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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 1, January/February 2017

44

AFRICA

30–40 minutes after EPACS (zero time sample: blood taken

immediately on admission) and peaked at six hours, thereafter

decreasing up to 72 hours. The concentration of CK was

significantly higher than the controls from two hours up to 48

hours in the EPACS patients (Fig. 4).

At four hours after EPACS, the serum adropin concentration

measurement had a sensitivity of 91.7% and specificity of 50% at

a confidence interval of 95% when the cut-off value was set at 4.12

ng/ml (Fig. 5). At six hours after EPACS, with the cut-off value set

to 5.37 ng/ml adropin for serum, the sensitivity was 91.7% and the

specificity 64% (Fig. 6). At four hours after EPACS, saliva adropin

exhibited 91.7% sensitivity and 57% specificity at a confidence

interval of 95%, when the cut-off value was 4.12 ng/ml. At six

hours after EPACS, when the cut-off value was 4.12 ng/ml, the

same sensitivity and specificity were found as at four hours for

saliva adropin level. Serum troponin I exhibited 100% sensitivity

and 100% specificity at a confidence interval of 95% when the

cut-off value was 0.141 ng/ml at four hours after EPACS, and when

the cut-off value was 0.226 ng/ml at six hours after EPACS (Fig. 6).

Discussion

Cardiovascular diseases are the leading cause of death in

both developed and developing countries. The World Health

Organisation predicts that by 2020, 37% of all deaths worldwide

will be from CVDs.

22

Health innovations are widely used, but

ACS, a lethal manifestation of CVD, remains the leading cause

of death worldwide.

28

Currently, cardiac biomarkers (especially

cTI and cTnT) are the most important diagnostic laboratory

tests for ACS.

8

Each year worldwide a million patients with

suspected ACS are admitted to emergency, cardiology and

cardiovascular surgery departments but only around 10% of

cases are then confirmed.

9

Therefore, an accurate, precise and

rapid diagnostic test for EPACS is needed to save lives.

In this context, recent animal studies and a human study have

suggested that adropin could be useful for diagnosing EPACS

in addition to other cardiac biomarkers, but these studies were

controversial.

19,20

Therefore the ability of adropin to identify

cardiac injury earlier than is possible with current biomarkers

should be re-investigated and the controversy resolved. In the

present study, therefore, we measured serum cardiac marker

enzymes and timed serum and saliva adropin concentrations in

EPACS patients and in age- and gender-matched controls.

Troponin I, CK, CK-MB and adropin concentrations

gradually increased in the EPACS group from up to six hours to

levels higher than in the controls (

p

<

0.05), and troponin I and

CK-MB continued to increase for up to 12 hours after EPACS.

After 12 hours, CK and adropin levels started to decrease for up

to 72 hours. These findings confirmed the value of the classical

parameters of troponin I, CK and CK-MB for diagnosing

EPACS in clinical practice.

Saliva adropin concentrations changed in parallel with

serum adropin concentrations in ACS. The saliva adropin

concentration was generally higher than the serum adropin,

possibly because the salivary glands produce adropin (see

below). Since adropin is expressed in many tissues, including

the heart, all contributing to the serum pool, we had assumed

that serum adropin concentration increased after EPACS, as do

troponin I or CK-MB, which are released from the myocardium,

mainly during EPACS and necrosis following heart injury.

9

Our clinical results agree with our previous animal

experiments, showing that adropin concentration gradually rose

above control levels in EPACS patients. This is in contrast to Yu

et al

., who found that serum adropin levels were significantly

lower in EPACS patients than in SAP patients or controls.

20

Yu

et

Hours

0 2 4 6 12 24 48 72

Concentration (IU/l)

800

700

600

500

400

300

200

100

0

Control

c

c

b

c c

c

c a

CK

CK-MB

c

c c

c

b

Fig. 4.

Differences in serum CK and CK-MB concentrations

between EPACS and control subjects.

a

p

<

0.05 and

b,c

p

<

0.01 compared with control.

1 – Specificity

0

0,2

0,4

0,6

0,8

1,0

Sensitivity

1,0

0,8

0,6

0,4

0,2

0

Serum adropin

Saliva adropin

Serum troponin I

Reference

Fig. 5.

Sensitivity and specificity of serum and saliva adropin

and serum troponin I for detecting EPACS at four

hours. The area under the ROC curve, adropin sensi-

tivity of 91.7% and specificity of 67%, were identified

when the cut-off was set at 5.37 ng/ml adropin.

1 – Specificity

0

0,2

0,4

0,6

0,8

1,0

Sensitivity

1,0

0,8

0,6

0,4

0,2

0

Serum adropin

Saliva adropin

Serum troponin I

Reference

Fig. 6.

Sensitivity and specificity of serum and saliva adropin

and serum troponin I for detecting EPACS at six hours.

The area under the ROC curve, adropin sensitivity of

91.7% and specificity of 50%, were identified when the

cut-off was set at 4.43 ng/ml adropin.