الفهرس 
Epidemiology of CADOnly 14 pages are availabe for public view
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Abstract
oronary artery disease (CAD), and its acute form acute
coronary syndrome (ACS), have been considered as a
major health problem and one of the most common leading
causes of death all over the world. The WHO has estimated that
the global number of deaths from CAD will rise from
7.2 million in 2002 to 11.1 million in 2020. ACS is the
umbrella term of clinical signs and symptoms of myocardial
ischemia including unstable angina (UA), non-ST segment
elevation myocardial infarction (NSTEMI) & ST-segment
elevation myocardial infarction (STEMI).
The extend of the disease burden and the rate of its
increase directed the attention to the imperative need to
investigate any potential serum surrogate marker for
atherosclerosis which holds a high risk for myocardial
infarction. In this regards, visfatin could be a good candidate;
owing to its obvious role in the pathophysiology of different
forms of cardiovascular diseases.
Adipose tissue (AT) is no longer considered an energy
storing depot but a real endocrine organ that synthesizes and
secretes a wide range of diverse bioactive factors, collectively
called adipokines. Visfatin a protein of 491 amino acids with a
molecular mass of 52 kDa, is one of the recent identified
Adipokines.
C
Summary and Conclusion
87
Visfatin is strongly expressed within symptomatic
atherosclerotic carotid plaques and is localized to areas with
lipid loaded macrophages,where it is also implicated in
atherosclerotic plaque instability. Additionally, visfatin is
involved in endothelial dysfunction which causes progression
of atherosclerosis to MI. Visfatin also act as a growth factor for
B-lymphocyte-precursors, produced by different lineages of
immune cells and induces expression of variety of cytokines.
The researchers concluded that visfatin is considered as a proinflammatory
adipocyte, associated with pro-inflammatory state
that contribute to a number of diseases rather than CAD such as
type 2 diabetes mellitus.
In addition to its obvious role in inflammation Visfatin
increased matrix metalloproteinase-9 (MMP-9) known by its
role in matrix degradation. It was also reported that visfatin
could induce angiogenesis in human umbilical vein endothelial
cells (HUVECs), whereas progressive angiogenesis in
atherosclerotic lesions has been considered one of the causes of
plaque expansion and vulnerability.
Nowadays coronary angiography is the most accurate
method for diagnosing the presence and the extent of CAD.
However, this technique is considered an invasive test which
has some major complications. Hence there is an urgent need
for an early, sensitive and non invasive laboratory marker that
can diagnose and predict the degree of disease severity.
Summary and Conclusion
88
The aim of this study was to investigate the association of
serum visfatin levels with the presence and extent of angiographic
lesions in patients with coronary artery disease (CAD) assessed by
coronary angiography. Moreover, our study aimed to assess the
ability of visfatin to differentiate them from patients with (AMI)
that also confirmed by coronary angiography.
This study included thirty (30) patients (27 males: 3
females) that have attended the Cardiology Department at Ain
Shams University Hospitals presenting with chest pain and
were subjected to elective coronary angiography and diagnosed
to have atherosclerotic CAD. Their ages ranged from 40 to 84
years with a mean age of 59.13±10.7 years. Along with another
group included thirty (30) adult patients (28 males: 2 females)
presenting with acute myocardial infarction (AMI) for the first
time and were assessed within 12 hours from the onset of chest
pain, recruited from the coronary care unit (CCU) at Ain Shams
University Hospitals. The diagnosis of AMI was confirmed by
coronary angiography (C.A) in addition to ST segment
elevation on ECG (if present) and the elevation of myocardial
necrotic marker Troponin I and CKMB in serum. Their ages
ranged from 40 to 70 years with a mean age of 54.63±7.64
years, vs (20) apparently healthy, age-and sex-matched subjects
serving as a healthy control group. Their ages ranged from 48 to
65 years with a mean age of 56.1 ±4.84 years.
Summary and Conclusion
89
Accordingly, they were further classified into three
subgroups; patients with one-vessel disease showing a significant
luminal narrowing of 50% or more, patients with two-vessel
disease and patients with three-vessel disease. In addition twenty
(20) age- and sex- matched apparently healthy with a strictly
normal coronary angiogram, served as a healthy control group.
Several risk factors may contribute to the occurrence of
CAD and or AMI. In our studied population the risk factors that
were present included: smoking, dyslipidemia, HTN in addition
to previous PCI, previous CABG or family history of any
ischemic heart disease.
The results of the current study shows that there was no
statistically significant difference between controls and
atherosclerotic patients regarding risk factors including
smoking, dyslipidemia, HTN in addition to previous PCI,
previous CABG or family history of any ischemic heart disease.
Also no statistically significant difference were found
between controls and patients with AMI regarding risk factors
including smoking, HTN in addition to previous PCI, previous
CABG or family history of any ischemic heart disease. A highly
statistically significant difference was found between the control
group and patients with AMI regarding total cholesterol and LDL,
were lowest mean serum total cholesterol and LDL levels
Summary and Conclusion
90
observed among control group while highest mean serum total
cholesterol and LDL levels were observed in patient group.
Comparing atherosclerotic and AMI groups, no
significant difference were found regarding risk factors;
including smoking, dyslipidemia, HTN in addition to previous
PCI, previous CABG, family history of any ischemic heart
disease.
A highly statistically significant increase were found
between controls and atherosclerotic patients, where lowest
median serum visfatin levels were observed among control
group while highest median serum visfatin levels were observed
in patient group reaching up to five folds.
Similar results were found between controls and patients
with AMI, where visfatin was highly statistically significant
increased closer to five folds.
Comparing atherosclerotic and AMI groups, no
significant difference in visfatin levels were found.
In atherosclerotic group,correlation studies found no
association between serum visfatin level and risk factors
including smoking, dyslipidemia, HTN in addition to previous
PCI, previous CABG, family history of any ischemic heart
disease in atherosclerotic group consistent with except for
inverse relation between serum HDL-C and visfatin level. No
Summary and Conclusion
91
association was found between serum visfatin levels and
number of affected vessels.
Also correlation studies found no association between
serum visfatin level and risk factors in AMI group. Also no
association was found between serum visfatin level and cardiac
biomarkers. No association was found between serum visfatin
level and number of affected vessels.
In our study diagnostic performance of visfatin was
evaluated; visfatin was able to discriminate between
atherosclerotic patients and healthy subjects with a diagnostic
sensitivity of 96.69% and diagnostic specificity of 95% at a cutoff
value of 10 ug/L with PPV of 96.7% and NPV of 95%.
Similar, visfatin at a cut-off value of 10 ug/L was able to
discriminate between AMI patients and healthy subjects with a
diagnostic sensitivity of 93.33% and diagnostic specificity of
95% with PPV of 96.6% and NPV of 90.5%.
In conclusion, the serum visfatin level is a strong
independent risk factor for diagnosis of CAD and/or AMI
development. Where, a cut-off of > 10 μg/L can distinguish
between the control group and patients groups with a sensitivity
of 95%, specificity of 95%, PPV of 98.3% and NPP of 86.4%.