Left atrial mechanics strongly predict functional capacity assessed by cardiopulmonary exercise testing in subjects without structural heart disease

Abstract

Left atrium function is essential for cardiovascular performance and is evaluable by two-dimensional speckle-tracking echocardiography (2D-STE). Our aim was to determine how echocardiographic parameters interrelate with exercise capacity and ventilatory efficiency in subjects with no structural heart disease. Asymptomatic volunteers, in sinus rhythm and with normal biventricular size and function, were recruited from a community-based population. Individuals with moderate-to-severe valvular disease, pulmonary hypertension, and history of cardiac disease were excluded. We performed a transthoracic echocardiogram and assessed left atrial (LA) and left ventricular (LV) mechanics via 2D-STE. Cardiopulmonary exercise testing by treadmill took place immediately thereafter. Peak oxygen uptake (VO) served as measure of functional capacity and ventilation/carbon dioxide output (VE/VCO) slope as surrogate of ventilation/perfusion mismatch. 20 subjects were included (age 51 ± 14 years, male gender 65%). Peak VO strongly correlated with age (r = -0.83; P < 0.01), with E/e' ratio (r = -0.72; P < 0.01), and with LA reservoir- and conduit-phase mechanics, particularly with LA conduit strain rate (SR) (r = -0.82; P < 0.01), but showed no correlation with LA volume index or LV mechanics. A similar pattern of associations was identified for VE/VCO slope. In multivariate analysis, LA conduit SR (β = -0.69; P = 0.02) emerged as sole independent correlate of peak VO, adjusted for age and for E/e' ratio (adjusted r = 0.76; P< 0.01). Conduit and reservoir components of LA mechanics displayed strong associations with peak VO and VE/VCO slope. LA conduit-phase SR seems best suited as echocardiographic marker of functional capacity in subjects with no structural heart disease.

Atrial function in Fontan patients assessed by CMR: Relation with exercise capacity and long-term outcomes

“…In the current study we demonstrated a limited role of atrial performance on outcomes in Fontan patients. These results are in strong contrast to results in a similarly sized group of healthy adults, in which atrial function assessed by echocardiography strongly predicted exercise performance [15].…”

“…The atria play an important role in diastole and during exercise atrial function might be augmented [14]. Atrial function assessed by echocardiographic strain has been shown to predict exercise capacity in healthy adults [15]. A predictive value of atrial function on exercise performance has also been confirmed in patients with dilated cardiomyopathy [16], heart failure with preserved ejection fraction [17], and tetralogy of Fallot [18].…”

Relationship between Cardiac Remodeling and Exercise Capacity in Elite Athletes: Incremental Value of Left Atrial Morphology and Function Assessed by Three-Dimensional Echocardiography

“…LV GLS was proved to be a strong marker of LV functional status, 34,35 and LA passive EF may be perceived as a composite marker of LV diastolic function, LA stiffness, and filling pressures, which may explain their predictive value. 36,37 Previous studies using cardiac magnetic resonance examinations in athletes observed strong correlations between cardiac size and cardiopulmonary fitness. 5,38 In parallel with our results, more pronounced LV and LA morphologic remodeling was found to be associated with better exercise capacity in echocardiographic studies as well.…”

Going beyond classic echo in aortic stenosis: left atrial mechanics, a new marker of severity

“…Currently, the management of patients with AS is based on the assessment of AS severity, left ventricular ejection fraction (LVEF), and symptom development [2]. In patients with aortic valve disease, the left atrium (LA) undergoes remodeling due to pressure overload, resulting in disturbances in three functional phases: reservoir, conduit, and contractile phase [3, 4]. In patients with AS, there is an increase in filling pressures and LA afterload, due to left ventricular (LV) hypertrophy.…”