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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 3, May/June 2017
AFRICA
183
testing. Complete blood counts (CBC), including haemoglobin,
haematocrit and WBC count were analysed using an automated
CBC device (Abbott Cell Dyn; Abbott Laboratories, Effingham,
Illinois, USA). Biochemical parameters were measured using
an Olympus AU 600 auto-analyzer (Olympus Optical Co. Ltd,
Schimatsu-Mishima, Japan). All study parameters were reviewed
and approved by the local ethics committee.
Statistical analysis
Statistical analysis was performed using the SPSS (version 20.0,
SPSS Inc, Chicago, Illinois) software package. Continuous
variables are expressed as mean
±
standard deviation (mean
±
SD)
and categorical variables as percentage (%). The Kolmogorov–
Smirnov test was used to evaluate the distribution of variables.
The Student’s
t
-test was used to evaluate continuous variables
showing normal distribution and the Mann–Whitney
U
-test
to evaluate variables that did not show normal distribution. A
p
-value
<
0.05 was considered statistically significant
Results
The study population consisted of 1 368 consecutive patients
undergoing coronary angiography. Out of the total population,
86 patients with MB were included in the study group. The
control group consisted of 88 age-matched subjects with normal
coronary angiograms, selected consecutively during the same
study period as the study group. The same exclusion criteria were
applied to the study and control groups.
The distribution of cardiovascular risk factors, demographic
characteristics, and laboratory parameters in the two groups are
shown in Table 1. The mean age of the MB group was 56
±
9
years and control group was 54
±
7 years (
p
=
0.468).
There was no statistically significant difference between the
two groups with regard to known CAD risk factors, such as
diabetes mellitus and smoking history, except hypertension was
more prevalent in the MB group than in the control group (25
vs 36%,
p
=
0.034; Table 1). The ejection fraction was similar
between the two groups (62.4
±
3.1 vs 60.2
±
4.2%,
p
=
0.471;
Table 1). The PDW (17.3
±
0.4 vs 16.1
±
0.5%,
p
=
0.003), NLR
(3.2
±
1.3 vs 2.2
±
0.9%,
p
=
0.034), and RDW (14.3
±
1.3 vs 13.1
±
1.1%,
p
=
0.032) were significantly increased in the MB group
relative to the control group (Table 2).
Discussion
In this study we examined the relationship betweenMB and PDW
and other haematological parameters. MB was independently
associated with increased values of PDW, NLR and RDW.
MB is a congenital variant of the coronary artery in which a
portion of the epicardial coronary artery takes an intramuscular
course.
12
This arrangement of a ‘tunnelled’ segment of the artery
under the ‘bridge’ of overlying myocardium frequently results
in vessel compression during systole. While this condition is
frequently asymptomatic, in many cases it may be responsible
for adverse complications, including coronary atherosclerosis,
angina, myocardial ischaemia,
13
acute coronary syndromes,
14-16
left ventricular dysfunction and stunning,
17
arrhythmias,
18
and
even sudden cardiac death.
19
Early pathological analysis of myocardial bridging recognised
‘sparing’ of the bridged segments from atherosclerotic lesions.
20
The intima of the tunnelled segment is significantly thinner
than the proximal segment, and includes a predominance of
the ‘contractile’ subtype of smooth muscle cells, thought to
be negatively associated with progression of atherosclerotic
lesions.
21
In addition, known as vasoactive agents, endothelial
nitric oxide synthase, endothelin-1 and angiotensin-converting
enzyme levels are decreased in the bridged coronary wall.
22
These agents have been implicated in the proliferation of
smooth muscle cells, resulting in increased size of atherosclerotic
lesions. Systolic kinking of the bridged segments and endothelial
dysfunction may also predispose to coronary vasospasm and
thrombus formation.
23
Conversely, the proximal segment of the bridge appears to
develop atherosclerosis at an increased rate, approximately 90%.
24
Endothelial cell morphology at the entrance to the tunnelled
segment reveals a ‘flat, polygonal and polymorphic’ structure,
indicative of a low-shear stress state, while the endothelial cells
within the tunnel maintain a helical orientation, a sign of laminar
flow and high shear.
24
This suggests a haemodynamic basis for
the increased plaque formation proximal to the tunnel, through
impairment of endothelial cell function and morphology. Also,
expression of the vasoactive agents, endothelial nitric oxide
synthase, endothelin-1 and angiotensin-converting enzyme are
all increased in the proximal segment.
22
Table 1. Distribution of baseline characteristic of all patients
Variables
Normal coronary
artery
(
n
=
88)
Myocardial
bridging
(
n
=
86)
p
-value
Age (years)
54
±
7
56
±
9
0.468
Male gender,
n
(%)
58 (66)
62 (72)
0.342
Family history,
n
(%)
28 (32)
24 (28)
0.580
Hyperlipidaemia,
n
(%)
19 (22)
22 (25)
0.385
Smoking,
n
(%)
23 (26)
21 (24)
0.486
Diabetes mellitus,
n
(%)
16 (18)
19 (22)
0.385
Hypertension,
n
(%)
22 (25)
31 (36)
0.034
SBP (mmHg)
121
±
11
125
±
8
0,548
DBP (mmHg)
78
±
9
81
±
6
0.783
Heart rate (bpm)
74
±
15
78
±
9
0.673
Ejection fraction (%)
62.4
±
3.1
60.2
±
4.2
0.471
Values are mean (
±
SD), SBP: systolic blood pressure, DBP: diastolic
blood pressure.
Table 2. Distribution of the haematological
parameters of all cases
Variables
Normal coro-
nary artery
(
n
=
88)
Myocardial
bridging
(
n
=
86)
p
-value
White blood cells (10
3
/ µl)
7.9
±
2.1
8.1
±
2.3 0.278
Mean corpuscular volume (fl)
88.9
±
8.3 86.9
±
7.8 0.878
Platelets (
×
1 000/mm
3
)
266
±
38
272
±
41 0.647
Haemoglobin (g/dl)
13.8
±
1.9 14.1
±
1.3 0.387
RDW (%)
13.1
±
1.1 14.3
±
1.3 0.032
Mean platelet volume (fl)
8.8
±
0.9
8.9
±
1.1 0.093
Platelet distribution width (%) 16.1
±
0.9 17.3
±
1.1 0.003
NLR
2.2
±
0.9
3.2
±
1.1 0.034
RDW: red blood cell distribution width, NLR: neutrophil-to-lympho-
cyte ratio.