Factors impacting on left ventricular hypertrophy in haemodialysis patients
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Date
2008-10-23T08:35:25Z
Authors
Chabu, James
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Abstract
Left ventricular hypertrophy (LVH) and increases in large artery stiffness predict
cardiovascular outcomes in patients with renal failure. What determines left ventricular mass
index (LVMI) and large artery stiffness and the contribution toward LVH and large artery
dysfunction is not entirely clear. Consequently, this cross sectional study was aimed at
assessing the various factors impacting on LVH in haemodialysis (HD), to contribute toward
our understanding of the pathophysiology of LVH and large artery dysfunction in 94 adult HD
patients. Pre- and post-dialysis blood pressures (BPs) were determined over 12 sessions of
dialysis and averaged. Pulse wave analysis performed at the carotid, femoral and radial
arteries was employed to determine pulse wave velocity (PWV) and central augmentation
index (AIc). Echocardiography was performed to determine left ventricular mass (LVM)
indexed to body surface area (LVMI). Natriuretic peptides, procollagen type I c-peptide (PIP),
c-terminal telopeptide of type I collagen (ICTP), matrix metalloproteinases and their inhibitors
were studied.
The prevalence of LVH was 72.8 % (67/92) .On multivariate analysis pre- (p≤
0.005), post- (p<0.05) and averaged dialysis (p < 0.015) systolic BP were associated with
LVMI and PWV. 24 hour (r = 0.260, p = 0.026), day (r = 0.247, p = 0.036), and night (r=
0.241, p = 0.042) systolic BP were not more closely associated with LVMI than the averaged
dialysis systolic BP (r = 0.272, p = 0.010). Similarly 24 hour (r = 0.41, p = 0.0003), day
(r=0.400, p = 0.0005), and night (r =0.416, p = 0.0003) systolic BP were not more closely
associated with PWV than the post-dialysis systolic BP (r=0.39, p=0.0001) indicating that
these BP measurements are as effective as 24-hour ambulatory BP in predicting cardiovascular target organ changes. No relationship between either PWV (r=-0.08), or AIc (r=-0.10) and
LVMI, between PWV (r=-0.11), or AIc (r=0.03) and LV MWT was noted. IVCD was
independently associated with LVMI (partial r adjusted for average dialysis SBP=0.27,
p=0.014; partial r adjusted for 24-hour SBP=0.29, p=0.013), and LV mean wall thickness
(p<0.01), but not with LV relative wall thickness (p=0.18), or LV end diastolic diameter
(p=0.88). An association between IVCD and AIc (partial r adjusted for average dialysis
SBP=0.21, p<0.05), but not PWV was noted. NT-proANP and NT-proBNP were
independently associated with LVMI (p<0.0001) but neither were associated with IVCD
independent of LVMI suggesting a close association with LVMI in HD. Serum concentrations
of matrix metalloproteinases 1, 2 and 9, and their tissue inhibitors (1 and 2) were not
associated with LVMI, remodelling or PWV and neither procollagen I nor the C-terminal
telopeptide of type I collagen (ICTP) were associated with LVMI. Thus, factors impacting on
LVH in this study were systolic BP, NT-proANP, NT-proBNP and IVCD.
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Keywords
haemodialysis, left ventricular hypertrophy