longitudinal with the mitral annulus moving back towards the rear of the atrium after the P-wave and during the PR interval and returning to its resting position at the time of the first heart sound, marking end-diastole. It is worth mentioning that not only does this pattern of function mirror that of the left ventricle, although in the opposite direction, but the atrium also does not function in isolation of the ventricle. Myocardial development studies have shown close relationship between age-related changes in the function of the atrium and the ventricle which themselves are closely related. As left ventricular lengthening velocities reduce with age, those of left atrial shortening reciprocally increase in order to secure normal stroke volume entering the left ventricle. 3 Conventional measurements of the left atrial size rely on longitudinal and transverse diameters as well as its area measurements. Segmental left atrial myocardial function is easily assessed from the longitudinal motion amplitude and velocity of the lateral, septal, and posterior segments as shown by the mitral annulus excursion during atrial systole. This is easily achieved using tissue Doppler or speckle tracking techniques. The amplitude of left atrial longitudinal motion is also assessed by the same techniques or by conventional M-mode. Similar to the left ventricle, the main determinant of left atrial contractile function is its intrinsic myocardial function, which has its well-established maturation course, between foetal life and adolescence. 4 As the atrium gets large in size due to various pathologies, with the commonest secondary to left ventricular and valve diseases, its overall contractile function falls and eventually pump failure and atrial fibrillation. Even in patients with paroxysmal atrial fibrillation and only small increase in atrial size we have shown significant reduction in segmental left atrial function particularly in areas adjacent to the pulmonary veins. 5 Critical investigation of atrial function shows that such pathophysiological course is not that simple. We and others have previously shown that atrial flutter and fibrillation are commonly preceded by progressive prolongation of P-wave duration which itself proved a good predictor for the occurrence of atrial arrhythmias. 6,7 This is explained on the basis of progressive atrial enlargement and myocardial stretching, which increase its surface area and hence the prolonged depolarization time. Such behaviour is similar to that occurring in dilated left ventricles with prolonged depolarization time and broad QRS duration. Another important component of left atrial function is its electromechanical delay, similar to that seen in the left ventricle. This can easily be studied by the same Doppler echocardiographic techniques mentioned above and left atrial motion measured with reference to the onset of its electrical depolarization, the P-wave. Studies have used the onset of segmental left atrial shortening (excursion) or peak shortening velocity as two possible landmarks for electromechanical delay. Normal values for the two measurements have been determined and well documented. Normally, the three left atrial segments shorten in a synchronous fashion with no more than few milliseconds time difference between them, again a finding similar to that seen in the left