Biomarkers in acute myocardial infarction: current perspectives
Vascular Health and Risk Management
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Biomarkers in acute myocardial infarction:
current perspectives
This article was published in the following Dove Medical Press journal:
Vascular Health and Risk Management
Suleyman Aydin 1
Kader Ugur 2
Suna Aydin 3
İbrahim Sahin 1,4
Meltem Yardim 1
1
Department of Medical Biochemistry
and Clinical Biochemistry (Firat
Hormones Research Group),
Medical School, Firat University,
Elazig 23119, Turkey; 2Department
of Internal Medicine (Endocrinology
and Metabolism Diseases), School
of Medicine, Firat University, Elazig
23119, Turkey; 3Cardiovascular
Surgery Department, Elazig Research
and Education Hospital, Health
Science University, Elazig 23119,
Turkey; 4Department of Medical
Biology, Medical School, Erzincan
Binali Yildirim University, Erzincan
24100, Turkey
Introduction
Correspondence: Suleyman Aydin
Department of Medical Biochemistry
(Firat Hormones Research Group),
School of Medicine, Firat University,
Hospital Street, Elazig 23119, Turkey
Tel +90 533 493 4643
Fax +90 424 237 9138
Email
Acute myocardial infarction (AMI) is one of the major causes of mortality and morbidity worldwide.1 About 10% of patients who are admitted to emergency departments
with chest pain every year are diagnosed with heart attack.2 AMI is a condition that
can be due to ischemic heart disease or coronary artery disease in conjunction, and it
becomes manifest when an atherosclerotic plate ruptures and a developing thrombus
occludes the coronary artery totally or partially, restricting blood access to the heart
(Figure 1).3,4 In this case, the opening of the occluded coronary artery is usually
provided by inserting a stent. However, when stents are insufficient, coronary bypass
is performed by cardiac pulmonary bypass surgery using the left internal mammary
artery or saphenous vein to maintain regular nourishment of the heart.5
AMI has found its place in the concept of acute coronary syndrome (ACS). ACS
includes a group of clinical syndromes ranging from unstable angina pectoris, AMI
with non-S (downward deflection immediately after ventricular contraction)-segment
elevation, and T (recovery of ventricles)-segment elevation to AMI, with ST-segment
1
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http://dx.doi.org/10.2147/VHRM.S166157
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Purpose: Acute myocardial infarction (AMI) is the most common cause of death in the world.
Comprehensive risk assessment of patients presenting with chest pain and eliminating undesirable
results should decrease morbidity and mortality rates, increase the quality of life of patients, and
decrease health expenditure in many countries. In this study, the advantages and disadvantages
of the enzymatic and nonenzymatic biomarkers used in the diagnosis of patients with AMI are
given in historical sequence, and some candidate biomarkers – hFABP, GPBB, S100, PAPPA, RP, TNF, IL6, IL18, CD40 ligand, MPO, MMP9, cell-adhesion molecules, oxidized LDL,
glutathione, homocysteine, fibrinogen, and D-dimer procalcitonin – with a possible role in the
diagnosis of AMI are discussed.
Methods: The present study was carried out using meta-analyses, reviews of clinical trials,
evidence-based medicine, and guidelines indexed in PubMed and Web of Science.
Results: These numerous AMI biomarkers guide clinical applications (diagnostic methods, risk
stratification, and treatment). Today, however, TnI remains the gold standard for the diagnosis
of AMI. Details in the text will be given of many biomarkers for the diagnosis of AMI.
Conclusion: We evaluated the advantages and disadvantages of routine enzymatic and nonenzymatic biomarkers and the literature evidence of other candidate biomarkers in the diagnosis of
AMI, and discuss challenges and constraints that limit translational use from bench to bedside.
Keywords: acute myocardial infarction, cardiac protein, cardiac peptide
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Aydin et al
Left coronary artery
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Circumflex branch
of left coronary artery
Right coronary artery
Anterior interventricular
branch of left coronary artery
Right marginal branch of right
coronary artery
Figure 1 Gross anatomy of heart.
elevation and sudden death.6 The sensitivity and specificity of electrocardiography (ECG) are low in ACS.7 In the
majority of cases with ST-segment elevation in ECG and
typical ischemic chest pain, AMI with a Q wave (downward
deflection immediately preceding ventricular contraction)
develops in most cases and AMI without a Q wave develops
in a few. However, the majority of cases without ST-segment
elevation develop unstable angina pectoris or AMI without
a Q wave, with a few developing AMI with a Q wave. STsegment elevation changes into ST-segment depression when
an oxygen-free environment persists.8
As the sensitivity and specificity of ECG are low in
diagnosing AMI, the criteria for AMI were decided by the
European Society of Cardiology (ESC) and the American
College of Cardiology (ACC).9,10 Accordingly, a patient has
to have at least two of the following: typical symptoms, a
characteristic elevation or decrease pattern in cardiac markers
(eg, CK-MB izoenzymes), preferably serum troponins (cTnI
or cTnT), or a typical ECG trace with Q waves that indicate
a diagnosis of AMI.4,11
Ischemia due to decreased coronary artery flow causes
deterioration of ventricular function and myocardial necrosis.12 Therefore, such enzymes as ALT, AST, LDH, CK, and
troponins have been indicators for years us a diagnosis of
2
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AMI.13,14 Therefore, in our study, cardiac markers (cTnI and
cTnT), CK-MB, and myoglobin, frequently used in diagnosing AMI and determining prognosis, are mentioned in
review, and our intention is to discuss some other important
candidate biomarkers, such as copeptin15 and irisin,16 which
may be relevant in diagnosing AMI and determining prognosis (Figure (...truncated)