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. 2023 Sep 29;13(10):1992. doi: 10.3390/life13101992

Table 1.

Biomarkers used and application in ACS.

Biomarker Mechanism of Action-Release Clinical Application & Abilities
hs-Troponin Regulates cardiac contraction.
Released at myocardium necrosis.
T & I isoforms cardiac specific
Modification above 99th URL diagnostic for MI
hs-cTn has high sensitivity & NPV at cost of specificity.
5x URL increase→high PPV (>90%) for type 1 MI
‘Rule-out’ & ‘rule-in’ MI algorithms
Differentiate NSTEMI & UA
Rises in 3–12 h, peak at 24 h.
Prognosis of all-cause mortality
CK-MB Released at myocardium necrosis.
CK-MB isoenzyme mostly at cardiac muscle (low levels in skeletal muscle)
Diagnosis: Rises after 4–6 h & peaks at 24 h
Normal at 48–72 h→detects reinfarction.
NPV 97% & sensitivity 91% at first 6 h
Prognostic for infarct size, wall motion abnormalities, mortality, HF, possibly LV remodeling, CI-AKI
Cystatin C Protease inhibitor secreted by nucleated cells.
Filtered through glomerulus and catabolized in proximal tubule.
Associated with Egfr
Prognostic/risk stratification for all-cause mortality, HF hospitalization, CVD after ACS
Peaks at 3rd day after ACS (vs. 6th Creatinine)
Prognostic for NRP, MACE & mortality after PCI
H-FABP Released from cytoplasm after cardiac injury and necrosis High sensitivity at decreased cutoffs (4 μg/L)
Early biomarker (<1 h), reinfarction detection
Possible value in early ruling out MI
Endocan Endothelial dysfunction & activation
Inflammation
Risk stratification and Prognosis of MACE, high SYNTAX score
Possibly indicates reperfusion after PCI or CABG
Possibly different levels in STEMI vs. NSTEMI/UA
Galectin Cardiac remodeling and fibrosis (fibroblasts→myofibroblasts & collagen synthesis)
Plaque Destabilization in CVD
Prognosis of MI and HF
Risk stratification (LVEF, MACE, mortality, HF, remodeling)
Interrelated with atherosclerosis & inflammation.
Possible therapeutic target
sST2 Decoy receptor for sST2/IL-33 interaction cardiac fibrosis, hypertrophy and remodeling Prognostic factor ADHF (>35 ng/mL)
Therapeutic guidance in Type 1 & 2 MI (>35 ng/mL likely adverse remodeling & >70 ng/mL aggressive treatment)
Prognostic for ACS (mortality, HF, remodeling)
Prognostic for reperfusion & NRP after PCI
D-dimers Breakdown of fibrin clot by plasmin at the site of coronary artery thrombosis Possibly diagnostic for MI and differentiate from UA (>500 ng/mL)
Prognostic for recurring MI, all-cause mortality, in hospital complications, NRP
CRP Acute-phase inflammation Prognostic factor of future myocardial infarction and stroke, levels > 3 mg/L upon discharge: increased risk of readmission within 1 year for recurrent cardiovascular instability or myocardial infarction
micro-RNA Control of gene expression, oxidative stress, inflammation, apoptosis, fibrosis, and cardiac remodeling processes Predictive factor for cardiovascular mortality and the development of heart failure
GDF-15 Increases in tissue damage and inflammation Risk predictor
Fibrinogen Clot formation, platelet aggregation, fibrinolysis, inflammation Induce coronary artery restenosis, baseline levels: increased risk of cardiovascular events within 2 years

ACS: Acute Coronary Syndrome; ADHF: Acute Decompensated Heart Failure; CABG: Coronary Artery Bypass Grafting; CI-AKI: Contrast Induced Acute Kidney Injury; CK-MB: Creatine Kinase-MB; CVD: Cardiac Vascular Disease; eGFR: estimated Glomerular Filtration Rate; GDF-15: Growth Differentiation Factor-15; HF: Heart failure; hs-cTn: high sensitivity troponin; LV: Left Ventricle; MACE: Major Adverse Cardiac Events; MI: Myocardial Infarction; NSTEMI: non-ST-elevation Myocardial Infarction; NPV: Negative Predictive Value NRP: No Reflow Phenomenon; PCI: Percutaneous Coronary Intervention; PPV: Positive Predictive Value; UA: Unstable Angina; URL: Upper Reference Limit.