filling through its reservoir, conduit, and booster pump function, whereas LV function influences LA function throughout the cardiac cycle. The LA can act to increase LA pressure (in significant atrial disease) and can react to increased LV filling pressure (in significant ventricular disease). LA remodelling is related to LV remodelling w1 and LA function has a central role in maintaining optimal cardiac output despite impaired LV relaxation and reduced LV compliance.1 Understanding how each component of LA function is influenced by LV performance, and how each LA phasic function contributes to maintain an optimal stroke volume in normal and diseased hearts, is important for interpreting data derived from quantification of LA function.During LV systole and isovolumic relaxation, the LA functions as a reservoir, receiving blood from the pulmonary veins and storing energy in the form of pressure. This atrial function is modulated by LV contraction, through the descent of the LV base during systole, by right ventricular systolic pressure transmitted through the pulmonary circulation, and by LA properties (ie, relaxation and chamber stiffness).w2 During early LV diastole and diastasis, the LA functions as a conduit. Blood is transferred into the LV through the LA via a small pressure gradient during early diastole and flows passively from the pulmonary veins into the LV during diastasis. The conduit function is modulated especially by LV diastolic properties (LV relaxation and early diastolic pressures). During late LV diastole, the LA functions as a pump, the LA contraction augmenting LV stroke volume by approximately 20e30% in normal subjects and substantially more in the presence of impaired LV relaxation. LA booster pump function is modulated by LV compliance, LV end-diastolic pressure, and LA intrinsic contractility.