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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 5, September/October 2016
296
AFRICA
CAE, 43 (27%) with type 2, 54 (34%) with type 3, and 36 (23%)
with type 4 CAE.
The histopathological characteristics of CAE are similar to
those of CAD, however the specific mechanism of abnormal
luminal dilatation seen in CAE remains to be elucidated.
Negative remodelling is found in stenotic CAD, however
positive remodelling is seen in CAE.
12
In a study by Yolcu
and colleagues, it was shown that serum levels of plasminogen
activator inhibitor-1, which causes an increase in activity of
matrix metalloproteinase, increased in patients with isolated
ectasia, suggesting different pathways other than atherosclerosis
in ectasia formation.
12
Yetkin and colleagues showed that carotid–intima media
thickness was statistically lower in CAE patients with stenotic
CAD than in individuals who had CAD alone, and reported that
ectasia was not an atherosclerotic process limited to the coronary
arteries.
13
In previous studies, aortic aneursym, dilatations in
lower-extremity varicose veins, basillary artery aneurysm and
varicocele were reported to be more frequent in isolated ectasia
patients.
12
These findings propose that positive remodelling in the
vessel wall, which is not common in the atherosclerotic process,
plays a role in the aetiopathogenesis of CAE.
Mg
2
+
, which works as an allosteric modulator of several
proteins, controls nucleotide and protein synthesis, regulates
Na
+
, K
+
, and Ca
2
+
channels, and plays a crucial role in enzymatic
reactions involving kinases, is an abundant intracellular divalent
cation.
14,15
Less than 1% of the total body Mg
2
+
concentration
circulates in the blood, and it is stored primarily in bone and the
intracellular compartments of muscle and soft tissue.
15,16
Mg
2
+
regulates vascular tone, cardiac rhythm and platelet-activated
thrombosis.
17,18
Mg stimulates nitric oxide release, which has a potent
vasodilatory effect, from the endothelium. It is a co-factor for
the delta-6-desaturase enzyme, which plays an important role
in the synthesis of prostoglandin E1 (it has vasodilatory and
antiplatelet effects) from linoleic acid.
19
An increase in extracellular Mg concentration causes
vasodilatation, a reduction in vascular resistance, an increase
in capacitance function in peripheral, coronary and cerebral
arteries, and a decrease in agonist-induced vasoconstriction.
Mg deficiency causes oxidative stress, inflammation, decreased
luminal diameter, medial hypertrophy, vascular remodelling,
it potentiates agonist-evoked vasoconstriction, and increases
vascular tonus.
20
As a result of increased intracellular Mg
2
+
concentration
[(Mg
2
+
)i], vasodilation occurs and agonist-induced vasoconstric-
tion decreases. Reduced (Mg
2
+
)i leads to hypercontractility and it
impairs vasorelaxation.
21
Mg is a unique calcium antagonist, has an effect on most
types of calcium channels in vascular smooth muscle, and
can decrease intracellular calcium levels.
22
Inactivation of
calmodulin-dependent myosin light-chain kinase activity and
decreased contraction are among the major effects of decreased
intracellular calcium levels.
22
Consequently, this causes arterial
relaxation, lower peripheral and cerebral vascular resistance,
it relieves vasospasm, and results in a decline in arterial blood
pressure.
22
As a calcium antagonist, Mg decreases the activity of voltage-
dependent calcium channels, diminishing calcium release from
the sarcoplasmic reticulum.
23
In some
in vivo
and
in vitro
studies,
Mg was shown to have vasodilatory effects on the aorta, and
mesenteric, skeletal muscular, uterine and cerebral arteries.
23
In previous studies, Mg was reported to play a role in
the aetiopathogenesis and management of eclampsia
and hypertension. Eclampsia is characterised by myogenic
vasoconstriction of the cerebral arterioles and arteries,
increased permeability of the blood–brain barrier, and oedema
formation due to acute blood pressure increase.
23
In those
patients, intravenous Mg, due to its calcium antagonist effect on
smooth muscle, caused relaxation and vasodilatation.
23
It also
limits vasogenic oedema in cerebral endothelium by a calcium-
dependent secondary messenger system, leading to decreased
paracellular permeability and stress fibre contraction.
23
Mg is now being used in coronary stents because of its strong
antiproliferative and vasodilatory effects. In a study by Yener
and colleagues, it was shown that Mg supplementation after
coronary artery bypass surgery may delay the onset of atrial
fibrillation.
24
Table 2. Comparisons of clinical parameters and magnessium
Clinical parameters
Isolated CAE (
n
=
62)
CAD (
n
=
73)
CAD
+
CAE (
n
=
95)
NCA (
n
=
57)
p-value
Fasting blood glucose (mg/dl)
(mmol/l)
109
±
28
(6.05
±
1.55)
113
±
25
(6.27
±
1.39)
118
±
39
(6.55
±
2.16)
108
±
25
(5.99
±
1.39)
0.197
Urea (mg/dl)
35
±
10
35
±
10
36
±
10
32
±
10
0.114
Serum creatinine (mg/dl)
(mmol/l)
0.91
±
0.20
(80.44
±
17.68)
0.88
±
0.22
(77.79
±
19.45)
0.92
±
0.31
(81.33
±
27.40)
0.80
±
0.15
(70.72
±
13.26)
0.024
¥
Sodium (mg/dl)
139
±
2.09
139
±
2.67
140
±
2.24
139
±
2.60
0.102
Potassium (mEq/l)
4.32
±
0.43
4.17
±
0.42
4.28
±
0.43
4.12
±
0.57
0.054
Total cholesterol (mg/dl)
(mmol/l)
192
±
43
(4.97
±
1.11)
188
±
35
(4.87
±
0.91)
180
±
39
(4.66
±
1.01)
179
±
36
(4.64
±
0.93)
0.142
Triglycerides (mg/dl)
(mmol/l)
146
±
79
(1.65
±
0.89)
171
±
112
(1.93
±
1.27)
151
±
82
(1.71
±
0.93)
136
±
59
(1.54
±
0.67)
0.133
HDL cholesterol (mg/dl)
(mmol/l)
46
±
12
(1.19
±
0.31)
39
±
8.8
(1.01
±
0.23)
42
±
9.5
(1.09
±
0.25)
44
±
10
(1.14
±
0.26)
0.003
µ√
LDL cholesterol (mg/dl)
(mmol/l)
118
±
36
(3.06
±
0.93)
114
±
27
(2.95
±
0.70)
108
±
34
(2.80
±
0.88)
105
±
29
(2.72
±
0.75)
0.095
TSH (mIU/l)
0.99
±
0.87
1.10
±
1.45
1.12
±
1.21
1.16
±
1.35
0.895
Magnesium (mg/dl)
1.90
±
0.19
1.75
±
0.19
1.83
±
0.20
1.80
±
0.16
0.000
√£&
Calcium (mg/dl)
9.69
±
0.32
9.64
±
0.28
9.67
±
0.33
9.58
±
0.41
0.103
¥
NCA vs CAD
+
CAE (
p
<
0.05);
µ
CAD vs NCA (
p
<
0.05);
√
CAD vs CAE (
p
<
0.05);
£
CAE vs NCA (
p
<
0.05);
&
CAD vs CAD
+
CAE (
p
<
0.05).