Atrial fibrillation (AF) is the most common arrhythmic disease at 1 to 2% of the U.S population, with the forecast of increasing prevalence [17]. AF originates from a trigger and substrate, with substrate being a large fibrotic atrium. As atrial fibrosis stiffens the LA [5], this may cause additional increased atrial pressure, or reduced LA strain. The role of elevated cardiac pressure in AF and left atrial (LA) remodeling is important [32, 39]. Firstly, elevated pressure is thought to increase LA volumes, ultimately leading to stretch and to development of atrial fibrosis [33], and potentially lead to new onset AF [22]. Secondly, many categories of patients with elevated cardiac pressure progress to AF, including patients with heart-failure [1], hypertrophic cardiomyopathy [26], and obstructive sleep apnea [21] among others.
The triad of strain, pressure and stiffness (e.g. fibrosis) are crucial in understanding atrial remodeling. A simple to understand model of strain (e, equals stress / stiffness) on a spherical shell of radius r, and thickness b, yields [34, 37] :
\(\epsilon \propto \frac{ P\bullet r}{\left(b\bullet E\right)}\) Eq. 1.
This equation describes a relationship between strain (e), pressure (P), stiffness (E, atrial fibrosis, etc. ) and volume (r3). The equation also explains the origin of left atrial “stiffness index” (E\(\propto \text{P}/{\epsilon }_{LA}\)) (pressure/LA reservoir strain) [4] [16] employed by echocardiography (using E/e’ for pressure). Atrial stiffness is partly attributable to atrial fibrosis, which can be evaluated using 3D high resolution late gadolinium enhancement (LGE) [29] with cardiac magnetic resonance (CMR). Increased atrial LGE (fibrosis causing increased stiffness) is associated with reduced LA function (both strain and EF), as confirmed by many studies [6, 11, 12, 13, 19, 27, 30].
In non-AF subjects, atrial strain changes are often advocated as an early sign of pressure increase [3, 4, 14, 35, 36]. LA strain as a correlate of pressure is an attractive possibility. To date, there are no imaging biomarkers to estimate cardiac pressure accurately; many echo correlates (E/e’, etc) are not fully robust. Others have studied LA strain as a direct biomarker of LV filling pressure [3, 4], or its role in grading diastolic dysfunction (itself a disease indicative of elevated pressure) [35]. The pressure-strain relationship varied from strong to modest [3] [4] [14] [36]. These findings have not been attempted or replicated in an AF cohort. We hypothesized that pressure-strain relationships may be modulated in AF cohort, because of the range of LA volumes and atrial fibrosis, as is suggested by Eq. 1. We examined the relationship of LA strain with elevated pressure in an AF cohort, with the hypothesis that atrial stiffness might impact this relationship.
Even while LA strain is an area of increasing interest, it is rarely noted the very tight correlations between LA strain, LA volume, and LA EF. In AF, where LA volumes span a wide range, this becomes even more important. Complete strain analysis (including strains in three phases, systolic, early diastolic and during the atrial kick; also strain rates, and timings of peak strains and strain rates) is not often performed and the unique contributions of these metrics are not known.