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Left ventricular mass and hemodynamic overload in normotensive hemodialysis patients

โœ Scribed by Lin, Yao-Ping; Chen, Chen-Huan; Yu, Wen-Chung; Hsu, Tsei-Lieh; Ding, Philip Yu-An; Yang, Wu-Chang


Publisher
Nature Publishing Group
Year
2002
Tongue
English
Weight
124 KB
Volume
62
Category
Article
ISSN
0085-2538

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โœฆ Synopsis


Background:

It remains uncertain whether the hemodynamic parameters are important determinants of left ventricular mass (lvm) in normotensive chronic hemodialysis (nthd) patients, as has been found in their hypertensive counterparts.

Methods:

Forty nthd patients (mean age, 53.7 +/- 14.4 years; male/female, 18/22) without the requirement of antihypertensive drugs for at least six months were studied. controls were 41 hypertensive hemodialysis patients (hthd) and 46 normotensive subjects with normal renal function (ntnr). the influence of anthropometrics, cardiovascular structure and function, and volume status on lvm (by two-dimensional echocardiography) was analyzed by steps of multiple linear regression.

Results:

As compared with the ntnr and nthd group, the hthd group had obvious pressure and volume/flow overload, and greater lv wall thickness, chamber size and mass. in contrast, nthd subjects had similar blood pressure, large artery function, lv chamber size and stroke volume as the ntnr subjects. however, the nthd patients still had greater wall thickness and lvm, along with greater cardiac output, lower total peripheral resistance and lower end-systolic meridional stress to volume ratio (essv) than the ntnr group. lvm in the nthd group was significantly positively related to averaged systolic blood pressure (sbpavg), body surface area, extracellular fluid (ecf), carotid intima-media thickness (imt), aortic pulse wave velocity (pwv), and negatively related to essv and kt/v. the independent significant noncardiac structural determinants of lvm in nthd subjects were essv, sbpavg, pwv and sv (model r2 = 0.617, p < 0.001).

Conclusions:

The nthd patients, without significant pressure and volume overload, still had increased lvm that was partially explained by the persistent flow overload and subclinical lv dysfunction.


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