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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 1, January/February 2017
40
AFRICA
Adropin as a potential marker of enzyme-positive acute
coronary syndrome
Suna Aydin, Mehmet Nesimi Eren, Musa Yilmaz, Mehmet Kalayci, Meltem Yardim, Omer Dogan Alatas,
Tuncay Kuloglu, Huseyin Balaban, Tolga Cakmak, Mehmet Ali Kobalt, Ahmet Çelik, Suleyman Aydin
Abstract
Aim:
Enzyme-positive acute coronary syndrome (EPACS) can
cause injury to or death of the heart muscle owing to prolonged
ischaemia. Recent research has indicated that in addition to
liver and brain cells, cardiomyocytes also produce adropin.
We hypothesised that adropin is released into the bloodstream
during myocardial injury caused by acute coronary syndrome
(ACS), so serum and saliva levels rise as the myocytes die.
Therefore, it could be useful to investigate how ACS affects the
timing and significance of adropin release in human subjects.
Methods:
Samples were taken over three days after admis-
sion, from 22 EPACS patients and 24 age- and gender-
matched controls. The three major salivary glands (subman-
dibular, sublingual and parotid) were immunohistochemically
screened for adropin production, and serum and saliva adro-
pin levels were measured by an enzyme-linked immuno-
sorbent assay (ELISA). Salivary gland cells produce and
secrete adropin locally.
Results:
Serum adropin, troponin I, CK and CK-MB concen-
trations in the EPACS group became gradually higher than
those in the control group up to six hours (
p
<
0.05), and
troponin I continued to rise up to 12 hours after EPACS. The
same relative increase in adropin level was observed in the
saliva. Troponin I, CK and CK-MB levels started to decrease
after 12 hours, while saliva and serum adropin levels started
to decrease at six hours after EPACS. In samples taken four
hours after EPACS, when the serum adropin value averaged
4.43 ng/ml, the receiver operating characteristic curve showed
that the serum adropin concentration indicated EPACS with
91.7% sensitivity and 50% specificity, while when the cut-off
adropin value in saliva was 4.12 ng/ml, the saliva adropin
concentration indicated EPACS with 91.7% sensitivity and
57% specificity.
Conclusion:
In addition to cardiac troponin and CK-MB
assays, measurement of adropin level in saliva and serum
samples is a potential marker for diagnosing EPACS.
Keywords:
saliva, serum, adropin, acute coronary syndrome,
enzyme-positive acute coronary syndrome, myocardial infarc-
tion, immunohistochemistry
Submitted 3/7/15, accepted 17/4/16
Published online 19/5/16
Cardiovasc J Afr
2017;
28
: 40–47
www.cvja.co.zaDOI: 10.5830/CVJA-2016-055
Acute coronary syndrome (ACS) [acute myocardial infarction
(AMI), enzyme-positive acute coronary syndrome (EPACS)] is
the dominant cause of death and disability in children and in
young,
1
middle-aged and elderly adults in both developed and
developing countries.
2
Coronary arteriosclerosis is a chronic
disease with stable and unstable periods.
3
During unstable
periods, increased cholesterol deposition and activated local
inflammation in the vascular wall can cause atheromatous
plaque rupture and thrombus formation, resulting in unstable
angina (chest pain) or MI (heart attack).
4,5
EPACS is currently diagnosed, according to criteria
proposed by the American College of Cardiology (ACC) and
European Society of Cardiology (ESC),
6,7
as the presence of
three or more of the following abnormalities: a history of
the presenting illness, prolonged chest pain, ‘silent infarct’,
pathological Q waves in the electrocardiogram (ECG), typical
rise and/or fall of cardiac biomarkers (preferably troponin I)
with at least one value above the 99th percentile of the upper
reference limits.
8
Department of Anatomy – Cardiovascular Surgery, Elazig
Education and Research Hospital, Elazig, Turkey
Suna Aydin, MD, PhD,
cerrah52@hotmail.comDepartment of Cardiovascular Surgery, School of
Medicine, Dicle University, Diyarbakir, Turkey
Mehmet Nesimi Eren, MD
Department of Medical Biochemistry (Firat Hormones Research
Group), School of Medicine, Firat University, Elazig, Turkey
Musa Yilmaz, MD
Meltem Yardim, MD
Suleyman Aydin, PhD
Laboratory of Medical Biochemistry, Elazig Education and
Research Hospital, Elazig, Turkey
Mehmet Kalayci, MD
Department of Emergency, Mugla Sitki Kocman University,
Education and Research Hospital, Mugla 48000, Turkey
Omer Dogan Alatas, MD
Department of Histology and Embryology, School of
Medicine, Firat University, Elazig, Turkey
Tuncay Kuloglu, MD
Department of Internal Medicine, 29 May State Hospital,
Ankara, Turkey
Huseyin Balaban, MD
Department of Cardiology, Ercis State Hospital, Van, Turkey
Tolga Cakmak, MD
Department of Cardiology, School of Medicine, Firat
University, Elazig, Turkey
Mehmet Ali Kobalt, MD
Department of Cardiology, School of Medicine, Mersin
University, Mersin, Turkey
Ahmet Çelik, MD