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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 2, March/April 2017
106
AFRICA
diameter was found to be an important variable predicting the
development of postoperative AF.
The role of Vitamin D deficiency in the onset of AF was
suggested because of several potential mechanisms described
previously.
16
Vitamin D regulates inflammatory responses and
up-regulates the expression of anti-inflammatory cytokines, such
as IL-10, according to
in vitro
experiments.
17
Also, Vitamin D
regulates activity of the renin–angiotensin–aldosterone system
(RAAS). Activated RAAS can lead to oxidative stress and
inflammation, both of which could culminate in AF.
18
It is
assumed that tissue angiotensin II may induce apoptosis of the
cardiomyocytes and contribute to changes in atrial structure.
19
There were conflicting results regarding low 25-(OH) Vitamin
D levels and AF. On one hand, several studies demonstrated a
close association between Vitamin D deficiency and AF, such as
Demir
et al
.,
20
who found a strong relationship between Vitamin
D deficiency and non-valvular AF. Chen and co-workers
found that serum 25-(OH) Vitamin D level correlated with
high-sensitivity C-reactive protein and left atrial diameter, and
was significantly associated with AF in Chinese patients with
non-valvular persistent AF.
21
Hanafy
et al
.
22
revealed the direct
electromechanical effects on the left atrium after Vitamin D
administration, and found that Vitamin D could effectively
prevent or terminate AF.
On the other hand, no association was found between 25-(OH)
Vitamin D levels and ischaemic heart disease, stroke or acute
myocardial infarction, despite previous studies showing Vitamin
D deficiency to be associated with increased incidence of these
conditions.
23-25
Rienstra
et al
.
26
evaluated 2 930 participants of the
Framingham Heart study during a follow-up period of 9.9 years
and found no relationship between Vitamin D status and incident
AF, concluding that Vitamin D deficiency does not promote the
development of AF. Additionally, Qayyum
et al
.
27
showed that
there was no association between Vitamin D deficiency and type
of AF or complications of AF. Another prospective cohort study
based on the Rotterdam study did not support the hypothesis
that Vitamin D level is associated with AF.
28
Our study was the first to evaluate the predictive value of
25-(OH) Vitamin D level in the development of POAF. In recent
studies, there has been a paradox between Vitamin D levels and
AF, and a negative correlation between Vitamin D and left atrial
diameter.
15
In our study, although there was a significant negative
correlation between Vitamin D and left atrial diameter, Vitamin
D level was not an independent predictor for the development
of POAF.
We believe that the paradoxical results between Vitamin D
and AF could be related to the activation of the RAAS caused
by Vitamin D insuffiency, increased levels of reactive oxygen
radicals, and individual differences in receptor activity. Also,
because of the negative correlation between Vitamin D level
and left atial diameter, it could be hypothesised that Vitamin D
insuffiency could lead to atrial dilatation, causing AF. Further
randomised clinical studies are needed in this field.
Our study has some limitations. First, it was a retrospective
study design. Second, AF was diagnosed by ECG monitoring in
a hospital setting without performing a follow up after discharge.
Third, the small sample size of this study was problematic. Fourth,
measurement of Vitamin D levels occurred at a single point in
time. Fifth, we did not determine parathyroid hormone levels.
Conclusion
To the best or our knowledge, this study is the first to evaluate
the relationship between POAF and 25-(OH) Vitamin D levels.
Table 2. Laboratory and echocardiograpic parameters
Laboratory and echocardiographic
parameters
POAF
p
-value
Present
mean
±
SD
(median)
Absent
mean
±
SD
(median)
Haemoglobin (g/dl)
13.5
±
1.7
(13.1)
13.7
±
1.5
(13.7)
0.316
Platelets (10
3
/µl)
218.9
±
59.7
(212)
234.1
±
66.6
(230)
0.68
White blood cells (10
3
cells/µl)
7.8
±
2.3
(7.6)
7.6
±
2.2
(7.5)
0.647
Mean platelet volume (fl)
10.5
±
1.1
(10.5)
10.4
±
0.9
(10.4)
0.303
Neutrophils (10
3
cells/µl)
4.7
±
2.1
(4.6)
4.3
±
1.2
(4.2)
0.384
Lymphocytes (10
3
cells/µl)
1.9
±
0.8
(1.9)
2.3
±
1.5
(1.9)
0.072
Neutrophils:lympocytes
2.9
±
2.0
(2.5)
2.1
±
0.8
(1.9)
0.136
Platelet:large cell ratio
33.6
±
16.2
(29.4)
27.5
±
6.7
(27)
0.006
Sedimentation (mm/h)
27.4
±
23.2
(23.5)
24.9
±
20.4
(19)
0.758
Urea (mg/dl)
46.8
±
22.2
(41)
36.7
±
4.3
(32)
0.012
Creatinine (mg/dl)
(mmol/l)
1.07
±
0.29
(1)
(94.59
±
25.64)
(88.4)
0.94
±
0.24
(0.8)
(83.10
±
21.22)
(70.72)
0.013
Fasting plasma glucose (mg/dl)
(mmol/l)
136.7
±
52.2
(110)
(7.59
±
2.90)
(6.11)
120.3
±
40.3
(106)
(6.68
±
2.24)
(5.88)
0.340
C-reactive protein (mg/dl)
1.6
±
2.5
(0.5)
0.8
±
1.2
(0.3)
0.053
Total cholesterol (mg/dl)
(mmol/l)
179.2
±
45.1
(178)
(4.64
±
1.17)
(4.61)
183.8
±
53.3
(179)
(4.76
±
1.38)
(4.64)
0.680
High-density lipoprotein choles-
terol (mg/dl)
(mmol/l)
39
±
8.3
(37)
(1.01
±
0.21)
(0.96)
39.3
±
11.6
(37)
(1.02
±
0.30)
(0.96)
0.760
Low-density lipoprotein
cholesterol (mg/dl)
(mmol/l)
112.6
±
38.5
(111.5)
(2.92
±
1.00)
(2.89)
114.9
±
46.9
(101)
(2.98
±
1.21)
(2.62)
0.920
Trigylicerides (mg/dl)
(mmol/l)
180.1
±
95.1
(168)
(2.04
±
1.07)
(1.90)
150.1
±
60.9
(140.5)
(1.70
±
0.69)
(1.59)
0.231
25-hydroxy Vitamin D (ng/ml)
19.9
±
6.1
(19.5)
26
±
8.2
(26.4)
<
0.001
Calcium (mg/dl)
9.2
±
0.5
(9.1)
9.4
±
0.4
(9.4)
0.034
Magnesium (mg/dl)
2.1
±
0.3
(2)
2.1
±
0.4
(2.1)
0.086
Albumin (g/dl)
4
±
0.4
(4.1)
4.2
±
0.3
(4.1)
0.163
Potassium (mmol/l)
4.1
±
0.5
(4.1)
4.3
±
0.3
(4.3)
<
0.001
Uric acid (mg/dl)
6.4
±
1.5
(6.19
5.5
±
1.2
(5.4)
0.004
Left atrium (mm)
41.2
±
4.3
(41)
37.8
±
3.9
(38)
<
0.001
Ejection fraction (%)
51.3
±
9.1
(55)
55.2
±
6.7
(55)
0.043
POAF, postoperative atrial fibrillation.