INTRODUCTION
The term acute coronary syndrome (ACS) refers to any clinical symptoms
that may result in a diagnosis of acute myocardial ischemia. These
symptoms include unstable angina (UA), non-ST segment elevation
myocardial infarction (NSTEMI), and ST segment elevation myocardial
infarction (STEMI) 1 . An important type of ACS, UA is
often diagnosed in emergency services situations, although diagnoses of
UA often decrease with the emergence of biomarkers susceptible to
myocardial damage, resulting in the patient’s condition being
reclassified as NSTEMI 2. Despite this emerging
clinical finding, when diagnosing and treating UA patients, there are
still practitioners who follow guidelines that were created as a result
of studies carried out in the era of cardiac troponins instead of high
sensitive cardiac troponins (hsTn), which are no longer commonly used.
Current guidelines do not differ so much in terms of the management of
biomarker-positive or negative non-ST segment elevation acute coronary
syndromes (UA and NSTEMI)3,4. Although some existing
studies and the resultant guidelines have demonstrated the positive
effects of early invasive interventions on cardiac endpoints in hsTn
positive NSTEMI patients, these positive effects may be delayed in
patients with UA due to hsTn negativity 5 . Although
assessing hsTn levels is the gold standard in identifying myocardial
damage, it may not be sufficient for early risk evaluation. There have
been many subsequent studies examining the value of hsTns in diagnosing
ACS, and these studies have emphasized that complementary biomarkers are
important 6. One of these biomarkers is copeptin,
which is the C-terminal part of the prohormone for vasopressin
(pro-vasopressin); copeptin becomes prominent in conditions of acute
endogenous stress due to its rapid release pattern 7.
Many studies have investigated the accuracy and sensitivity of copeptin
in diagnosing ACS disorders 8-10. There are many
studies on the joint use of hsTn and copeptin levels for diagnosing ACS;
however, there are insufficient studies assessing copeptin levels among
non-ST segment elevation acute coronary syndrome patients with negative
hsTn levels during admission to the emergency room and during
follow-ups. The aim of our study is to identify serum copeptin levels in
patients with UA and to evaluate the relationship between copeptin
levels and the clinical and angiographic severity of these patients.