Comparison of left ventricular diastolic filling with myocyte bulk modulususing Doppler echocardiography and acoustic microscopy in pressure-overload left ventricular hypertrophy and cardiac amyloidosis

Background: The myocardial bulk modulus has been described as the constitut ive properties of the left ventricular (LV) wall and is measured as rho V-2 (rho = density, V = sound speed) using acoustic microscopy. Hypothesis: The study was undertaken to assess the relationship between the myocyte bulk modulus and transmitral inflow patterns in patients with pres sure-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 echocardiog raphy before death, and myocardial tissue specimens were obtained at autops y. The tissue density and sound speed in the myocytes were measured by micr ogravimetry and acoustic microscopy, respectively. The diameters of the myo cytes were measured on histopathologic specimens stained by the elastica Va n Gieson method. Results: In the subendocardium, the myocyte bulk modulus was larger in LVH (2.98 x 10(9) N/m(2), p < 0.001) and smaller in AMD (2.61 x 10(9) N/m(2), p < 0.001) than in the controls (2.87 x 10(9) N/m(2)). The myocyte diameter in LVH (26 +/- 1 mu m) was larger than that in the control (21 +/- 1 mu m, p < 0.001) and AMD (20 +/- 1 mu m, p < 0.001). The bulk modulus in the sube ndocardial myocyte significantly correlated with the deceleration time (DT) of the early transmitral inflow (r = 0.689, p = 0.028 in control, r = 0.77 4, p = 0.024 in LVH, and r = 0.786, p = 0.021 in AMD). Conclusion: The changes in the myocyte elasticity as represented by the bul k modulus were limited to the subendocardial layers and may be related to r elaxation abnormalities in LVH and a reduction in LV compliance in AMD.