CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 7, August 2012
398
AFRICA
indicate arterial elasticity, which includes structure, elastin and
collagen.
It has been shown that
β
-adrenergic blocking agents,
diuretics, and some direct vasodilators such as hydralazine and
dihydralazine, only lowered blood pressure but had no effect on
vascular elasticity, whereas the ACE inhibitors, calcium channel
blockers in general and nitroprusside, in addition to their blood
pressure-lowering properties, also improved arterial elasticity.
10,14
In a six-month study it was shown that perindopril improved
arterial elasticity in hypertensive patients independent of its
blood pressure-lowering properties.
11
In a number of studies, possible mechanisms were
investigated. It was suggested that vascular collagen metabolism
plays a role. However, no correlation could be found between
matrix metalloproteinase (MMP)-1, the tissue inhibitor of
MMP-1 (TIMMP-1), PWV and blood pressure in patients who
received perindopril for six months.
15
A more recent study
showed that ET-1 contributed to a decreased arterial compliance
in hypertension through inhibition of collagen degradation.
13
Furthermore, it has been shown that captopril therapy in
congestive heart failure decreased endothelin production.
12
However, in our study, no correlation could be found between
ET-1 levels and arterial elasticity in any arterial segment or at any
of the measured intervals. This was in contrast to a study done in
endurance-trained men, where a linear correlation between ET-1
and aortic PWV was found.
16
The segment in which the arterial elasticity is measured is
important. In a previous study it was found that perindopril
had a smaller effect on the elasticity in the carotid artery than
the femoral artery.
17
In contrast to our study where the arterial
elasticity in the brachial–ulnar segment was not affected by
perindopril, another study showed an improvement in brachial
elasticity.
18
Conclusion
In addition to its blood pressure-lowering effect, our study
confirms the improvement in arterial elasticity in the carotid–
femoral segment but not the brachial–ulnar segment in patients
on perindopril therapy. Furthermore, we have shown that ET-1
was not correlated to arterial elasticity in patients receiving
perindopril.
As referenced by Milan
et al.
,
the European Society
of Hypertension has now included in their guidelines the
improvement of arterial elasticity as one of the therapeutic aims
in the treatment of hypertension.
19
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TABLE 2. EFFECT OF PERINDOPRIL 4 MG DAILY ON PWVAND ET-1 IN BLACK HYPERTENSIVE
PATIENTSAFTERA NINE-MONTHTREATMENT COMPARED TO HEALTHYVOLUNTEERS
Patients (
n
=
39)
Variable median (IQF 1–3)
Control (
n
=
51)
M0
M1
M3
M6
M9
Carotid–femoral PWV (m/s)
8.2**
(7.0–10.7)
11.6
(7.1–14.0)
9.3
(6.9–11.5)
7.96
(7.4–10.8)
9.6
(7.5–10.0)
7.5*
(6.3–10.5)
Brachial–ulnar PWV (m/s)
6.4 ns
(4.4–9.8)
6.4
(5.4–9.5)
6.4
(5.3–10.1)
6.8
(4.6–8.5)
7.2
(4.4–8.8)
6.1
(5.0–8.4)
ET-1 (pmol/l)
4.69**
(3.0–5.4)
6.15
(3.5–7.89)
7.55
(4.66–9.42)
7.96
(6.36–8.87)
8.15
(5.32–9.63)
4.53
(3.68–9.25)
Values are median IQF 25–75% (1st–3rd).
*Compared to baseline M0, M1, M3, M6 M9 after one, three, six and nine months of therapy (
p
<
0.05 Mann-Whitney rank sum test).
**Comparison between healthy volunteers (control) and baseline (M0) of patients before treatment. (
p
<
0.05 Mann-Whitney rank sum test).
