High-sensitivity troponin

Troponin is a regulatory protein composed of three subunits, namely troponin C, troponin I and troponin T. High-sensitive troponin I is often used in clinical diagnosis, mainly for the diagnosis of acute myocardial infarction. Some patients with severe skeletal muscle damage may produce false positives, and severe hemolysis will also affect the test results. Let's take a closer look at high-sensitivity troponin I.

Diagnosis of myocardial injury Among the many clinical biochemical indicators for diagnosing acute myocardial infarction (AMI), CK-MB (serum myocardial enzyme) was once considered the "gold standard" for diagnosing AMI and has been widely used for many years. With the in-depth study of cardiac troponin (cTn), the status of CK-MB has been seriously challenged both in terms of myocardial specificity and diagnostic sensitivity. cTn is considered to be the best definite marker at present and is gradually replacing CK-MB as the "gold standard" for the diagnosis of AMI.

Patients with various coronary artery diseases will inevitably suffer from myocardial cell damage. The clinical manifestations of some patients may not fully meet the WHO diagnostic criteria for AMI (unstable angina is one of them), but are accompanied by an increase in certain myocardial injury markers (such as cTnT, etc.), which causes the intracellular components to leak into the peripheral blood circulation. This makes the detection of myocardial cell injury markers possible. The blood concentrations of cTnT and cTnI increase rapidly after AMI (3-6h), which is equivalent to or slightly earlier than CK-MB (3-8h). Their specificity and sensitivity are significantly higher than CK-MB. cTn has a fairly long diagnostic window (cTnI 7~9 days, cTnT longer). cTn is better than CK-MB in diagnosing patients with acute chest pain (regardless of whether they have skeletal muscle damage or not). Studies have shown that there is no significant difference between cTnI and cTnT in the diagnosis of AMI, and both can identify myocardial damage that CK-MB cannot detect. Compared with cTnT, cTnI shows lower initial sensitivity and higher specificity. In terms of the relative value of increase, cTnT is higher than cTnI; in patients with unstable angina, the frequency of cTnT increase is higher than cTnI. In terms of predicting 30-day mortality after AMI, cTnT is better than cTnI.

Whether it is unstable angina or myocardial infarction without Q waves, cTnT in the first 24 hours has the greatest prognostic value. Follow-up of patients with unstable coronary artery disease found that only 1% of patients with normal cTnT and exercise test had death or AMI; if abnormal, death or AMI could reach 50%. Follow-up studies of patients with acute coronary artery disease (including myocardial infarction) found that the mortality rate of patients with cTnT less than 0.1μg/L was only 4%. In comparison, the mortality rate of patients with cTnT greater than 0.1μg/L was 3 times higher, the percentage of shock was 3 times higher, and the percentage of congestive heart failure was also increased by 1 time. Observational studies on cTnI have obtained similar results. Among patients with unstable coronary artery disease, the mortality rate of patients with cTnI greater than 0.1μg/L was more than 3 times higher than that of patients with cTnI less than 0.1μg/L. Therefore, any patient with acute coronary artery disease who is simultaneously tested for elevated cTn should be considered to be at high risk.

Diagnosis of perioperative myocardial infarction The diagnosis of myocardial infarction after coronary artery bypass grafting plays an important role in cardiac surgery. cTn is a sensitive and specific marker of perioperative myocardial infarction, which can identify minor perioperative myocardial injuries that do not meet the conventional perioperative myocardial infarction judgment criteria. Compared with CK activity, cTnT has a higher detection sensitivity in the diagnosis of myocarditis due to its relatively high serum detection value and longer rise time. Serum cTnT can be used as a diagnostic marker for acute myocarditis. Relationship with renal failure Ischemic heart disease is one of the main causes of morbidity and mortality in patients with advanced renal disease, accounting for about 40% of the total mortality rate; about 25% of these ischemic heart diseases develop into AMI. Therefore, in the clinical treatment of patients with advanced renal disease, the diagnosis of cardiovascular complications becomes a crucial issue. There are differences in the detection values ​​of cTnT and cTnI in the serum of patients with advanced renal disease. There are three possible reasons for the increase of cTnT in patients with advanced renal disease: cross-reaction of the detection method; over-expression of cTnT in skeletal muscle; and the presence of minor myocardial damage. The second-generation cTnT analysis method will not produce false positives due to the over-expression of cTnT in the skeletal muscle of patients with advanced renal disease, thereby eliminating the cross-reaction of the analysis method. The results of the study suggest that the increase of cTnT in the serum of patients with advanced renal disease may be due to a certain degree of myocardial damage.