Function over form? Assessing the left atrium in heart failure

Abstract

This editorial refers to 'Left atrial function measured by cardiac magnetic resonance imaging in patients with heart failure: clinical associations and prognostic value' † , by P. Pellicori et al., on page 733.The understanding of heart failure (HF) haemodynamics has traditionally focused on left ventricular (LV) structure and function, with the left atrium being viewed simply as a passive transport chamber that empties into the left ventricle. Over the last decade, there has been increasing recognition of the importance of left atrial (LA) structure and function in the pathophysiology of HF. LA volume was first to be established as a biomarker integrating the magnitude and duration of LV diastolic function, and a predictor of cardiovascular outcomes in HF. More recently, LA function has emerged as a novel determinant of clinical status and outcomes in HF, and perhaps an even more robust prognostic marker than LA volume ( Table 1). Pellicori et al. have now explored the prognostic relevance of one summary measure of LA function-LA emptying fraction (LAEF)-by magnetic resonance imaging (MRI) in HF.1 In this single-centre study of 759 patients with suspected HF and in sinus rhythm undergoing cardiac MRI, LAEF was lower on average among 664 patients with the confirmed diagnosis of HF. Lower LAEF correlated with larger LA maximal and conduit volumes, smaller LA reservoir volume, lower LV and right ventricular (RV) ejection fraction, greater LV and RV remodelling, and higher circulating N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. Over a median follow-up of 3-4 years, LAEF, but not LA volume, was independently associated with incident HF hospitalization, cardiovascular mortality, all-cause mortality, and atrial fibrillation in multivariable models that included clinical predictors and NT-proBNP level. Importantly, LAEF provided incremental value in predicting these outcomes, beyond clinical variables alone but not in addition to NT-proBNP levels. The left atrium modulates LV filling and cardiovascular performance by three distinct functions: (i) as a reservoir for pulmonary venous return during LV systole; (ii) as a conduit for passive flow of blood from the pulmonary veins into the ventricle during early LV diastole and diastasis, and (iii) as a pump during late LV diastole that augments LV stroke volume (by 15-30% in healthy individuals and more in the presence of abnormal LV relaxation) (Figure 1). LA reservoir function is influenced by LA compliance as well as LV contraction via descent of the LV base during systole, and RV systolic pressure transmitted via the pulmonary circulation. LA conduit function is inversely related to reservoir function and strongly modulated by LV relaxation and compliance. LA pump function reflects LA contractility and is also dependent on both LA preload (venous return) and LA afterload (LV end-diastolic pressure). Of note, the Frank -Starling mechanism applies to LA mechanics (as with LV mechanics), wherein LA ejection volume increases as LA filling volume increases, ...

Echocardiographic estimation of left ventricular and pulmonary pressures in patients with heart failure and preserved ejection fraction: a study utilizing simultaneous echocardiography and invasive measurements

“…An inverse relation exists between LA strain and LV end‐diastolic filling pressures and conventional indices of diastolic function . Recently, LA function has gained recognition as an important focus area in the assessment of LV diastolic function, especially in heart failure . We demonstrated that LA reservoir strain was a better predictor of mean PAWP than LAVi, which is currently one of the major indices for structural abnormalities in the ASE/EACVI recommendations and ESC guidelines .…”

“…25 Recently, LA function has gained recognition as an important focus area in the assessment of LV diastolic function, especially in heart failure. 20,21,26,27 We demonstrated that LA reservoir strain was a better predictor of mean PAWP than LAVi, which is currently one of the major indices for structural abnormalities in the ASE/EACVI recommendations and ESC guidelines. 1,13,14 It is suggested that a decrease in LA function might precede LA remodelling 20 and is the best parameter to distinguish asymptomatic patients with diastolic dysfunction from those with HFpEF.…”

Muscle Contraction and Pressure-Volume Loops in the Left-Heart

“…It is worth noting that active contraction of LA modulates both LV filling and LV stroke volume. This latter can be increased by ~15-30% in healthy individuals and even more in the presence of abnormal relaxation (Pagel et al 2003, Shah & Lam 2015.…”

Heart Failure in Patients with Preserved Ejection Fraction: Questions Concerning Clinical Progression

“…The above relocation of interest to endothelial inflammation shifts attention to concentric LVH remodeling and diastolic dysfunction in contrast to the HFrEF remodeling, which is driven by progressive loss of cardiomyocytes [ 49 ]. Pellicori et al [ 50 ] believe that left atrial emptying function (LAEF) is a better prognostic marker in outpatients referred for HF, while the improvement of the LA structural remodeling after therapy is associated with better clinical outlook in patients with HF [ 51 ].…”

“…The relevant clinical trials are suboptimal in their design, and the treatment to a great extent remains largely empiric [ 1 ]. The present limited natural history data on follow-up in all clinical stages of PDD and HFpEF patients raise a number of questions: (1) there is an unspecified relationship between PDD and progression to HFpEF; (2) there are no data for the relationship between the degree of PDD and clinical progression, as people with the same degree of PDD develop different clinical phenotypes; (3) there is an undetermined connection of the progression rate from PDD to HFpEF for each particular comorbidity; (4) there are no data for similarities or differences between the two clinical phenotypes on clinical deterioration and progression up to the final stages of HF; (5) there are no clear data on the mortality rate of HFpEF patients during the whole period of clinical deterioration up to the final stages; more data are required for the duration and survival in each step of the syndrome ( Figure 2 ); (6) robust data are needed to support the notion that in HFpEF, the left ventricular remodeling is the most probable cause of the clinical decline; (7) it is speculated that the two phenotypes differ in their remodeling mechanism, and as a consequence, they have developed different clinical progression rates; (8) novel prognostic imaging biomarkers are required; probably, LA function is emerging as an important prognostic biomarker [ 51 ].…”