Abstract
Introduction: The diagnostic utility of B-type natriuretic peptide (BNP) has prompted interest in its use as an aid in the detection of early heart failure and assessment of diseases. The first objective of this study was measurement of BNP and troponin I (TnI) blood levels in patients with acute myocardial infarction (AMI) and unstable angina. The second objective of this study was to find a correlation between TnI and BNP in blood.Methods: The concentrations of BNP and TnI in 150 blood levels were determined using CMIA (chemiluminescent microparticle immunoassay) Architect and 2000 (Abbott diagnostics). The retrospective study included 100 patients who were hospitalized at the Department of Internal Medicine of the University Clinical Center Sarajevo and 50 healthy control. The reference blood range of BNP is 0-100 pg/mL and TnI is 0.00-0.4 ng/mL.Results: In the patients with AMI the mean value of BNP is 764.48 ± 639.52 pg/mL and TnI is 2.50 ± 2.28ng/mL. The patients with unstable angina have BNP 287.18 ± 593.20 pg/mL and TnI 0.10 ± 0.23 ng/mL. Our studies have shown that the correlation between BNP and TnI was statistically significant for p< 0.05 using Student t test with correlation coefficient r = 0.36. Conclusions: BNP and TnI levels can help to identify the patients with a high risk for cardiovascular diseases.
Highlights
The diagnostic utility of B-type natriuretic peptide (BNP) has prompted interest in its use as an aid in the detection of early heart failure and assessment of diseases
BNP and troponin I (TnI) levels can help to identify the patients with a high risk for cardiovascular diseases
The clinical spectrum of acute coronary syndrome (ACS) consists of ST elevated myocardial infarction (STEMI) and non-ST elevated myocardial infarction (NSTEMI)/or unstable angina (UA), which are classified using electrocardiography (ECG) changes
Summary
The diagnostic utility of B-type natriuretic peptide (BNP) has prompted interest in its use as an aid in the detection of early heart failure and assessment of diseases. BNP was first isolated from porcine brain tissue, but heart has been determined to be the major source It is synthesized and released in the blood in response to volume overload or conditions that cause ventricular stretch, to control fluid and electrolyte homeostasis by interaction with. BNP is realized from cardiac myocytes due to their stretching, volume overload and high filling pressure [3,4,5]. It is a neurohormone produced in the ventricular myocardium in response to dilatation and pressure overload, and its plasma concentration correlates with the magnitude of pressure and/or volume overload. Plasma BNP values increase with increasing age and are higher in women than in men [2]
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