ARTICLE
Auteur(s) : P
Kozielec1, L Kotkowiak1, J
Późniak1, A Salacka1, I
Hornowska1, J Brodowski2, P
Michón1
1Pomeranian Medical University, Department of Family
Medicine, Szczecin, Poland
2Pomeranian Medical University, Laboratory of Family
Nursing, Szczecin, Poland
Magnesium is one of the most significant elements necessary for the
proper function of the human body. Like potassium it is an
intracellular cation. Magnesium takes part in the majority of
metabolic and energetic processes as an activator and co-factor of
more than 300 enzymes. Magnesium also influences the other
electrolyte concentrations acting through the calcium and sodium-
potassium pump.In the human body magnesium is found mainly within
the intracellular space. Only approximately 1% of the general
magnesium pool is found in the extracellular fluids [5]. Ionized
fraction is a biologically active form of magnesium that
constitutes ca 60-80% of the serum magnesium concentration. The
function of the organism is best described by the ionized fraction
that is the active pool of the bioelements [13, 16].Magnesium
deficiency is best documented in severe diseases and acute
life-threatening states in patients treated in gynecology,
cardiosurgery and intensive care. Correction of the magnesium
deficiency is one of the life-saving procedures performed in these
patients [3, 8, 10, 17].Because of the well recognized, significant
role of magnesium in the human body new research on chronic
diseases that afflict modern society is needed. The aim of the
study was to evaluate the ionized fraction of serum magnesium in
patients with circulatory system abnormalities: arterial
hypertension and stable coronary disease.
Material and methods
The study enrolled 437 ambulatory patients referred for routine
check-up in the chosen period of 4 months. Review of the patient’s
history, physical examination and analysis of medical files were
performed in all patients with special regard to the risk of
disease of circulatory system and other coexisting diseases. The
study group enrolled 113 individuals with diagnosed arterial
hypertension, 26 individuals with diagnosed stable coronary artery
disease, and 25 individuals with diagnosed arterial hypertension
and coexisting coronary artery disease.
All patients from the study group had ECG, funduscopy, lipid and
carbohydrate metabolism checked during the few past months. The
patients with diagnosed diabetes mellitus, lipid disturbances,
thyroid gland function disturbances and patients taking magnesium
preparations and individuals on any type of diet were excluded from
the study. Only individuals with BMI ranging from 20 to 30 were
enrolled into the study.
Group A comprised 113 patients with WHO Io or
IIo arterial hypertension without any coexisting
diseases; 68 patients in that group were treated with ACE
inhibitors, 23- with beta-blockers, and 22- with calcium channel
blockers as monotherapy.
Group B comprised of 26 patients with a positive history, ECG
and exercise ECG findings, USG for coronary artery disease, with
Io or IIo degree of chest pain, without any
additional diseases. Patients with cardiac infarction and
circulatory failure were excluded from the examined group. The
following medications were administered in that group: 8 patients
had beta-blockers combined with nitrates, 14 patients had
beta-blockers as monotherapy, and 4 patients had calcium channel
blockers combined with nitrates. In addition, 24 patients in that
group had acetylsalicylic acid and 2 had ticlopidine.
Group C comprised of 25 patients with stable coronary artery
disease (Io and IIo CCS) with coexisting
arterial hypertension (WHO Io and IIo). The
diagnostic criteria for these diseases were the same as applied in
groups A and B. 18 patients received ACE inhibitor agents and
beta-blockers, 7–ACE inhibitor and calcium channel blockers. All
patients were administered acetylsalicylic acid.
Group D comprised of 273 individuals seen around the same time,
most frequently for a routine check-up required for employment
purposes. Arterial hypertension, ischemic disease of the heart,
diabetes mellitus, other endocrinologic diseases and renal failure
were excluded, based on physical examination and medical files in
patients from that group. These individuals did not take any drugs
or other preparations containing magnesium. They were on a standard
diet without any dietary restrictions.
Patients fasted before blood sampling for at least 8 hours.
Blood samples were collected from the ulnar vein using the Vacuum
syringes. The serum concentration of the ionized magnesium (iMg)
was evaluated immediately after centrifugation in order to diminish
the influence of increasing pH on ionized magnesium concentration.
The measurements were performed using AVL 988-4 apparatus equipped
with an ion selective magnesium electrode.
The data obtained underwent statistical analysis using
Statistica PL software. Evaluation of quantitative variables
included analysis of minimum, maximum, arithmetic mean, median and
standard deviation. The distribution of all qualitative parameters
was tested using the Shapiro-Wilk test and homogeneity was tested
using Levene’s test. The Kruskal-Wallis test was used to evaluate
the significance of differences because the distribution was not
normal. The level of significance was p < 0.05.
Results
The results are shown in table 1( Table
1 ). It contains serum ionized magnesium concentrations in
the groups studied and in the control group. The results obtained
indicate moderate, statistically insignificant differences in mean
serum magnesium concentrations in the groups analysed when compared
to the results obtained in controls (Kruskal-Wallis test).
Table 1 Serum ionized magnesium concentration in group
A- patients with arterial hypertension; group B- patients with
stable coronary artery disease; group C- patients with arterial
hypertension and stable coronary artery disease; group D-
controls.
|
Group
|
n
|
X
|
Min-max
|
Me
|
SD
|
p < 0.05
|
|
|
[mmol/L]
|
[mmol/L]
|
|
|
|
|
Study group A
|
113
|
0.631
|
0.48 – 0.8
|
0.62
|
0.073
|
|
|
Study group B
|
26
|
0.640
|
0.52 – 0.77
|
0.66
|
0.06
|
n.s
|
|
Study group C
|
25
|
0.670
|
0.55 – 0.98
|
0.65
|
0.127
|
|
|
Control group D
|
273
|
0.633
|
0.48 – 0.89
|
0.62
|
0.075
|
|
Discussion
In the world literature there are numerous reports on dismagnesemia
in circulatory system diseases [12, 14, 20, 21] Dacey found
decreased concentrations of ionised magnesium in the serum of
individuals with both ventricular and supraventricular arrhythmias
[4]. Sasaki et al. confirmed these findings and emphasised the
presence of increased magnesium concentrations in erythrocytes in
patients with arterial hypertension and normal serum magnesium
levels [18].
Touyz in his report stated that magnesium played an important
role in the pathogenesis of hypertension; however, any information
on application of that element in therapy frequently was confusing
[21].
Jee et al. [9] conducted a meta-analysis of clinical trials on
application of magnesium in treatment of arterial hypertension and
concluded that the influence of magnesium supplementation on
lowering of arterial hypertension was minimal; however, they also
stated the positive correlation between high magnesium intake and
biggest drop in arterial blood pressure.
In our studies we evaluated the concentrations of ionised
magnesium in hypertensive patients. The concentrations of ionised
magnesium in hypertensive patients and in controls did not differ
significantly.
Similar conclusions were found by Kosch et al. They compared
serum magnesium concentrations in 39 patients with arterial
hypertension and 40 with normal blood pressure. They found the
following serum magnesium concentrations in the analysed groups:
0.87 mmol/L and 0.83 mmol/L, respectively [11].
Resnick et al. found statistically a significantly lower level
of serum ionised magnesium in hypertensive patients not treated
pharmacologically compared with healthy individuals. The
differences were more distinct in Caucasians (0.579 hypertensive
versus 0.620 healthy controls). The ionised to non-ionised
magnesium ratio was increased in both studied black patient groups
(with and without arterial hypertension) and in hypertensive
Caucasians. The results cited indicate disturbances in calcium and
magnesium regulation – most likely both the cause and the result of
the disease. It is worth mentioning that the blood pressure values
did not influence the changes in magnesium levels [15].
When analysing the above mentioned data one should underline the
prevalence of sodium-dependent arterial hypertension among black
hypertensive patients. Evaluation of the concentration of ionised
magnesium associated with sodium-dependent arterial hypertension
requires further studies.
Numerous data from the literature indicate the significant role
of hypomagnesemia in the development of coronary artery disease and
the possibility of risk reduction for CAD by magnesium
supplementation [1, 2]. Researchers e.g. Ueshima et al., Guo,
Elming et al. underline in their papers that the concentration of
total and ionised magnesium is lower in patients with acute
ischemia of the heart when compared to concentrations of that
element in healthy individuals [6, 7, 22].
The mean serum ionised magnesium concentration obtained in our
research of patients with coronary artery disease was higher than
in the control group; however, the differences were not
statistically significant.
Confusing data on the benefits from magnesium supplementation in
the treatment of coronary artery disease, underlined also by
Schechter et al. indicate the need for further studies [19].
Conclusion
The highest differences in serum concentrations of ionized
magnesium were found between healthy controls and patients with
arterial hypertension coexisting with coronary artery disease.
However, these differences were not statistically significant.
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