title: Comparison of left ventricular diastolic filling with myocyte bulk modulus using Doppler echocardiography and acoustic microscopy in pressure-overload left ventricular hypertrophy and cardiac amyloidosis.
abstract: BACKGROUND
  The myocardial bulk modulus has been described as the constitutive properties of the left ventricular (LV) wall and is measured as rho V2 (rho = density, V = sound speed) using acoustic microscopy.
  
  
  OBJECTIVE
  The study was undertaken to assess the relationship between the myocyte bulk modulus and transmitral inflow patterns in patients with pressure-overload LV hypertrophy (LVH) and cardiac amyloidosis (AMD).
  
  
  METHODS
  In 8 patients with LVH, 8 with AMD, and 10 controls without heart disease, the transmitral inflow pattern was recorded by Doppler echocardiography before death, and myocardial tissue specimens were obtained at autopsy. The tissue density and sound speed in the myocytes were measured by microgravimetry and acoustic microscopy, respectively. The diameters of the myocytes were measured on histopathologic specimens stained by the elastica Van Gieson method.
  
  
  RESULTS
  In the subendocardium, the myocyte bulk modulus was larger in LVH (2.98 x 10(9) N/m2, p < 0.001) and smaller in AMD (2.61 x 10(9) N/m2, p < 0.001) than in the controls (2.87 x 10(9) N/m2). The myocyte diameter in LVH (26 +/- 1 microns) was larger than that in the control (21 +/- 1 microns, p < 0.001) and AMD (20 +/- 1 microns, p < 0.001). The bulk modulus in the subendocardial myocyte significantly correlated with the deceleration time (DT) of the early transmitral inflow (r = 0.689, p = 0.028 in control, r = 0.774, p = 0.024 in LVH, and r = 0.786, p = 0.021 in AMD).
  
  
  CONCLUSIONS
  The changes in the myocyte elasticity as represented by the bulk modulus were limited to the subendocardial layers and may be related to relaxation abnormalities in LVH and a reduction in LV compliance in AMD.
authors.affiliation: Second Department of Internal Medicine, Kagawa Medical University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Masugata
authors.forename: K
authors.initials: K
authors.lastname: Mizushige
authors.forename: S
authors.initials: S
authors.lastname: Senda
authors.forename: A
authors.initials: A
authors.lastname: Kinoshita
authors.forename: H
authors.initials: H
authors.lastname: Sakamoto
authors.forename: S
authors.initials: S
authors.lastname: Sakamoto
authors.forename: H
authors.initials: H
authors.lastname: Matsuo
mesh_terms: D000162:Acoustics; D000368:Aged; D000686:Amyloidosis / Q000000981:diagnostic imaging / Q000503:physiopathology*; D001783:Blood Flow Velocity; D009202:Cardiomyopathies / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003971:Diastole; D015150:Echocardiography, Doppler; D004548:Elasticity; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008853:Microscopy; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D009206:Myocardium / Q000166:cytology*; D016277:Ventricular Function, Left / Q000502:physiology*