الفهرس 
Acute Coronary Syndrome
Coronary AtherosclerosisOnly 14 pages are availabe for public view
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Abstract
Acute myocardial infarction (AMI) remains one of the
principal causes of death around the world. Early diagnosis
is of great importance in the ED to ensure early effective
treatment.
The gold standards for the diagnosis of AMI are ECG
and determination of serum cTn concentration, which
complement clinical assessment. Cardiac troponin is
superior to other biomarkers available for AMI diagnosis,
including myoglobin and CK-MB.
However, ECG is of little help in ruling out of AMI in
20-30% of patients with AMI as no significant ECG
changes are detected in those patients despite the presence
of ongoing acute cardiac ischemia.
Moreover, ruling out of AMI is still a demanding
point of interest especially within the early hours of
myocardial injury, in the so-called ‘troponin-blind period’.
This is due to the fact that cTn levels do not increase during
the first few hours of AMI. Therefore, the ruling out of
AMI requires monitoring of patients between 6 to 9 hour
period and serial blood sampling for measurement of cTn
concentration. Thus, many biomarkers are being evaluated, alone or
in combination with cTn for enhancing the early diagnosis
of AMI with higher sensitivity. In this regards, markers
with pathophysiologic background independent of cell
necrosis might improve rapid diagnosis of AMI, including
Copeptin.
Copeptin as a marker of acute stress, is excreted into
circulation independent of necrosis of cardiac cells in cases
of AMI. Also, inadequate filling of the left ventricle caused
by AMI stimulates cardiac baroreceptors or causes direct
damage to baroreceptors which subsequently leads to AVP
and Copeptin secretion from the posterior pituitary gland.
Copeptin rises early at a time when other biomarkers are
still undetectable.
In this regard, our study aimed to examine the role of
serum Copeptin in enhancing the sensitivity of cardiac
troponin during the early hours of admission of ACS
patients in emergency department.
For this purpose, we recruited fifty (50) subjects
including: forty (40) patients who presented to ED in AinShams University Hospital complaining of chest pain and
were highly suspicious to have acute cardiac ischemia, in
addition to ten (10) subjects serving as a healthy controlgroup. Patients were classified into fifteen (15) patients with
UA and twenty five (25) patients with AMI.
All participants were subjected to routine
investigations as (fasting blood glucose, fasting lipid
profile, kidney function tests and liver function tests),
specific investigations as cTnI, Total CK and CK-MB, in
addition to serum Copeptin assay by ELISA technique.
Both serum cTnI and serum Copeptin were measured
twice; at 3 hours and then at 6-9 hours from admission
time.
Results of the current study revealed that median serum
levels of Copeptin in AMI group showed highly significant
increase in the first sample (3hours) than the second sample
(6-9 hours). While the median serum levels of cTnI and
CKMB showed a highly significant increase in the second
sample (6-9hours) than the first sample (3hours).
A remarkable finding was that there was a highly
significant difference in serum level of Copeptin observed
in AMI group when compared to UA in the first sample.
While the median serum levels of cTnI and CKMB showed
a non-significant difference in AMI group when compared
to UA in the first sample. This augments the theory that the
Copeptin rises early at a time when other biomarkers are
still within normal range. Receiver operating characteristic (ROC) curve
analysis was applied to assess the diagnostic performance
of Copeptin for discriminating AMI group from UA group
in the first sample. The best cut-off point was150 pg/mL.
At this cutoff level, the sensitivity was 100%, specificity of
100%, PPV100%, NPV100% and AUC was 1.0. While in
the second sample, the best cutoff level of Copeptin was 40
pg/mL. At this cutoff level, the sensitivity was 96%,
specificity of 100%, PPV 100%, NPV 93.7% and AUC was
0.98.
Another ROC curve analysis was applied to assess the
diagnostic performance of cTnI for discriminating AMI
group from UA group in the first sample. The best cut-off
point was 12.6 pg/mL. At this cutoff level, the sensitivity
was 92%, specificity 46.67%, PPV 74.2%, NPV 77.8% and
the AUC was 0.669. While in the second sample, the best
cutoff level of cTnI was 47.8 pg/mL at which 100% of the
AMI patients can be diagnosed correctly and no false
positive. At this cutoff level the sensitivity was 100%,
specificity 100%, PPV 100%, NPV 100% and the AUC
was 1.0.
In conclusion, the present study indicates that
determination of Copeptin as a single marker in early
diagnosis of AMI has diagnostic value being superior to aconventional cTn-I within the first three hours after acute
chest pain but still single Copeptin determination is unable
to displace or challenge a serial cTn-I measurement to
detect myocardial necrosis within a rule-in approach. The
improvement in the early diagnosis of AMI offered by
Copeptin testing may have the potential to improve
prognosis of cases with AMI, as they would be early
managed. In addition, by showing a role in ruling out AMI,
Copeptin can improve allocation of resources in the ED and
markedly reduce total treatment cost. Copeptin is
considered to be an important biomarker in diagnosing
AMI which should be applicable in the daily work not only
the experimental field.