Left atrial disease and left atrial reverse remodelling across different stages of heart failure development and progression: a new target for prevention and treatment

Abstract

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

Pathogenetic mechanism of atrial failure. Left atrial (LA) remodelling is a multifactorial clinical entity driven by different electrical, mechanical and metabolic stressors. These ones lead to volume/pressure overload, activate the renin–angiotensin–aldosterone (RAA) system and determine the release of different cytokines and hormones. The time‐dependent adaptation of atrial myocytes finally results in a chronic LA dilatation and a loss of elasticity, with a consequent stiffer chamber, less affected by changes in pressure. Without removing the causative stressor, this adaptive process inexorably progresses and the alterations become persistent. However, by treating the underlying diseases or risk factors and with heart failure therapies, atrial failure progression may be halted and, in some cases, reversed.