Bio-Markers of Acute Myocardial Infarction

Bio-Markers of Acute Myocardial Infarction

Acute myocardial infarction (AMI) is the most common cause of death in the world. Early detection of acute myocardial infarction (AMI) is crucial for deciding the course of treatment to preserve and prevent further damage to the myocardial tissue.The ideal bio marker to rule in and rule out AMI rapidly and reliably is still lacking.Many tissue peptides and proteins have been discovered in recent years, due to advances in molecular biology and biochemistry.  Therefore, we need to see whether these molecules that are synthesized and released from the heart tissue (synthesized and released from myocytes) have a role in the diagnosis of AMI. The main objective in the search for new markers is to make comprehensive risk assessments of patients with chest pain at the earliest time and eliminate any undesirable consequences.

Candidate cardiac proteins with potential in future diagnosis of  AMI- 

 hFABP-FABPs are released from the damaged cells into the blood very quickly, and their half-life is 20 minutes after release from kidneys into the circulation.The increase starts just 3 hours after the onset of chest pain. It returns to normal after 12–24 hours and is detected in lesser amounts than myoglobin, but it is more useful in diagnosing AMI. Metabolism is primarily controlled by the kidneys. Therefore, an increase in blood hFABP levels, as in myoglobin, should be combined with other suspected criteria in favor of MI.Glycogen phosphorylase isoenzyme BB(GPBB) – It is released from damaged  myocardial cells in the early  period due to myocardial oxygen deficiency.It rises  in the first 1–4 hours of AMI, peaks at 6–10 hours, and  returns to reference values within 1–2 days. Ischemia-modified albumin-IMA  rise can  be detected by this test 3 hours after the appearance of  ACS symptoms (sensitivity 70%, specificity 80%, positive predictive value 96%).However,  the detection of high IMA levels in patients with cancer, infection, brain ischemia, liver disease, and end-stage renal disease limits the specificity of this test in the diagnosis of  AMI. S100A- It  is an  intracellular  calcium-binding  protein dimer in vertebrates.S100A serum levels increase in trauma and acute ischemic stroke, and are highly sensitive in showing myocardial injury.Choline-Concentrations of  WBCho and PlCho increase during the early period of  AMI, due to coronary plaque destabilization and stimulation  of PLD by macrophages in tissue ischemia. Therefore, it has  been suggested that cardiac ischemia can be detected early if choline levels of patients with ischemic symptoms are observed. lrisin- In  the case of  AMI, irisin decreases, unlike other known cardiac markers. Probably, it would be appropriate to diagnose  AMI in future by using ECG+ CK and CK-MB+ TnI+ irisin, due to the advantage of this feature of irisin.copeptin-  Another  novel peptide,  may be used as a diagnostic marker in combination with other biomarkers in patients with suspected AMI diagnosis. Copeptin alone cannot be a single diagnostic marker in patients with suspected AMI diagnosis.Adropin- molecules have been reported to increase after  AMI in 1–24 hours. Therefore, this is a new parameter that will probably contribute to the sensitivity of TnI  in the diagnosis of AMI.

Markers of myocyte rupture-The CD40 and CD40 ligand (CD40L) system is expressed on a variety of cell types. Studies suggest that elevated serum levels of soluble CD40L (sCD40L) identify patients with ACS at higher risk of recurrent MI and death independent of other prog-nostic biomarkers including cTnI and CRP,and the subgroup of patients who will benefit from antiplatelet treatment can be identified.

Markers of plaque destabilisation- Myeloperoxidase (MPO) is a component of granules within the neutrophils. It plays a crucial role in inflammation and oxidative stress in the cellular level. Studies have shown that MPO is infe-rior to current biomarkers for diagnostic purposes, but elevated levels independently predict future risk of coronary artery disease in both patients with ACS and healthy individuals.MMPs, in particular MMP-9, are important in the collagen breakdown and structural changes associated with ventricular remodelling after AMI and a distal biomarker for inflammation.

Inflammatory biomarkers-Serum IL-6 was shown to be useful for predicting mortality in patients with ACS and identifying individuals who could benefit from targeted interventional or intensive therapy.TNF-α is a cardio-inhibitory cytokine, detected in several tissues including endothelial cells, smooth muscle cells and macrophages that reduces cardiac contractility either directly or via induction of NOS. It was reported that inflammatory cytokines, including TNF-α and hs-CRP, could predict the 6-month survival of patients with ACS.Procalcitonin concentration increases in patients with AMI. Other studies also have found that PCT have prognostic value for predicting mortality or other ischaemic events.Several  studies have reported that upregulation of CRP is an independent prognostic marker of recurrent non-fatal MI or cardiac death. It also reflects the extent of myocardial  injury in STEMIs.

Neuroendocrine biomarkers-Serum levels of cardiac  natriuretic peptides, especially  BNP and NT-proBNP, are upregulated following ACS. Elevated BNP levels in patients with AMI were also found to be associated with myocardial infarct size.Although BNP/NT-proBNP levels are increased  in patients with ACS, they cannot be used as diagnostic markers since they are also upregulated in other conditions with similar symptoms such as heart failure and pulmonary embolus. Elevated adrenomedullin levels are indicative of cardiac  remodelling and may improve risk stratification in heart failure and MI.

During the last several years, there has been a  increasing interest in circulating microRNAs(miRNAs) as potential novel biomarkers for AMI. miRNA is a type of single-stranded, noncoding small ribonucleic acid (about 22nucleotides in length) located within introns of protein-coding genes that functions in suppressing protein synthesis via gene silencing.Recent animal and clinical studies have demonstrated that miRNAs increase in the plasma shortly after the onset of a coronary event. Among  these miRNAs,  four  cardiac-enriched  miRNAs (miR-208, miR-499,  miR-1 and miR-133)  are consistently found to be increased in the plasma of patients with  AMI. A recent explosion of clinical data has provided evidence that circulating miRNAs have utility not only in diagnosis but also in predicting survival outcome and atherosclerotic burden. Certain miRNA isoforms occur exclusively in the circulation after an AMI and appear to display faster release kinetics than seen for troponins detected with high-sensitivity assays. Furthermore, testing for circulating miRNA seems to match the benefits of high sensitivity troponin testing in terms of clinical sensitivity and specificity. In some instances, miRNA testing improves the diagnostic potential when such testing is used togethervwith cardiac biomarkers or as an independent test. Moreover, some groups have identified unique signature patterns of circulating miRNAs that accurately distinguish between nonSTEMI and STEMI patients—a diagnosis that has important implications for early management in the acute-care setting.

Others markers PAPP-A is elevated 2–30 hours after the onset of chest pain.  CRP is  useful  for monitoring  inflammatory process,  coronary artery pathologies,  and the course of coronary artery  disease. Sometimes hs-CRP levels in healthy people are higher than in those patients with high revascularization and the risk of myocardial incidence.TNF, IL6, IL18, CD40 ligand, MPO, MMP9, cell-adhesion molecules, oxidized LDL, glutathione, homocysteine, fibrinogen, and D-dimer procalcitonin could be valuable in the diagnosis and prognosis of  AMI. It has also been emphasized that lipid biomarkers, LpA,  ApoA, ApoB, particle density, and particle size may have roles in the diagnosis of  AMI. In addition, these molecules may be descriptive  concerning the severity of coronary artery disease and may show increased risk of future MI.Suppression of tumourigenicity 2 (ST2)  is a biomarker of cardiomyocyte stress and fibrosis, which has  been shown to be induced in conditions of MI and acute heart failure which causes myocardial overload.Studies have suggested that circulating concentration of Growth differentiation factor-15 (GDF-15) is elevated in patients with AMI and can independently predict mortality or a composite of death  and non-fatal AMI.

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