CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 9/10, October/November 2013
362
AFRICA
acute myocardial infarction and hypertension.
19,20
There have
been several hypotheses suggested for slow coronary flow
phenomenon since first described in 1972 by Tambe
et al
.
11
In this theory, endothelial activation and inflammation, which
have been reported to be a major contributing factor to many
cardiovascular events and demonstrated to be associated with
different clinical settings of coronary artery disease, are the most
acceptable hypotheses for SCF.
13,
21-23
The biological oxidative effects of free radicals on cells, DNA,
proteins and lipids are controlled by a spectrum of exogenous
dietary and endogenous antioxidants.
24,25
Oxidative stress occurs
when there is an imbalance between free radical production and
antioxidant capacity. This may be due to increased free radical
generation and/or loss of normal antioxidant defense.
In the vascular wall, decreases in antioxidant defense are
thought to alter several important physiological functions.
Regulation of blood flow, inhibition of platelet aggregation,
inhibition of leukocyte adhesion and control of cellular growth
are influenced by oxidant stress. These phenomena ultimately
modulate vessel diameter, remodelling and lesion formation.
26,27
Within the lipid interior of membranes, lipophilic radicals
are formed that are different from those seen in the intracellular
aqueous milieu. Lipophilic radicals require different types of
antioxidants such as vitamin E,
β
-carotene, co-enzyme Q
10
and
membrane structural organisation (phospholipids: cholesterol,
different types of phospholipids and fatty acids important for
membrane integrity) for their removal.
Vitamin E has a unique biochemical role with both a chain-
breaking property and lipoprotein antioxidant. In fact, vitamin
E is a poor antioxidant outside the membrane bilayer, but very
effective when incorporated into the membrane. Therefore, it can
protect cell membranes from oxidative damage and this explains
why vitamin E is the most important biological antioxidant but
also one of the least important plasma antioxidants.
28
Oxidative stress has been implicated in over a hundred
disorders, including cardiovascular diseases,
1,6,27,29
but there have
been only a few investigations on oxidative stress or antioxidant
status in patients with SCF.
23
Furthermore, to the best of our
knowledge, there is no study about vitamin E levels in patients
with SCF in the literature.
In the present study, we investigated AOA producing hydroxyl
radicals
in vitro
using the Fenton reaction to observe antioxidant
defense potential in patients with SCF, and measured vitamin
E levels as a component of the antioxidant systems. We
observed no difference between the two groups with regard
to plasma antioxidant activity, but there was a significant
difference in vitamin E levels between the two groups (
p
=
0.001). These results suggest that decreased vitamin E levels
as a component of the antioxidant systems can be inadequate
to protect endothelial cells from oxidative damage at the tissue
level, which is less associated with total plasma activity of
hydrophilic compartments.
Concerning the lack of significant difference among smokers
in both groups, we have no explanation other than the potentially
negative influence of smoking on vitamin E levels. Since we did
not evaluate the TIMI frame counts individually, it would have
been interesting to see how smoking and its frequency could
affect coronary flow in smokers, even if they were within the
normal range of TIMI frame counts.
Since we did not include TIMI frame counts individually,
our study was limited in terms of correlative association
between the coronary flow rate and vitamin E levels. This
could be investigated in another study. There may also be other
confounding factors that were not considered in the current study.
However, given the lack of information on the pathophysiology
of slow coronary flow, this can be regarded as an initial study.
The negative influence of smoking on vitamin E levels is
interesting. Smoking, in addition to its many hazardous effects
on the whole body, appears to render the endothelial membrane
weak and exposed to the harmful influences of lipophilic radical
attacks by having a negative effect on vitamin E levels.
Conclusion
Our study has shown that levels of vitamin E, a membrane
protector against oxidative stress, were decreased in patients with
slow coronary flow. There also appeared to be a clear negative
influence of smoking on vitamin E levels. The association
between smoking and vitamin E levels is worth further
investigation in larger samples.
References
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TABLE 3. VITAMIN E LEVELSWITHIN GROUPS
AND BETWEEN GROUPS
Variables
Smokers
Non-smokers
p
-value*
n
Vitamin E (
μ
mol/l)
n
Vitamin E (
μ
mol/l)
NCF group 12
95.4
±
25.4
28 115.5
±
32.4
0.082
SCF group
27
84.4
±
28.6
13
88.2
±
29.2
0.665
p
-value*
0.248
0.015
*Mann-Whitney
U
-test
TABLE 4.ANTIOXIDANTACTIVITY LEVELSWITHIN GROUPS
AND BETWEEN GROUPS
Variables
Smokers
Non-smokers
p-value*
n
Antioxidant activity
(
μ
mol/l)
n
Antioxidant activity
(
μ
mol/l)
NCF group 12
2.4
±
0.5
28
2.7
±
0.7
0.070
SCF group
2.7
±
0.6
2.7
±
0.3
0.938
p
-value* 27
0. 072
13
0.752
*Mann-Whitney
U
-test.
