CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 1, January/February 2014
AFRICA
7
vascular calcification is not directly responsible for aortic
stiffening and the association of calcification with PWV is
not causative. There are many other factors such as elastin
fragmentation, endothelial dysfunction and advanced glycation
that affect aortic stiffness other than calcification.
11
Alternatively, since vascular micro-calcifications may be
present in uraemic subjects without radiologically visible
calcium,
27
it is possible that vascular stiffening occurs earlier on
and obscures any differences in CASP.
Unfortunately, we were unable to measure PWV. As left
ventricular mass index is strongly determined by CASP,
8,28
the
lack of association with vascular calcification supports our
controversial findings.
Non-dipping was particularly prevalent, as in other studies
of CKD,
29
and although it has been associated with vascular
calcification,
30
it was not different in those with and without
vascular calcification in this cohort. However, the very poor
dipping status overall may have obscured any clinically
meaningful difference between the two groups.
Both inter-dialytic office blood pressure and CASP correlated
well with ambulatory blood pressure measurements. This has
important implications since the FDA has called for the inclusion
of CASP into clinical studies of blood pressure.
4
Office CASP
could therefore also represent ambulatory CASP well in other
CKD-5D populations, although this requires further study. Our
observations support findings by other groups where inter-
dialytic measurement of blood pressure was superior to office
blood pressure in predicting ambulatory measurements for
CKD-5D patients.
31,32
There were several limitations to our study. First, the patients
in our cohort were young and one cannot be certain whether
these findings would be reproduced in an older cohort. Second,
we were not able to measure PWV in our study and it would have
been useful to do this in attempting to reconcile the lack of effect
of vascular calcification on central aortic pressures. It remains
to be determined in this cohort whether vascular calcification
occurs independently of changes in pulse-wave velocity. Third,
CASP was indirectly measured, although a recent publication
showed excellent correlation of BPro with direct measurement
of CASP.
17
Conclusion
Coronary and abdominal aortic calcification was not associated
with changes in central aortic systolic pressure or dipping
status in young South African dialysis patients. Inter-dialytic
office blood pressure and central aortic systolic pressure, when
measured according to ESH standards, correlated very well with
ambulatory measurements.
We are indebted to the staff at Groote Schuur Renal Unit as well as the
2-Military Hospital Radiology Department for their willing assistance. We
thank Genzyme Corporation (Cambridge, MA) and Discovery Health (South
Africa) for unrestricted research grants that made this possible. RF is grateful
to National Renal Care (South Africa) for salary funding.
Genzyme Corporation provided statistical advice during protocol design
but was at no stage involved in the collection, analysis, interpretation and
reporting of data herein. The authors declare no conflict of interest.
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