title: Left atrial myopathy in cardiac amyloidosis: implications of novel echocardiographic techniques.
abstract: OBJECTIVE
  To assess left atrial (LA) function and determine the prevalence of LA dysfunction in AL amyloidosis (AL) using conventional and strain echocardiography.
  
  
  RESULTS
  LA ejection fraction, LA filling fraction, LA ejection force, peak LA systolic strain rate (LAsSR), and LA systolic strain (LA epsilon) were determined in 95 AL patients (70 with and 25 without echocardiographic evidence of cardiac involvement, abbreviated CAL and NCAL, respectively), 30 age-matched controls (CON), and 20 patients with diastolic dysfunction and LA dilatation (DD). Peak LAsSR >2 standard deviations below mean CON value was used as the cut-off for normal LA function. LA ejection fraction was lower in CAL when compared with CON (40.4+/-13.6 vs. 67.0+/-6%, P=0.01). Left atrial septal strain rate and strain were lower in CAL (0.8+/-0.5 s(-1) and 5.5+/-4%, respectively) compared with CON (1.8+/-0.8 s(-1) and 14+/-4%, respectively, P=<0.0001), NCAL (1.6+/-0.8 s(-1) and 13+/-7%, respectively, P<0.0001) and DD (1.3+/-0.4 s(-1) and 10+/-2%, respectively, P<0.0001). Based on peak LA systolic strain rate criteria, the cut-off values for normal LA function were -1.1 s(-1) and -1.05 s(-1) for lateral and septal walls. Using these criteria, LA dysfunction was identified in 32% (lateral LA criteria) and 60% (septal LA criteria) of CAL patients. Lateral and septal LAsSR were lower in CAL patients with vs. those without symptoms of heart failure. Inter- and intra-observer agreement was high for LA strain echocardiography.
  
  
  CONCLUSIONS
  LA function assessment using strain echocardiography is feasible with low intra- and inter-observer variability. LA dysfunction is observed in AL patients without other echocardiographic features of cardiac involvement and may contribute to cardiac symptoms in CAL.
authors.affiliation: Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN, USA.
authors.forename: Karen M
authors.initials: KM
authors.lastname: Modesto
authors.forename: Angela
authors.initials: A
authors.lastname: Dispenzieri
authors.forename: Sanderson A
authors.initials: SA
authors.lastname: Cauduro
authors.forename: Martha
authors.initials: M
authors.lastname: Lacy
authors.forename: Bijoy K
authors.initials: BK
authors.lastname: Khandheria
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Pellikka
authors.forename: Marek
authors.initials: M
authors.lastname: Belohlavek
authors.forename: James B
authors.initials: JB
authors.lastname: Seward
authors.forename: Robert
authors.initials: R
authors.lastname: Kyle
authors.forename: A Jamil
authors.initials: AJ
authors.lastname: Tajik
authors.forename: Morie
authors.initials: M
authors.lastname: Gertz
authors.forename: Theodore P
authors.initials: TP
authors.lastname: Abraham
mesh_terms: D000368:Aged; D000686:Amyloidosis / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D009202:Cardiomyopathies / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D016022:Case-Control Studies; D004452:Echocardiography / Q000379:methods*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D010138:Pacemaker, Artificial; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology