title: Detection of left ventricular systolic dysfunction in cardiac amyloidosis with strain rate echocardiography.
abstract: BACKGROUND
  We examined the potential role of Doppler myocardial imaging including tissue velocity imaging, strain imaging, and strain rate imaging for detection of left ventricular systolic dysfunction in cardiac amyloidosis (CA) and determined the minimum dataset required to make the diagnosis.
  
  
  RESULTS
  Doppler myocardial imaging was performed in 103 patients with amyloidosis (AL). Peak longitudinal systolic tissue velocity, systolic strain rate (sSR), and systolic strain (sS) were determined for 16 left ventricular segments. Radial and circumferential sSR and sS were also measured. Patients with increased left ventricular wall thickness were classified with advanced-CA, and the remainder of the patients were classified with AL-normal-wall-thickness. The global means of peak systolic tissue velocity (3.6 +/- 1.0 vs. 3.9 +/- 0.9, P = .007), sSR (-0.8 +/- 0.3 vs. -1.0 +/- 0.2, P < .001), and sS (-9.9 +/- 3.7 vs. -15.6 +/- 3.3, P < .001) were significantly lower in advanced-CA compared with AL-normal-wall-thickness. The mean of either sSR or sS from 6 middle or all 16 segments similarly differentiated patients with advanced-CA from AL-normal-wall-thickness.
  
  
  CONCLUSIONS
  Longitudinal sS most accurately detects longitudinal systolic dysfunction in AL and best differentiates patients with advanced-CA with increased ventricular thickness from patients with AL-normal-wall-thickness. Interrogation of six middle segments was sufficient in identifying patients with advanced-CA. Further studies are warranted to define the incremental prognostic value of these new parameters in predicting outcomes for patients with AL.
authors.affiliation: Cardiovascular Division, Mayo Clinic and Foundation, Rochester, Minneosota 55905, USA.
authors.forename: Diego
authors.initials: D
authors.lastname: Bellavia
authors.forename: Theodore P
authors.initials: TP
authors.lastname: Abraham
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Pellikka
authors.forename: Ghormallah B
authors.initials: GB
authors.lastname: Al-Zahrani
authors.forename: Angela
authors.initials: A
authors.lastname: Dispenzieri
authors.forename: Jae K
authors.initials: JK
authors.lastname: Oh
authors.forename: Kent R
authors.initials: KR
authors.lastname: Bailey
authors.forename: Christina M
authors.initials: CM
authors.lastname: Wood
authors.forename: Salvatore
authors.initials: S
authors.lastname: Novo
authors.forename: Chinami
authors.initials: C
authors.lastname: Miyazaki
authors.forename: Fletcher A
authors.initials: FA
authors.lastname: Miller
mesh_terms: D000368:Aged; D000686:Amyloidosis / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D001706:Biopsy; D001783:Blood Flow Velocity / Q000502:physiology; D003937:Diagnosis, Differential; D018619:Echocardiography, Doppler, Pulsed / Q000379:methods*; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D015588:Observer Variation; D011379:Prognosis; D015203:Reproducibility of Results; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology