Page 14

Cover Story Cardiac Biomarkers - An Overview concentrations than the 99th percentile value used for MI diagnosis may identify patients who have not had an MI but still have a risk of having an adverse cardiac event.

with myocardial infarction. Increase may not be seen if patients present 24 hours after development of symptoms. The reporting units for hsTnT should be ng/L.

Troponin I is released into the blood within 4 hours after the onset of symptoms of myocardial ischemia; peaks at 14-24 hours and remains elevated for 3-5 days post-infarction. Therefore, CTI is very useful as a marker at any time interval after the heart attack. It is not increased in muscle injury; whereas CK2 may be elevated in some muscle injury. Cardiac isoform of CTnT and CTnI are mainly (95%) located in myofibrils and the remaining 5% is cytoplasmic. The initial increase is due to liberation of the cytoplasmic fraction and sustained elevation is due to the release from myofibrils.

CREATINE KINASE (CK) Normal serum value for CK is 15–100 U/L for males and 10–80 U/L for females. CK value in serum is increased in myocardial infarction. The time course is shown in Table 3. The CK level starts to rise within 3-6 hours of infarction. Therefore, CK estimation is very useful to detect early cases, where ECG changes may be ambiguous. A second peak may indicate another ischemic episode.The area under the peak and slope of initial rise are proportional to the size of infarct. Iso-enzymes of CK CK is a dimer; the subunits are called B for brain and M formuscle. Therefore, three iso-enzymes are seen in circulation. Normally CK2 (heart iso-enzyme) is only 5% of the total activity. Even doubling of the value of CK2 (MB) iso-enzyme may not be detected, if total value of CK alone is estimated. Hence the estimation of MB isoenzyme is the best diagnostic marker in myocardial infarction. CK and Muscle Diseases The level of CK in serum is very much elevated in musculardy strophies (500 -1500 IU/L). CK level is highly elevated in crush injury, fracture and acute cerebrovascular accidents. Therefore, estimation of total CK is employed in muscular dystrophies and MB isoenzyme is estimated in myocardial infarction. Brain Natriuretic Peptide (BNP)

Serum level of Troponin T (TnT) increases within 6 hours of myocardial infarction, peaks at 72 hours and then remains elevated up to 10-14 days. Elevated cTn levels indicate cardiac injury, including acute coronary syndrome (ACS), stroke, pulmonary embolism, sepsis, acute perimyocarditis, acute heart failure and tachycardia. Therefore more precise tests are needed. To satisfy this necessity, High sensitive TnT (hsTnT) has been developed. It enables determination of very low cTn concentrations. The higher sensitivity of this assay has allowed for improved identification of patients with AMI presenting in the first 3 hours following symptom onset. Even small increases are associated with a higher risk of death and other adverse outcomes. Two measurements of hsTnT are required for the assessment of patients with chest pain; the first measurement should be at presentation and the second sample should be measured 3 hours after. However, if the second sample does not show an incremental rise yet and clinical suspicion remains, then a further sample should be taken 12 hours after presentation. A rise of 20-100% is equivocal and needs further evaluation. Greater than 100% rise is consistent




The natriuretic peptide family consists of three peptides: atrialnatriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The clinical significance of CNP is not clear. ANP is produced primarily in the cardiac atria. BNP is present in human brain, but more in the cardiac ventricles. Human pro– BNP contains 108 amino acids. It is cleaved by enzymes within cardiacmyocytes into the active C-terminalBNP (32 amino acids) and an inactive peptide (proBNP 1–76). Both are seen in circulation. These natriuretic peptides defend against excess saltand water retention. BNP and NT-proBNP are released by the cardiac muscle in response to various stimuli such as increased cardiac wall tension from pressure and volume overload in the heart. Patients with congestive heart failure have high plasma concentrations of ANP and BNP. The concentrations are correlated with the extent of ventricular dysfunction. High concentrations of BNP predict poor long-term survival. In breathlessness, BNP test helps in the differentiation of the cause as a heart failure or an obstructive lung disease. Patients with COPD and worsening of their cor pulmonale with signs of RV volume overload (including edema and ascites) had increased BNP

Techagappe 15th edition (April - June 2018) E-book  

Agappe Diagnostics Limited is the first Indian IVD company publishing an International Diagnostic News Journal “Techagappe” for the public t...

Techagappe 15th edition (April - June 2018) E-book  

Agappe Diagnostics Limited is the first Indian IVD company publishing an International Diagnostic News Journal “Techagappe” for the public t...