Diagnostic potential<unk>  is a sensitive biomarker for myocardial infarction and can be detected in the blood within one to three hours of the pain. The diagnostic potential of the biomarker<unk>  for<unk>  injury was discovered in 1988 by Professor Jan Glatz (Maastricht, Netherlands).<unk>  is 20 times more specific to cardiac muscle than myoglobin, it is found at 10-fold lower levels in skeletal muscle than<unk>  muscle and the amounts in the kidney, liver and small intestine are even lower again.<unk>  is recommended to be measured with troponin to identify myocardial infarction and acute coronary syndrome in patients presenting with chest pain.<unk>  measured with troponin shows increased sensitivity of 20.6% over troponin at 3–6 hours following chest pain onset. This sensitivity may be explained by the high concentration of<unk>  in myocardium compared to other tissues, the stability and solubility of<unk> , its low molecular weight; 15kDa compared to 18, 80 and 37kDa for MYO, CK-MB and cTnT respectively, its rapid release into plasma after myocardial injury – 60 minutes after an ischemic episode, and its relative tissue specificity. Similarly this study showed that measuring<unk>  in combination with troponin increased the diagnostic accuracy and with a negative predictive value of 98% could be used to identify those not suffering from MI at the early time point of 3–6 hours post chest pain onset. The effectiveness of using the combination of<unk>  with troponin to diagnose MI within 6 hours is well reported. Prognostic potential In addition to its diagnostic potential,<unk>  also has prognostic value. Alongside D-dimer, NT-proBNP and peak troponin T, it was the only cardiac biomarker that proved to be a statistically significant predictor of death or MI at one year. This prognostic information was independent of troponin T, ECG and clinical examination. The risk associated with raised<unk>  is dependent upon its concentration. Patients who were TnI negative but<unk>  positive had 17% increased risk of all cause mortality within one year compared to those patients who were TnI positive but<unk>  negative. Currently these TnI positive patients are prioritised for angioplasty, and the TnI negative patients are considered to be of a lower priority, yet the addition of the<unk>  test helps identify patients who are currently slipping through the net and allows physicians to more appropriately manage this hidden high risk group. If both biomarkers were negative, there is 0% mortality at 6 months, in the authors own words this “represents a particularly worthwhile clinical outcome, especially because it was observed in patients admitted into hospital for suspected ACS.”<unk>  indicates risk across the ACS spectrum including UA, NSTEMI or STEMI where low<unk>  concentrations confer low risk whereas high<unk>  concentrations indicate patients who are at a much higher risk of future events.<unk>  in other diseases<unk>  has been proven to significantly predict 30-day mortality in acute pulmonary embolism.<unk>  is more effective than Troponin T in risk stratifying Chronic<unk>  Failure patients.<unk>  is beginning to create interest with researchers who have found emerging evidence that indicates a role in differentiating between different neurodegenerative diseases.<unk>  Point of care testing To obtain diagnostic and prognostic information a precise and fully quantitative measurement of<unk>  is required. Commercial tests include a Cardiac Array on Evidence MultiStat; and an automated biochemistry assay
Heart-type fatty acid binding protein
LDL receptor
Lipoprotein lipase
Low-density lipoprotein receptor gene family
VLDL receptor
Growth hormone secretagogue receptor
Apolipoprotein
Retinoblastoma protein