The Clinical Value of Copeptin in Acute Coronary Syndrome

Nora M Aborehab

doi:10.4172/2155-9880.1000278

Abstract

(1) The introduction of a novel immunoassay measuring copeptin, the c-terminal part of the vasopressin prohormone provided a unique window in common medical disorder. We examined the ability of copeptin in combination with cardiac troponin-I (cTn-I) in diagnosis of AMI, the differentiation between AMI and UA and finally evaluate the ability of copeptin in enhancing sensitivity of cTn-I at early hours of admission in emergency department. (2) This study was carried on 50 subjects; they were divided into 33 patients with AMI and 17 patients with UA. Concentrations of copeptin, cTn-I and CK-MB were determined in their sera. (3) In AMI group, the mean serum level of copeptin was highly significant in three hours than admission time and six hours. The mean serum level of cTn-I was highly significant in six hours than the admission time and three hours. The sensitivity and specificity of copeptin and cTn-I combination were 100% and 100% at the admission time versus 72.7% and 82.4% with cTn-I alone also versus 97% and 94.1% with combination of cTn-I and CK-MB. The AUC of the combination of copeptin and cTn-I was 1 which was significantly higher than the AUC of cTn-I alone 0.81 and the AUC of combination of cTn-I and CK-MB 0.92 (4) Copeptin as a single marker has diagnostic value being superior to cTn-I within the first three hours after acute chest pain. Dual marker strategy combining cTn-I and copeptin show incremental value in the early rule out of AMI.

Highlights

Acute coronary syndrome (ACS) encompasses a broad and heterogeneous population ranging from a patient with atypical chest discomfort, nonspecific electrocardiographic (ECG) changes, and normal cardiac biomarkers to the patient with a large ST-segment elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) [1].Atherosclerosis is the underlying reason for most causes of coronary artery disease, peripheral arterial disease and many cases of stroke
Regarding cardiac troponin-I (cTn-I), it was found from Table 8 and Figure 11 that cTn-I value 1.017 can be used as a cut-off point at which 90.9% of the AMI patients can be diagnosed correctly but 35.3% of normal persons are false positive
The elevation of copeptin in the AMI group during the first three hours may be due to two hypothesis; first the stress hypothesis where copeptin/Arginine vasopressin (AVP) is a substantial part of the endocrine stress response resulting in a synergistic release of ACTH and cortisol

Summary

Introduction

Acute coronary syndrome (ACS) encompasses a broad and heterogeneous population ranging from a patient with atypical chest discomfort, nonspecific electrocardiographic (ECG) changes, and normal cardiac biomarkers to the patient with a large ST-segment elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) [1].Atherosclerosis is the underlying reason for most causes of coronary artery disease, peripheral arterial disease and many cases of stroke. Acute coronary syndrome (ACS) encompasses a broad and heterogeneous population ranging from a patient with atypical chest discomfort, nonspecific electrocardiographic (ECG) changes, and normal cardiac biomarkers to the patient with a large ST-segment elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) [1]. Myocardial infarction; known as heart attack, is defined in pathology as the death of cardiac muscle due to prolonged severe ischemia. The criteria meets the diagnosis when there is rise or fall in cTn-I with at least one value above the 99th percentile upper reference limit with symptoms of ischemia, ECG changes, Angiology [3]. Myocardial infarction can be recognized by clinical features, including ECG findings, elevated values of biochemical markers of myocardial necrosis and by imaging or may be defined by pathology [3]

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Conclusion