CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 7, August 2012
396
AFRICA
Effect of perindopril on pulse-wave velocity and
endothelin-1 in black hypertensive patients
ELZBIETA OSUCH, WILLEM J DU PLOOY, SANDRA H DU PLOOY, LINDE H BÖHMER
Abstract
Introduction:
We investigated the effect of perindopril on
pulse-wave velocity (as indicator of arterial elasticity) and
endothelin-1 (ET-1) levels in black hypertensive patients.
Methods:
Forty-four newly diagnosed hypertensive patients
who received 4 mg perindopril daily were monitored for
nine months. Pulse-wave velocity (PWV) was measured non-
invasively along the carotid–femoral arterial segment (high
elastic content) and the brachial–ulnar segment (low elastic
content).
Results:
There was a significant increase in arterial elastic-
ity, as indicated by a slower PWV in the carotid–femoral
segment of the treatment group, from 11.6 to 7.5 m/s after
nine months. The PWV of the treatment group (7.5 m/s) after
nine months was lower than that of the healthy volunteer
group (8.2 m/s) but it was not statistically significant. No
correlation between ET-1 and PWV could be found.
Conclusion:
In addition to its blood pressure-lowering effect,
our study confirmed the improvement in arterial elasticity in
patients on perindopril therapy, without involvement of ET-1.
Keywords:
arterial elasticity, pulse-wave velocity, perindopril,
endothelin-1, hypertension
Submitted 20/1/12, accepted 3/5/12
Cardiovasc J Afr
2012;
23
: 396–399
DOI: 10.5830/CVJA-2012-043
Pulse-wave velocity (PWV) has become the standard for
measuring arterial elasticity or stiffness.
1,2
A higher PWV
indicates decreased elasticity. The elasticity of the larger arteries
ensures a dampening of the pulse wave and it is stored as recoil
energy to ensure continuous blood flow, with better perfusion.
3
PWV was found to be higher in patients with sustained essential
hypertension compared to normotensives subjects.
4
Decreased arterial elasticity and endothelial dysfunction
are associated with end-organ damage and, together with pulse
pressure, are independent predictors of cardiovascular risk
in hypertensive patients.
5-7
Therefore, besides lowering blood
pressure, structural and functional vascular properties have
become important.
1,8
Department of Pharmacology and Therapeutics, School of
Medicine, MEDUNSA Campus, University of Limpopo, South
Africa
ELZBIETA OSUCH, MB ChB, PhD (Pharmacol), MSc (Med)
(Pharmacol), Dip Fam Med
WILLEM J DU PLOOY, PhD, FCP (ACCP), BSc (Hons) (Pharmacol),
Dip Intl Bio-ethics,
Department of Physiology, School of Medicine, MEDUNSA
Campus, University of Limpopo, South Africa
SANDRA H DU PLOOY, MSc
LINDE H BÖHMER, PhD
Only a few studies, however, have reported the effect of
different drug therapies on abnormal arterial elasticity. The
methods differed widely and the patient numbers varied between
10 and 20.
9,10
In the Complior
®
study, 4 mg perindopril daily over
six months showed an improvement in arterial elasticity.
11
In patients with congestive heart failure it has been shown
that captopril decreased endothelin production.
12
It has also been
shown that increased endothelin-1 (ET-1) was associated with
decreased arterial elasticity in hypertensive patients.
13
In this study we investigated the effect of a nine-month
treatment of the angiotensin converting enzyme inhibitor (ACEI)
perindopril on arterial elasticity, brachial pulse pressure and the
role of ET-1 in black hypertensive patients.
Methods
Newly diagnosed hypertensive patients with a diastolic pressure
of
>
85 mmHg and/or a systolic pressure of
>
135 mmHg
were enrolled in the study. Only treatment-naïve patients were
admitted into the trial, after informed consent was obtained.
Patients with secondary hypertension or any concomitant
disease were excluded from the study. Those who needed
any treatment other than 4 mg of perindopril to control their
hypertension were excluded. Patients who were on any chronic
or acute medication were also excluded.
Forty-four patients received 4 mg of perindopril daily for a
period of nine months. Fifty-one healthy volunteers served as a
reference group.
PWV was used as a surrogate indicator of arterial elasticity
and was measured non-invasively using a Powerlab 4 SP system
(AD Instruments Pty, Ltd, Australia) and connected to a desktop
computer. PWV was measured along two segments of the arterial
tree, the carotid–femoral segment (representing an arterial
segment with a high elastic content) and the brachial–ulnar
segment (representing an arterial segment with little elastic
content).
The carotid–femoral PWV was calculated from the time
delay (
∆
t
) between the recorded proximal (carotid) and distal
(femoral) beginning of the upstroke of the wave, and the distance
(
∆
d
) separating the two respective transducers, according to the
equation:
speed (
v
)
=
∆
d
___
∆
t
Peripheral pulses were detected by miniature infrared
plethysmo-Doppler sensors. The same operator placed the
sensors, to limit bias. Each recording lasted for 15 seconds and
the average of five consecutive pulses was used. Baseline values
for volunteers and patients were recorded on three occasions
prior to commencement of the study.
Blood pressure was measured using calibrated non-invasive
blood pressure (NIBP) equipment (Welch Allyn, Model 5200-
103A). Other parameters and measurements included pulse
pressure, body mass index (BMI) and lead II of an ECG.
