Brain natriuretic peptide release in acute myocardial infarction

  • Azra Durak-Nalbantić Clinic for Heart Disease and Rheumatism, Clinical Center, University of Sarajevo
  • Alen Džubur Clinic for Heart Disease and Rheumatism, Clinical Center, University of Sarajevo
  • Mirza Dilić Institute for Vascular Disease, Clinical Center, University of Sarajevo
  • Žana Pozderac Institute for Health Protection of Students, University of Sarajevo
  • Alma Mujanović-Narančić Clinic for Endocrinology, Clinical Center, University of Sarajevo
  • Mehmed Kulić Heart Center, Clinical Center, University of Sarajevo
  • Enisa Hodžić Clinic for Heart Disease and Rheumatism, Clinical Center, University of Sarajevo
  • Nerma Resić Clinic for Heart Disease and Rheumatism, Clinical Center, University of Sarajevo
  • Snežana Brdjanović Clinic for Heart Disease and Rheumatism, Clinical Center, University of Sarajevo
  • Faris Zvizdić Clinic for Heart Disease and Rheumatism, Clinical Center, University of Sarajevo
Keywords: brain natriuretic peptide, acute myocardial infarction, left ventricle systolic dysfunction

Abstract

Brain natriuretic peptide (BNP) is released from ventricular myocites due to their stretching and volume overload. In heart failure there is BNP release. Aim of this study was to observe BNP release in acute myocardial infarction (AMI).

We measured BNP in 75 patients with AMI. Control group (n=61) was similar by age and gender to AMI group.

We found statistically significant elevation of BNP compared to controls (462.875 pg/ml vs 35.356 pg/ml,p< 0.001). Patients with severe systolic dysfunction had the highest BNP levels, while patients with the preserved systolic function had the lowest BNP levels (Group with EF<30% BNP= 1129.036 pg/ml vs Group with EF31-40 % BNP= 690.177 pg/ml vs Group with EF 41-50% BNP= 274.396 pg/ml vs Group with EF>51% BNP= 189.566 pg/ml, p< 0.001). We found statistically significant light positive correlation between BNP and left ventricle end-diastolic diameter (LVDd) (r= 0.246,p<0.05). and real positive correlation between BNP and peak troponin levels (r= 0.441,p < 0.05). BNP levels were higher in anteroseptal allocation of AMI compared to inferior allocation (835.80 pg/ml vs 243.03 pg/ml, p< 0.001) and in patients who were treated with heparin compared to fibrinolitic therapy (507.885 pg/ml vs 354.73 pg/ml, p< 0.05).

BNP is elevated in AMI and is a quantitative biochemical marker related to the extent of infarction and the left ventricle systolic dysfunction. Besides echocardiographic calculation, elevation of BNP could be used for quick and easy determination of the left ventricle systolic dysfunction.

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Brain natriuretic peptide release in acute myocardial infarction
Published
2012-08-20
How to Cite
1.
Durak-NalbantićA, Džubur A, Dilić M, Pozderac Žana, Mujanović-NarančićA, Kulić M, Hodžić E, Resić N, Brdjanović S, Zvizdić F. Brain natriuretic peptide release in acute myocardial infarction. Bosn J of Basic Med Sci [Internet]. 2012Aug.20 [cited 2020Nov.27];12(3):164-8. Available from: https://bjbms.org/ojs/index.php/bjbms/article/view/2470
Section
Biochemistry