Sensitive detection of myocardial contraction abnormality in chronic hemodialysis patients by ultrasonic tissue characterization with integrated backscatter

Citation
K. Mizushige et al., Sensitive detection of myocardial contraction abnormality in chronic hemodialysis patients by ultrasonic tissue characterization with integrated backscatter, ANGIOLOGY, 51(3), 2000, pp. 223-230
Citations number
20
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
ANGIOLOGY
ISSN journal
00033197 → ACNP
Volume
51
Issue
3
Year of publication
2000
Pages
223 - 230
Database
ISI
SICI code
0003-3197(200003)51:3<223:SDOMCA>2.0.ZU;2-V
Abstract
Since acoustic properties of the myocardium are sensitive to the myocardial structure and the contractile conditions of myocyte, the authors evaluated cardiac dysfunction based on the integrated ultrasonic backscatter in 18 h emodialysis (HD) patients (duration: 102 +/-84 months, mean age: 57.6 +/-9. 7 years) and 11 age-matched normals. The cyclic variation of integrated bac kscatter (CV-IB) at interventricular septum (IVS) and left ventricular post erior wall (PW) was measured and compared with percent fractional shortenin g (%FS) and percent wall thickening (%Th). The CV-IB of HD patients was sma ller than that of control subjects (IVS: 6.2 +/-1.1 dB vs 8.2 +/-1.1 dB, p = 0.0003 and PW: 8.4 +/-2.2 vs 10.3 +/-1.3, p = 0.025). No significant diff erence was observed in %FS and %Th between HD patients and control subjects . In HD, the ratio of velocities of early diastolic inflow (E) to late atri al inflow was decreased (0.7 +/-0.2 vs 1.1 +/-0.7, p = 0.049) and decelerat ion time of E was prolonged significantly (200 +/-28 msec vs 159 +/-30 msec , p = 0.0082). In the absence of overt cardiac systolic dysfunction, myocar dial damage indicated as a decrease in CV-IB and diastolic dysfunction iden tified on transmitral velocity waveform were detected, which may reflect fr om the myocardial fibrosis. As a mechanism, pressure overload, hyperparathy roidism, and anemia were neglected, and the other humoral factors may contr ibute to the myocardial damage in chronic renal failure.