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The importance of atrial cardiomyopathy (AtCM) as a specific clinical entity is increasingly recognized. Past definitions have varied, and the lack of consistent cut-offs for imaging parameters and biomarkers have limited clinical utility to diagnose and track AtCM progression. While research has mainly focused on AtCM in the context of atrial fibrillation, emerging evidence underscores its relevance in remodelling and development of heart failure. The aim of this consensus document was to provide a contemporary framework for AtCM, evolve the definitions of AtCM and atrial failure for more widespread clinical use, and help to direct emerging research and future clinical trials. Supporting the work of early career researchers, this consensus document evaluates diagnostic markers and summarizes the underpinning mechanisms, clinical characteristics and prognostic impact of AtCM. Our objective was to bring together new translational scientific progress, catalyse future research and enable clinical application to facilitate better management, for example in patient groups where aggressive control of risk factors or comorbidities could prevent AtCM progression. We redefined AtCM as a graded disorder that includes electrical dysfunction of the atria along with evidence of either mechanical atrial dysfunction, atrial enlargement and/or atrial fibrosis. Atrial failure is the end-stage manifestation of AtCM, characterized by progressive structural, electrophysiological and functional changes. Earlier identification, risk stratification and ongoing research into therapeutic options have the potential to prevent the clinical consequences of AtCM and atrial failure, including adverse patient outcomes and poor quality of life associated with atrial fibrillation and heart failure.

Background: Speckle tracking echocardiographic global longitudinal strain (GLS) predicts outcome in patients with new onset heart failure. Still, its incremental value on top of left ventricular ejection fraction (LVEF) in patients with nonischemic, nonvalvular dilated cardiomyopathy (DCM) after optimal heart failure treatment remains unknown. Methods and Results: Patients with DCM were included at the outpatient clinics of 2 centers in the Netherlands and Italy. The prognostic value of 2‐dimensional speckle tracking echocardiographic global longitudinal strain was evaluated when being on optimal heart failure medication for at least 6 months. Outcome was defined as the combination of sudden or cardiac death, life‐threatening arrhythmias, and heart failure hospitalization. A total of 323 patients with DCM (66% men, age 55±14 years) were included. The mean LVEF was 42%±11% and mean GLS after optimal heart failure treatment was −15%±4%. Twenty percent (64/323) of all patients reached the primary outcome after optimal heart failure treatment (median follow‐up of 6[4–9] years). New York Heart Association class ≥3, LVEF, and GLS remained associated with the outcome in the multivariable‐adjusted model (New York Heart Association class: hazard ratio [HR], 3.43; 95% CI, 1.49–7.90, P =0.004; LVEF: HR, 2.13; 95% CI, 1.11–4.10, P =0.024; GLS: HR, 2.24; 95% CI, 1.18–4.29, P =0.015), whereas left ventricular end‐diastolic diameter index, left atrial volume index, and delta GLS were not. The addition of GLS to New York Heart Association class and LVEF improved the goodness of fit (log likelihood ratio test P <0.001) and discrimination (Harrell’s C 0.703). Conclusions: Within this bicenter study, GLS emerged as an independent and incremental predictor of adverse outcome, which exceeded LVEF in patients with optimally treated DCM. This presses the need to routinely include GLS in the echocardiographic follow‐up of DCM.

Aim: Diagnosing heart failure with preserved ejection fraction (HFpEF) in the non-acute setting remains challenging. Natriuretic peptides have limited value for this purpose, and a multitude of studies investigating novel diagnostic circulating biomarkers have not resulted in their implementation. This review aims to provide an overview of studies investigating novel circulating biomarkers for the diagnosis of HFpEF and determine their risk of bias (ROB). Methods and results: A systematic literature search for studies investigating novel diagnostic HFpEF circulating biomarkers in humans was performed up until 21 April 2020. Those without diagnostic performance measures reported, or performed in an acute heart failure population were excluded, leading to a total of 28 studies. For each study, four reviewers determined the ROB within the QUADAS-2 domains: patient selection, index test, reference standard, and flow and timing. At least one domain with a high ROB was present in all studies. Use of case-control/two-gated designs, exclusion of difficult-to-diagnose patients, absence of a pre-specified cut-off value for the index test without the performance of external validation, the use of inappropriate reference standards and unclear timing of the index test and/or reference standard were the main bias determinants. Due to the high ROB and different patient populations, no meta-analysis was performed. Conclusion: The majority of current diagnostic HFpEF biomarker studies have a high ROB, reducing the reproducibility and the potential for clinical care. Methodological well-designed studies with a uniform reference diagnosis are urgently needed to determine the incremental value of circulating biomarkers for the diagnosis of HFpEF.

This study assessed the prognostic implications of mechanical atrial dysfunction in heart failure with preserved ejection fraction (HFpEF) patients with different stages of atrial fibrillation (AF) in detail. HFpEF patients (n = 258) systemically underwent an extensive clinical characterization, including 24-h Holter monitoring and speckle-tracking echocardiography. Patients were categorized according to rhythm and stages of AF: 112 with no history of AF (no AF), 56 with paroxysmal AF (PAF), and 90 with sustained (persistent/permanent) AF (SAF). A progressive decrease in mechanical atrial function was seen: left atrial reservoir strain (LASr) 30.5 ± 10.5% (no AF), 22.3 ± 10.5% (PAF), and 13.9 ± 7.8% (SAF), P < 0.001. Independent predictors for lower LASr values were AF, absence of chronic obstructive pulmonary disease, higher N-terminal-pro hormone B-type natriuretic peptide, left atrial volume index, and relative wall thickness, lower left ventricular global longitudinal strain, and echocardiographic signs of elevated left ventricular filling pressure. LASr was an independent predictor of adverse outcome (hazard ratio per 1% decrease =1.049, 95% confidence interval 1.014–1.085, P = 0.006), whereas AF was not when the multivariable model included LASr. Moreover, LASr mediated the adverse outcome associated with AF in HFpEF (P = 0.008). Mechanical atrial dysfunction has a possible greater prognostic role in HFpEF compared to AF status alone. Mechanical atrial dysfunction is a predictor of adverse outcome independently of AF presence or stage, and may be an underlying mechanism (mediator) for the worse outcome associated with AF in HFpEF. This may suggest mechanical atrial dysfunction plays a crucial role in disease progression in HFpEF patients with AF, and possibly also in HFpEF patients without AF.