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The left atrium is a dynamic chamber with peculiar characteristics. Stressors and disease mechanisms may deeply modify its structure and function, leading to left atrial remodelling and disease. Left atrial disease is a predictor of poor outcomes. It may be a consequence of left ventricular systolic and diastolic dysfunction and neurohormonal and inflammatory activation and/or actively contribute to the progression and clinical course of heart failure through multiple mechanisms such as left ventricular filling and development of atrial fibrillation and subsequent embolic events. There is growing evidence that therapy may improve left atrial function and reverse left atrial remodelling. Whether this translates into changes in patient's prognosis is still unknown. In this review we report current data about changes in left atrial size and function across different stages of development and progression of heart failure. At each stage, drug therapies, lifestyle interventions and procedures have been associated with improvement in left atrial structure and function, namely a reduction in left atrial volume and/or an improvement in left atrial strain function, a process that can be defined as left atrial reverse remodelling and, in some cases, this has been associated with improvement in clinical outcomes. Further evidence is still needed mainly with respect of the possible role of left atrial reverse remodelling as an independent mechanism affecting the patient's clinical course and as regards better standardization of clinically meaningful changes in left atrial measurements. Summarizing current evidence, this review may be the basis for further studies. [ABSTRACT FROM AUTHOR]

Aims Only 30% of patients receiving an implantable cardioverter defibrillator (ICD) for primary prevention receive appropriately therapy. We sought to investigate the value of tissue Doppler imaging (TDI) to predict ventricular tachycardia (VT), ventricular fibrillation (VF), and cardiovascular mortality (CVD) in patients with primary prevention ICD. Methods and results In total, 151 ICD patients meeting primary prevention criteria and with no history of ventricular arrhythmias were included. All participants were examined by conventional 2D echocardiography and TDI echocardiography. Longitudinal systolic (s'), early diastolic (e'),and late diastolic (a') myocardial velocities were measured using TDI at six mitral annular sites and averaged to provide global estimates. Forty patients experienced the combined endpoint of VT, VF, or CVD during a median follow-up of 2.3 years. Left ventricular ejection fraction, global longitudinal strain, E/e', global s', and global e' were not significantly different in patients who developed VT/VF/CVD compared with those who did not. In contrast, global a' was significantly lower in patients with an unfavourable outcome compared with those without (4.8 + 2.0 vs. 5.7 +1.8 cm/s, P = 0.020). Global a' remained an independent predictor of VT/VF/CVD after multivari-able adjustment for age, gender, b-blocker therapy, and deceleration time (HR = 1.25 [1.02,1.54], P = 0.032). Regional analysis revealed that a depressed a' in the inferior wall drives the predictive capability of a'. Conclusion Late diastolic velocity by TDI seems to be a superior echocardiographic predictor of VT/VF/CVD in ischaemic cardiomyopathy. Additionally, impaired late diastolic velocity in the inferior myocardial wall seems to be a paramount marker of future VT/VF/CVD. [ABSTRACT FROM AUTHOR]

Aims Mitral annular (MA) displacement reflects longitudinal left ventricular (LV) deformation and systolic velocity measurements reflect the rate of contraction; both are valuable in the diagnosis and prognosis of cardiac disease. The aim of this study was to test the agreement and reproducibility between motion mode (M-mode), colour tissue Doppler imaging (TDI), and two-dimensional strain imaging (2DSI) when measuring MA displacement and systolic velocity. Methods and results Using GE Healthcare Vivid 7 and E9 and Echopac BT11 software, MA displacement and velocity measurements by 2DSI, TDI, and M-mode determined in the septal and lateral walls in the apical four-chamber view were assessed in 50 control subjects and in 168 patients with various cardiac anomalies known to affect longitudinal displacement such as heart failure, mitral regurgitation, LV hypertrophy, and LV dilation. Intra- and inter-observer variability were tested using the Bland–Altman method in 125 patients. A relatively low bias between M-mode and TDI with respect to MA displacement (mean difference ± 1.96 standard deviation: 0.08 ± 0.35 cm) and a low bias between TDI and 2DSI with respect to MA peak systolic velocity (−0.13 ± 1.87 cm/s) were found. Reproducibility was acceptable for all methods with TDI having the lowest intra- and inter-observer variability. Conclusion LV function could be assessed in terms of MA displacement and systolic velocity using M-mode, TDI, and 2DSI. None of the measurement techniques are, however, interchangeable. Overall, TDI seems to be the most robust method, having the lowest observer variability. [ABSTRACT FROM PUBLISHER]