title: 'Hypersynchronisation' by tissue velocity imaging in patients with cardiac amyloidosis.
abstract: OBJECTIVE
  It is unknown if some patients with cardiac amyloidosis (CA) have mechanical dyssynchrony, as has been demonstrated in patients with ischaemic and dilated cardiomyopathies. The aim of this study was to assess mechanical dyssynchrony in patients with CA using tissue velocity imaging (TVI) and to define its usefulness for risk stratification.
  
  
  METHODS
  We included 121 patients with primary amyloidosis and 37 age-matched and sex-matched controls. Patients were divided into two groups: 60 with advanced-CA and 61 with no-advanced-CA, according to left ventricular (LV) wall thickness and diastolic dysfunction. Dyssynchrony assessment included: (1) atrioventricular dyssynchrony (dys), (2) interventricular dys, (3) intraventricular dys assessed longitudinally, using the standard deviation of time to systolic peak velocity (Ts-SD) of the 12 basal and mid level LV segments, and (4) intraventricular dys assessed radially, using the difference in radial Ts between mid anteroseptal and mid posterior segments.
  
  
  RESULTS
  Primary end-point was all-cause death. During a median follow-up of 13 months there were 35 events among patients.
  
  
  RESULTS
  Contrary to the hypothesis, the intraventricular dys indices in advanced-CA patients were reduced compared to either the no-advanced-CA group or to controls (Ts-SD: 12.1 (9.0); 35.1 (18.6); 24.5 (14.1), respectively, p<0.001). This reduction was primarily the result of decreased ejection time (ET). Moreover, ET was the most significant predictor of survival (HR = 0.98, p<0.001).
  
  
  CONCLUSIONS
  The regional timing of systolic motion measured by TVI was abnormally synchronised in the patients with advanced-CA. ET reduction plays a prominent part in this process and should be considered an essential parameter for assessment of patients with cardiac amyloidosis.
authors.affiliation: Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
authors.forename: D
authors.initials: D
authors.lastname: Bellavia
authors.forename: P A
authors.initials: PA
authors.lastname: Pellikka
authors.forename: T P
authors.initials: TP
authors.lastname: Abraham
authors.forename: G B
authors.initials: GB
authors.lastname: Al-Zahrani
authors.forename: A
authors.initials: A
authors.lastname: Dispenzieri
authors.forename: J K
authors.initials: JK
authors.lastname: Oh
authors.forename: R E
authors.initials: RE
authors.lastname: Espinosa
authors.forename: C G
authors.initials: CG
authors.lastname: Scott
authors.forename: C
authors.initials: C
authors.lastname: Miyazaki
authors.forename: F A
authors.initials: FA
authors.lastname: Miller
mesh_terms: D000686:Amyloidosis / Q000000981:diagnostic imaging / Q000503:physiopathology*; D001283:Atrioventricular Node / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D002037:Bundle-Branch Block / Q000503:physiopathology; D016022:Case-Control Studies; D015150:Echocardiography, Doppler; D005260:Female; D054143:Heart Failure, Systolic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D011379:Prognosis; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D015415:Biomarkers