À LA mode atrioventricular mechanical coupling.

eft atrial (LA) size and function have been popularized as barometers of left ventricular (LV) filling pressure and diastolic function. However, the specific role of the left atrium, independent of the left ventricle, and its clinical assessment remain challenging. Several recent investigations have suggested that measuring changes in LA volume (1), wall deformation (2), or the extent of wall fibrosis (3) may be clinically useful for predicting adverse cardiac events such as atrial fibrillation (AF) and mortality in patients with LV diastolic dysfunction. In this issue of iJACC, Neilan et al. (4) and the accompanying editorial (5) revisit the structural and functional tenets of atrioventricular coupling for understanding the rate-limiting pathophysiological features of patients with diastolic dysfunction that are finally associated with atrial arrhythmias. LA function shows phasic variations during different periods of the cardiac cycle (1). The left atrium functions as a receiving and dilating chamber (reservoir) during ventricular systole, allowing uninterrupted flow to arrive into the atrium even when the mitral valve is closed. The flow from the left pulmonary veins enters the LA cavity (Fig. 1) and starts rotating along a crescent-like axis to parallel the C-shaped closure line of the mitral valve leaflets (6). In contrast, the flow from the right pulmonary veins travels separately along the LA wall, creating noncolliding streams of blood flow. These blood flow streams wash the LA surface, avoiding hemodynamic stasis and thrombus formation, while the LA reservoir expands to reach its maximal volume. One could surmise that the lack of an intervening atrial chamber would halt the forward movement of venous blood flow when the mitral valve is closed and let the kinetic energy of the moving blood convert to a surge of static pressure that