CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 9/10, October/November 2013
358
AFRICA
modulating the vasodilator response to tachycardia and exercise.
6
NO formed via eNOS plays a crucial role in the regulation of
coronary blood flow, resulting in reduction of vascular resistance
by vasodilation and in the inhibition of platelet aggregation and
adhesion.
20
It has also been shown that decreased plasma eNOS
levels are an important indicator of endothelial dysfunction.
9,21
There are many studies indicating endothelial function
is impaired in patients with SCF. Sezgin
et al.
found that
endothelial function was impaired in people with SCF, and the
TIMI frame count was correlated with endothelial dysfunction.
14
Pekdemir
et al
. showed that endothelin-1 (ET-1) was higher
and NO concentration was lower in patients with SCF than in a
matched group of control subjects, and it was suggested that this
situation was due to endothelial dysfunction.
22
The plasma levels
of NO were also found to be lower in patients with SCF than in
normal subjects.
23,24
In another study, plasma NO levels were found to be lower
in patients with SCF than in controls, and negatively correlated
with TIMI frame count.
25
Likewise, we found in our study that
plasma levels of eNOS were lower and inversely correlated with
TIMI frame count in SCF patients than in control subjects. These
findings support the notion that endothelial function is impaired
in SCF patients.
Çamsari
et al
. found that baseline and peak exercise ET-1
and NO concentrations were impaired in patients with SCF and
suggested that endothelial dysfunction may play an active role
in the pathophysiology of SCF.
26
In our study, we found that
plasma levels of eNOS involved in the synthesis of NO were
significantly lower in patients with SCF than in control subjects.
In addition, this decline became even more pronounced after
exercise. These findings appear to support the previous studies.
Rate–pressure product (heart rate × systolic blood pressure) is
well correlated with myocardial oxygen consumption. Therefore,
failure of the oxygen supply to the myocardium when demand
is high may result in severe cardiovascular events. In SCF
patients, a negative correlation was previously reported between
rate–-pressure product and post-exercise NT-proBNP levels,
and a positive correlations was reported for post-exercise NO
concentrations and maximal heart rate as well as exercise
duration.
26,27
On the basis of these concepts, the severity of ischaemia
caused by exercise is generally considered to be closely related
to increased ventricular wall stress or damage.
27
In our study,
we found a positive correlation between rate–pressure product
and plasma levels of eNOS after exercise in SCF patients. We
believe that our results are consistent with previous studies,
22,26
in which lower NO levels have been found due to the response
of endothelial dysfunction to increased myocardial oxygen
consumption in patients with SCF.
Some limitations of this study should be considered. The
design of our study was cross-sectional, and the sample size of
the study population may not have been quite adequate.
Conclusion
Our findings indicate that an important pathophysiological
relationship exists between the severity of SCF in which
endothelial dysfunction plays a role in the pathogenesis and
level of circulating plasma levels of eNOS. To the best of our
knowledge, this is the first study on this issue reported in the
literature, and we believe that it will direct future large-scale
studies.
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Fig. 3. Relationship between TIMI frame count and basal
plasma levels of eNOS after exercise.
80.00
60.00
40.00
20.00
0.00
30.00
40.00 50.00 60.00 70.00
TIMI frame count
Plasma levels of eNOS
after exercise (pg/ml)
r
=
–0.58,
p
=
0.005
Fig. 4. Relationship between rate–pressure product and
plasma levels of eNOS.
400.00
375.00
350.00
325.00
300.00
275.00
0.00
20.00 40.00 60.00 80.00
Plasma levels of eNOS (pg/ml)
Rate–pressure product
r
=
0.494,
p
=
0.019
