Three items of myocardial damage

How to determine myocardial damage? In fact, there are strict regulations in medicine. Of course, when our body shows symptoms of myocardial damage, we go to the hospital for examination. Only by judging by the three values ​​of myocardial damage can the doctor tell the patient whether myocardial damage has occurred. In fact, there are some differences between the early markers and definite markers of myocardial injury. Let me introduce them to you below!

Early markers

Refers to markers whose blood levels increase within 6 hours after myocardial injury. Currently known early markers for diagnosing acute coronary syndrome (ACS) mostly appear in the early stages of the pathological process (before myocardial necrosis). The use of early markers can help with early diagnosis and, in turn, early treatment.

C-reactive protein (CRP) CRP increases abnormally in the early stage of myocardial operation and has a short window period. It has good clinical value in the early stage of myocardial injury and prognosis estimation. With the application of high-sensitive CRP (hs-CRP) detection method, its clinical application value has received increasing attention in recent years.

Myoglobin (Mb) Although Mb has low myocardial specificity, it can be rapidly released from the necrotic myocardium after myocardial infarction and has a high sensitivity. Mb has a short blood half-life, so it helps to observe whether reinfarction occurs during the course of AMI and whether the infarction expands. Mb is also a sensitive and accurate indicator for evaluating reperfusion during thrombolytic therapy of AMI.

Identify markers

A biochemical marker that appears in the blood 6 to 9 hours after the onset of myocardial injury and persists for several days, and has a high sensitivity and specificity for myocardial injury.

There are many methods for analyzing and measuring creatine kinase isoenzyme (CK-MB). The commonly used method to measure its activity (u/L) is immunosuppression analysis. The CK-MB mass (CK-MBmass) analysis method is to measure its protein concentration (μg/L), avoiding interference (such as giant CK, etc.) that may be encountered in activity determination. It has high sensitivity (minimum detection limit <1μg) and accuracy, short measurement time (the fastest takes only 7 minutes), is suitable for automatic analysis, and has been widely recognized.

Cardiac troponin (cTn) cTn has two isoforms: cTnI and cTnT. Because of its high sensitivity, strong specificity, and long duration after onset, cTn is currently a better definite marker for diagnosing myocardial injury.

cTn detection: cTn abnormalities can be detected in peripheral blood 6 to 8 hours after myocardial injury, and the increase can last for 7 to 10 days (cTnI) or 10 to 14 days (cTnT). The half-life of cTn in the blood is about several hours. cTn can be quantitatively detected using a highly sensitive labeled immunoassay, or rapidly quantitatively or qualitatively using solid phase immunochromatography. There are many reagents and methods for detecting cTnI. Some scholars have suggested that the use of serum specimens may be more appropriate than plasma specimens〔1〕. Hemolysis or fibrinogen, and even rheumatoid factor can sometimes affect certain cTnI determination methods. The stability of cTnI in the specimen should be considered, and attention should be paid to the specimen storage time and temperature. When using cTnI, different cTnI detection methods have different critical values. In addition, blood samples should be collected at least 6 to 9 hours after myocardial injury, which should be given full attention by clinicians. The current detection technology is highly sensitive and specific, and can even detect myocardial tissue necrosis <1.0g. Once cardiac troponin (cTn) is detected, it indicates that the patient has myocardial damage with clinical consequences.

Use of cTn in clinical diagnosis〔2〕cTn is mainly used for the clinical diagnosis, risk estimation and prognosis judgment of myocardial ischemic injury such as ACS (including latent angina and unstable angina as well as acute myocardial infarction). In addition, it can also be used to determine the effect of clinical thrombolytic therapy after MI, estimate the area of ​​myocardial ischemic injury, clinically diagnose myocarditis, myocardial trauma (cardiac surgery), perioperative cardiac complications, severe sepsis or left heart failure caused by sepsis, congestive heart failure, and observe the clinical efficacy of certain therapeutic drugs.