{"id":10491,"date":"2013-08-17T12:55:46","date_gmt":"2013-08-17T12:55:46","guid":{"rendered":"http:\/\/cardiophile.org\/?p=8964"},"modified":"2013-08-17T12:55:46","modified_gmt":"2013-08-17T12:55:46","slug":"biomarkers-in-acute-coronary-syndrome-2","status":"publish","type":"post","link":"https:\/\/johnsonfrancis.org\/professional\/biomarkers-in-acute-coronary-syndrome-2\/","title":{"rendered":"Biomarkers in acute coronary syndrome"},"content":{"rendered":"

Biomarkers in acute coronary syndrome<\/span><\/h2>\n

Why do we need biomarkers in acute coronary syndrome (ACS)?<\/strong><\/p>\n

Electrocardiogram (ECG) may not be diagnostic in all cases of myocardial infarction and a normal ECG does not rule out myocardial infarction either. A normal ECG may place a patient in a lower risk category. Even angiography has limitations in the diagnosis of myocardial infarction. It is not uncommon to find a recanalized vessel on coronary angiography after a myocardial infarction. It is for these reasons that we need the support of biomarkers in the diagnosis of myocardial infarction in an acute coronary syndrome. It also helps in risk stratification of acute coronary syndrome and decide on therapeutic options available.<\/p>\n

What are biomarkers of myocardial infarction?<\/strong><\/p>\n

Myocardial necrosis causes disruption of the sarcolemma (muscle cell membrane). It causes the release of intracellular macromolecules into the extracellular space which are later carried into the general circulation. These macromolecules which can be measured by serial blood testing are the biomarkers of myocardial infarction. Pattern and level of rise of these biomarkers correlate with timing and size of the myocardial infarction.<\/p>\n

Historical aspects on biomarkers<\/strong><\/p>\n

Transaminases released from dying myocytes were reported as detectable in blood and aiding diagnosis of myocardial infarction in the 1950s [1]. The initial serum markers to be evaluated were aspartate aminotransferase (AST), lactic dehydrogenase (LDH), total creatine kinase (CK) and \u03b1-Hydroxybutyrate.\u00a0Total CK estimation became available in 1960s, but had poor sensitivity and specificity\u00a0for cardiac muscle necrosis. CK could be released very well from skeletal muscle damage so much so that even a single intramuscular injection given for alleviation of the pain could elevate serum CK levels.<\/p>\n

Reference<\/strong><\/span><\/p>\n

    \n
  1. Karmen A, Wroblewski F, Ladue JS.\u00a0Transaminase activity in human blood. J Clin Invest. 1955 Jan;34(1):126-31.<\/li>\n<\/ol>\n

    Next<\/strong><\/a><\/p>\n","protected":false},"excerpt":{"rendered":"

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