Abstract

Rapid diagnosis and management of AMI have great impact on morbidity and mortality. Diagnosis which is based on elevation of cardiac biomarkers has its limitations. Copeptin is the C-terminal part of the vasopressin prohormone. The pathophysiology mode of release should theoretically add diagnostic information of cardiac cell necrosis. One of the major limitations of cardiac biomarkers is the delayed release in circulation. So looking for a new marker with a short diagnostic time window is needed. Aim is to determine the role of copeptin as an early marker for acute non-ST elevation MI (NSTEMI). This study included 88 patients with chest pain. They were divided into 2 groups. Group (1); included 30 patients with diagnosis of NSTEMI. Diagnosis of AMI was established according to the universal definition of MI. Group (2); included 58 patients with diagnosis of unstable angina (UA). Full medical history, physical examination, 12 lead ECG, random blood glucose level, renal function, total cholesterol, triglyceride, cardiac troponin I and Copeptin were obtained on admission. Follow up cardiac troponin I was done. Inclusion criteria: Defined as chest pain of ⩽6 h duration since onset, suggestive of myocardial ischemia, and lasting >20 min. at rest. Exclusion criteria: Patients with positive First cardiac troponin were rolled out, patients with ST segment elevation were rolled out. Other exclusion criteria: Patients presenting after a cardiac arrest, Trauma or major surgery within the last 4 week; pregnancy; IV drug abuse; age less than 18 years; shock and sepsis. Patients who were included had second troponin I re- done and copeptin analysis done. In group 1 (NSTEMI) 28 patients had ECG changes and only 2 had NSTEMI without ECG changes. In group 2 (UA) 23 patients had ECG changes and 35 patients had normal ECG. Males and females were 49 and 39. Age in G1 and G2 was 60 ± 4 and 53 ± 5. Copeptin analysis was done 6 h after Infarction or chest pain. All the patients with NSTEMI (30) had positive copeptin and positive troponin except one only who had + troponin only and another one who had + copeptin only. Of the 58 patients without MI none had the two tests positive, only one had + troponin and one had + copeptin. Using ROC curve: copeptin had sensitivity 100% and specificity 82.8% with using cut off point 13.2 pmol/l. So copeptin can be used for early detection of myocardial infarction. Copeptin seems to be an ideal confirmatory marker for rapid rule out of AMI. If the two tests (with troponin) are positive, this is evident MI; if the two are negative it rules out MI.

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