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.