Biomarkers of Inflammation and Oxidative stress in the Prediction and Management of Acute Coronary Syndrome

The assessment of patients presenting with chest pain or symptoms indicative of cardiac ischemia remains a diagnostic challenge. Many types of research have focused on the search for ideal biological markers for the rapid detection of cardiac cell injuries. Markers of inflammation and oxidative stress are the way forward. At present, the biomarker most widely used for diagnosing acute coronary syndrome is cardiac troponin though it has some limitations. Apart from cardiac troponin, several other biomarkers, especially inflammation and oxidative stress markers in acute coronary syndrome, have been investigated. However, most of them still require validation in further studies. As markers of inflammation and oxidative stress address a particular aspect of the pathophysiology of acute coronary syndrome, these biomarkers may provide unique information to the managing clinician separate from that of markers of myocyte necrosis. Serum markers of inflammation and oxidative stress appear before cardiac necrosis markers and are valuable targets for early and timely diagnosis of an acute cardiac event. Using these markers in combination with biomarkers of plaque formation, unstable plaque development, plaque rupture, thrombosis, and myocardial necrosis (multimarker approach) could increase their diagnostic and prognostic value.

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Response to commentary on 'zinc supplementation is associated with a reduction in serum markers of inflammation and oxidative stress in adults: A systematic review and meta-analysis of randomized controlled trials'

Cytokine ◽

10.1016/j.cyto.2021.155460 ◽

2021 ◽

Vol 141 ◽

pp. 155460

Author(s):

Razieh Hosseini ◽

Gordon A. Ferns ◽

Amirhossein Sahebkar ◽

Mohammad Ali Mirshekar ◽

Mohammad Jalali

Keyword(s):

Oxidative Stress ◽

Systematic Review ◽

Randomized Controlled Trials ◽

Zinc Supplementation ◽

Meta Analysis ◽

Serum Markers ◽

Controlled Trials ◽

Randomized Controlled ◽

Markers Of Inflammation ◽

And Oxidative Stress

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MS366 CYTOKINE PROFILES AND OXIDATIVE STRESS IN ACUTE CORONARY SYNDROME

Atherosclerosis Supplements ◽

10.1016/s1567-5688(10)70867-9 ◽

2010 ◽

Vol 11 (2) ◽

pp. 184

Author(s):

M. Sahlawi ◽

M.O. Hamza

Keyword(s):

Oxidative Stress ◽

Acute Coronary Syndrome ◽

Coronary Syndrome ◽

Cytokine Profiles ◽

And Oxidative Stress

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Variation of Cardiac Troponin I and T Measured with Sensitive Assays in Emergency Department Patients with Noncardiac Chest Pain

Clinical Chemistry ◽

10.1373/clinchem.2011.179903 ◽

2012 ◽

Vol 58 (8) ◽

pp. 1208-1214 ◽

Cited By ~ 27

Author(s):

Volkher Scharnhorst ◽

Krisztina Krasznai ◽

Marcel van 't Veer ◽

Rolf H Michels

Keyword(s):

Emergency Department ◽

Acute Coronary Syndrome ◽

Chest Pain ◽

Cardiac Troponin ◽

Myocardial Necrosis ◽

High Sensitivity ◽

Noncardiac Chest Pain ◽

Short Term ◽

Coronary Syndrome ◽

Concentration Changes

Abstract BACKGROUND New-generation high-sensitivity assays for cardiac troponin have lower detection limits and less imprecision than earlier assays. Reference 99th-percentile cutoff values for these new assays are also lower, leading to higher frequencies of positive test results. When cardiac troponin concentrations are minimally increased, serial testing allows discrimination of myocardial infarction from other causes of increased cardiac troponin. We assessed various measures of short-term variation, including absolute concentration changes, reference change values (RCVs), and indices of individuality (II) for 2 cardiac troponin assays in emergency department (ED) patients. METHODS We collected blood from patients presenting with cardiac chest pain upon arrival in the ED and 2, 6, and 12 h later. Cardiac troponin was measured with the high-sensitivity cardiac troponin T (hs-cTnT) assay (Roche Diagnostics) and a sensitive cTnI assay (Siemens Diagnostics). Cardiac troponin results from 67 patients without acute coronary syndrome or stable angina were used in calculating absolute changes in cardiac troponin, RCVs, and II. RESULTS The 95th percentiles for absolute change in cardiac troponin were 8.3 ng/L for hs-cTnT and 28 ng/L for cTnI. Within-individual and total CVs were 11% and 14% for hs-cTnT and 18% and 21% for cTnI, respectively. RCVs were 38% (hs-cTnT) and 57% (cTnI). The corresponding log-normal RCVs were +46%/−32% for hs-cTnT and +76%/−43% for cTnI. II values were 0.31 (cTnI) and 0.12 (hs-cTnT). CONCLUSIONS The short-term variations and IIs of cardiac troponin were low in ED patients free of ischemic myocardial necrosis. The detection of cardiac troponin variation exceeding reference thresholds can help to identify ED patients with acute myocardial necrosis whereas variation within these limits renders acute coronary syndrome unlikely.

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