Three markers of myocardial injury

Many people are familiar with the term myocardial damage, and many people understand what myocardial damage is. But more people actually don’t know how to judge whether they have myocardial damage. In fact, if you want to determine myocardial damage, you still need to go to the hospital for professional examination. Among them, myocardial injury markers will tell us the condition and extent of myocardial damage.

Myocardial injury markers refer to proteins and/or enzymes that are released into the peripheral blood and detected when the myocardium is damaged. The detection of this type of substance can provide clues for the clinical diagnosis, disease monitoring and risk stratification of acute myocardial infarction and other diseases accompanied by myocardial damage. In addition to high sensitivity and specificity, an ideal myocardial injury marker should also have the following characteristics: ① It exists mainly or only in myocardial tissue, has a high content in the myocardium, and can reflect small-scale damage; ② It can detect early myocardial damage with a long window period; ③ It can estimate the size of the infarction and judge the prognosis; ④ It can evaluate the thrombolytic effect.

The main biochemical markers reflecting myocardial ischemic injury include myocardial enzymes and myocardial proteins. The former include serum aspartate aminotransferase, serum lactate dehydrogenase and its isoenzymes, serum creatine kinase and its isoenzymes; the latter include troponin, myoglobin, etc.

1. Serum aspartate aminotransferase

Aspartate aminotransferase (AST), also known as aspartate aminotransferase (GOT), is widely distributed in various tissues of the human body. It is abundant in the liver, skeletal muscle, kidney and myocardium. The AST of red blood cells is about 10 times that of serum, and mild hemolysis will increase the test results.

(1) Reference value: <40U/L (37°C), usually using the enzyme-coupled rate method.

(2) Clinical significance: AST increases 6 to 12 hours after acute myocardial infarction, reaches a peak within 24 to 48 hours, lasts for 5 days or 1 week, and then decreases. Because AST is not tissue-specific, elevated AST alone cannot diagnose myocardial injury.

2. Serum lactate dehydrogenase and its isoenzymes

Lactate dehydrogenase (LD) is a key enzyme that regulates the conversion of pyruvate into lactate during anaerobic glycolysis of glucose. It is widely present in the cytoplasm and mitochondria of tissue cells such as the liver, heart, skeletal muscle, lungs, spleen, brain, red blood cells, and platelets. LD is a tetramer with a molecular weight of 135KD, which is composed of M-type and H-type subunits and constitutes 5 isozymes: H4 (LD1), MH3 (LD2), M2H2 (LD3), M3H (LD4), and M4 (LD5).

(1) Reference values: ① Lactate dehydrogenase: 200-380 U/L when pyruvate is the substrate; 109-245 U/L when lactate is the substrate. ②LD1 was 28.4%±5.3%, LD2 was 41.0%±5.0%, LD3 was 19.0%±4.0%, LD46.6%±3.5%, and LD5 was 4.6%±3.0%. The total activity of lactate dehydrogenase is usually detected by rate method, while its isoenzymes are usually determined by electrophoresis.

(2) Clinical significance: When myocardial damage occurs, the myocardial cell membrane ruptures, and mitochondria and cytoplasmic substances leak into the intercellular fluid and peripheral blood. Lactate dehydrogenase and its isoenzyme LD1 begin to increase 8 to 12 hours after the onset of acute myocardial infarction, reach a peak in 48 to 72 hours, and return to normal in 7 to 12 days. Continuous measurement of lactate dehydrogenase has certain reference value for patients with acute myocardial infarction who seek medical treatment late and whose creatine kinase has returned to normal.