How to judge the severity of myocardial damage through troponin, myoglobin and creatine kinase?

Author: Jia Mei, Chief Physician, Peking University People's Hospital

Reviewer: Jin Mei, Chief Physician, Beijing Anzhen Hospital, Capital Medical University

The changes caused by inflammation, degeneration, edema, or necrosis of myocardial cells are called myocardial injury.

Mild myocardial cell damage may have no obvious symptoms, but severe cases may show severe chest tightness, chest pain, difficulty breathing, fatigue, nausea, vomiting, and even malignant arrhythmias, pericardial rupture, and sudden death.

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1. What factors can cause myocardial damage?

Severe myocardial ischemia caused by coronary artery disease, such as acute coronary syndrome, coronary heart disease, and acute myocardial infarction, can lead to myocardial damage;

Inflammation such as myocarditis and pericarditis can also cause myocardial damage;

Myocardial stress includes emotional and physical stress. Emotional stress, such as the death of a family member or divorce, can cause a heartbroken feeling, but this is actually myocardial damage. Physical stress, such as a car accident or major surgery, can cause myocardial damage.

Autoimmune diseases affecting the heart, such as heart disease caused by systemic lupus erythematosus, can cause myocardial damage;

Physical or chemical damage, such as knife or gun injuries to the myocardium, and toxic effects of drugs on the heart, such as cancer drugs and blood disease drugs, which are toxic to the heart and cause myocardial damage.

Once myocardial damage occurs, the severity of the damage needs to be determined. The severity of myocardial damage can be evaluated through electrocardiogram and myocardial injury markers.

When myocardial cells are damaged, some proteins or enzymes inside the cells can escape from the damaged myocardial cells and enter the blood. These substances can be detected by blood drawing and can provide clues for the diagnosis of myocardial injury, disease monitoring and risk stratification.

Figure 2 Original copyright image, no permission to reprint

The most commonly used myocardial injury markers now are troponin, myoglobin, and creatine kinase isoenzymes, which are mainly used in the diagnosis of acute coronary syndrome and prognosis assessment. When acute coronary syndrome or acute myocardial infarction is suspected, myocardial injury markers should be checked.

2. What is the significance of troponin in myocardial injury?

Troponins include troponin I, troponin T and troponin C. Among them, troponin I and troponin T are myocardial injury markers with high sensitivity, good specificity and long window period for diagnosing acute myocardial infarction in recent years.

After myocardial cells are damaged, troponin appears early and remains in the blood for a relatively long time. Among the myocardial injury markers, the concentration of troponin secretion is also the highest. At the same time, troponin will gradually decrease with the relief of ischemic symptoms, and the increase will last for up to 7-14 days. It has relatively high sensitivity and specificity, making it the best marker for diagnosing acute myocardial infarction.

3. What is the significance of myoglobin in myocardial injury?

Myoglobin is an oxygen-binding protein that is widely present in skeletal muscle, smooth muscle and myocardium. In the myocardium, it exists in the cytoplasm of myocardial cells. Once myocardial cells are damaged, myoglobin is the first to come out of the myocardial cells and enter the blood. It is the first to increase after an acute myocardial infarction occurs. It has the highest sensitivity and can be used as an exclusion indicator. If chest pain is still negative within 6 hours or 10 hours, acute myocardial infarction can be excluded.

Myocardial infarction patients will have chest pain that will appear in the blood within 1-2 hours, increase within 2-4 hours, generally reach the highest value within 6-9 hours, and return to normal within 24 hours. Therefore, for patients with chest pain who come to the hospital for treatment more than one day later, it is meaningless to test myoglobin, and there is no need to test it.

The negative predictive value of myoglobin can reach 100%. For example, if chest pain persists for 6-10 hours and the myoglobin test is negative, the possibility of acute myocardial infarction can be 100% ruled out.

The disadvantage is that it has poor specificity, because it exists in myocardium, skeletal muscle, and smooth muscle. For example, thoracotomy, excessive physical exercise, skeletal muscle injury, and injections can all cause an increase in specificity. Therefore, if myoglobin is positive in patients with chest pain, other indicators must be combined for diagnosis.

4. What is the significance of creatine kinase in myocardial injury?

Creatine kinase is composed of two different subunits, the M subunit and the B subunit, so it has three isoenzymes, namely CK-MM, CK-MB and CK-BB.

CK-MM mainly exists in skeletal muscle, accounting for 99% and CK-MB for 1%; in myocardium, CK-MM accounts for about 77% and CK-MB accounts for 22%; in brain tissue, almost 100% is CK-BB.

CK-MM is the main component in the serum. If CK-MB is released in large quantities from myocardial cells and its level in the serum increases, it indicates that the myocardium is damaged. It is mainly used for the diagnosis of acute myocardial infarction. In acute myocardial infarction, CK-MB begins to increase in 2-3 hours, reaches its peak in 6-12 hours, and returns to normal in 36-72 hours. Therefore, CK-MB is also a good indicator for diagnosing acute myocardial infarction.

Because it usually takes 3 days for CK-MB to return to normal, troponin usually returns to normal in 7-14 days, and myoglobin returns to normal in 24 hours, if CK-MB rises again after 3 days, it is suspected that another myocardial infarction has occurred, so CK-MB can be used as an indicator of acute myocardial infarction. Of course, some patients with non-acute myocardial infarction will also have a slight increase in CK-MB, such as patients with heart failure, hypertrophic cardiomyopathy, and tumors.

The detection of myocardial injury markers is done by drawing blood. The specific indicators checked depend on the duration of chest pain. If the chest pain is within 6 hours, troponin, creatine kinase isoenzyme and myoglobin should be checked. If the chest pain lasts for more than 24 hours, it is meaningless to check myoglobin because it returns to normal within 24 hours. If the chest pain lasts for 2-3 days, only troponin is needed.

Myocardial injury markers may also be affected by other factors. For example, non-acute myocardial infarction or non-acute coronary syndrome may slightly increase. Myocardial injury markers may also slightly increase in cases of hypertrophic cardiomyopathy, heart failure, pulmonary embolism, atrial fibrillation, and stroke. Some false positives should also be excluded. By drawing blood several times in a row and monitoring the increase or decrease in troponin, differential diagnosis can be made. Combined testing of multiple indicators is not as easy as misdiagnosis or missed diagnosis based on a single blood draw.