Functional and Anatomic Responses of the Left Atrium to Change in Estimated Left Ventricular Filling Pressure.
BACKGROUND
Left atrial (LA) remodeling and dysfunction reflect chronic exposure to elevated left ventricular (LV) filling pressures. The aim of this longitudinal cohort study was to define the effect of reducing LV filling pressures on reverse remodeling of LA volume (LAV) and function.


METHODS
This retrospective cohort included 195 patients (52% men; mean age, 64 ± 14 years) in sinus rhythm with LA dilatation and sequential echocardiograms (median interval, 1 year; interquartile range, 0.5-2.0 years). One hundred seventy-four patients underwent medical therapy (82 with reduced E/e' ratios), and 21 underwent surgery for valvular heart disease. Biplane LAV (normal value, ≤ 68 mL for men, ≤ 62 mL for women), LA strain (ε) (normal value, >32%) and LV filling pressures (assessed as E/e' ratio; normal value, <13) were measured.


RESULTS
Although LAV at baseline and follow-up were 88 ± 27 and 81 ± 24 mL, LA ε and E/e' ratio remained stable at 26 ± 11% and 14 ± 7, respectively. Changes in E/e' ratio were associated with changes in LAV (r = 0.37, P < .001) and LA ε (r = -0.51 P < .001). Although reduced E/e' ratio or improved LA ε at follow-up occurred in about 50% of the patients, only 26% (51 of 195) had normalized LAV. Compared with surgery, successful reduction of E/e' with medical therapy was less effective in reducing LAV (P < .001) but produced similar improvement in LA ε. Having normal or improved E/e' ratio at follow-up was not associated with normalization of LAV (relative risk, 1.29 [P = .326] and 1.22 [P = .421], respectively) but was associated with normalized LA ε (relative risk, 2.04 [P = .011] and 1.86 [P = .017], respectively) independently of LAV.


CONCLUSIONS
Reduction in LV filling pressures reduces but rarely normalizes LAV. The strong association of reduced LV filling pressure with improved LA function indicated by LA longitudinal ε supports the increasing interest of LA ε measurement.
Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.
Quan L
QL
Huynh
Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.
Kashif
K
Kalam
Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.
Andrea
A
Iannaccone
Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.
Kazuaki
K
Negishi
South Western Sydney Clinical School, The University of New South Wales, Liverpool Hospital, Sydney, Australia.
Liza
L
Thomas
Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Electronic address: tom.marwick@utas.edu.au.
Thomas H
TH
Marwick
D016279:Atrial Function, Left / Q000502:physiology*; D064752:Atrial Remodeling / Q000502:physiology*; D018619:Echocardiography, Doppler, Pulsed / Q000379:methods*; D005260:Female; D005500:Follow-Up Studies; D006325:Heart Atria / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013318:Stroke Volume / Q000502:physiology; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology*
Doppler; Echocardiography; Strain; Volume