Can elevated troponin be diagnosed as myocardial infarction?
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Can elevated troponin be diagnosed as myocardial infarction?
Can elevated troponin be diagnosed as myocardial infarction? Be cautious in this codition!
Troponin and creatine kinase isoenzyme (CK-MB) are both commonly used indicators to determine acute myocardial infarction, and both often increase consistently.
However, when the two changes are inconsistent, whether or not to still diagnose myocardial infarction, there are a lot of things worth thinking about and discussing. It is necessary to combine the medical history and other auxiliary examinations to analyze the results comprehensively.
1. Troponin is elevated, CK-MB is not high
1) Acute myocardial infarction, but not in the time window of CK-MB
CK-MB starts to increase within 3 to 8 hours after acute myocardial infarction, and returns to normal within 2 to 3 days. The troponin starts to rise in 2 to 4 hours, the troponin T lasts for 14 days, and the troponin I lasts for 5 to 8 days. High-sensitivity troponin is more sensitive than ordinary troponin, and it starts to increase 1 to 3 hours after the onset.
Therefore, for acute myocardial infarction with a short onset time (such as within 2 hours) or a long onset time (such as 3 days to 2 weeks), it can be manifested as elevated troponin and low CK-MB.
2) Acute myocardial infarction, but insufficient CK-MB sensitivity
The sensitivity of troponin (especially high-sensitivity troponin) is much higher than that of CK-MB, and it can identify a small area of focal myocardial necrosis. High-sensitivity troponin can be detected in half of healthy people. In addition to the diagnosis of myocardial infarction, a certain degree of increase can also be used as a basis for risk stratification of cardiovascular events.
Therefore, if the area of myocardial infarction is small, it can be manifested as increased troponin and low CK-MB, such as partial non-ST-segment elevation myocardial infarction.
3) Non-specific elevation of troponin
Although troponin has good sensitivity, in some cases the specificity is not good, even inferior to CK-MB. Especially when troponin is elevated and CK-MB is not high, a high degree of vigilance should be given to non-specific elevation of troponin.
In 2012, the ACCF of the United States issued the “Expert Consensus on the Explanation of Elevated Troponin Levels in Clinical Practice”, and some countries also issued the “Chinese Expert Consensus on the Clinical Application of High Sensitive Methods to Detect Cardiac Troponin” in 2014, in which how to analyze muscle troponin The reason for the increase in calcineurin is one of the key points of the consensus. Elevated troponin only indicates myocardial necrosis, but there are many reasons for myocardial necrosis.
In addition to myocardial infarction, diseases that can cause elevated troponin, including: chronic renal insufficiency, severe infection, heart failure, pulmonary embolism, chemotherapy-related cardiotoxicity, hypertensive emergencies, shock, aortic stenosis, aortic dissection , Stroke, etc. Among them, the most common influencing factors are kidney failure, severe infections, and heart failure. Please look at the following set of data:
Renal failure: In end-stage renal disease (ESRD), the proportions of troponin T and troponin I are 42% and 15% in patients with non-myocardial infarction, but the proportion of CK-MB is only 4%. Therefore, in patients with renal failure, we can see a large amount of elevated troponin, and most patients with low CK-MB are not acute myocardial infarction. While troponin I and troponin T have similar sensitivity, and troponin I is more specific in renal failure, so troponin I is not high, only troponin T is elevated, regardless of acute cardiac stem.
Severe infections: A comprehensive analysis of related studies published from 1998 to 2008 shows that up to 62% (43-85%) of severely infected patients have no ACS, but have elevated troponin I and T.
Heart failure: Among patients with heart failure, 6.2% of patients have troponin I higher than 1.0 ug/L (patients with abnormal renal function have been excluded). If troponin I is greater than 0.4 ug/L and troponin T is greater than 0.01 ug/L as the standard, up to 75% of patients with heart failure have abnormal troponin.
Although CK-MB can also increase non-specifically in severe infections and heart failure, the increase in troponin is more common due to its high sensitivity. Therefore, when troponin is elevated, CK-MB is not high, and there is a lack of typical chest pain and ECG changes, a high degree of suspicion of non-specific elevation of troponin is required, and the diagnosis of myocardial infarction needs to be very cautious.
2. CK-MB is elevated, troponin is not high
CK-MB is elevated, troponin is not high, and myocardial infarction is basically not considered. It can be seen in the following situations:
1) Skeletal muscle injury
Skeletal muscle damage can lead to a significant increase in CK, while CK-MB is only “proportionally” increased, and does not indicate myocardial infarction. The value of CK-MB at the time of myocardial infarction accounts for about 5% to 10% of CK. If the ratio is less than 5%, the possibility of skeletal muscle damage should be considered.
2) Falsely elevated CK-MB
In clinical practice, occasionally, CK-MB accounts for a high proportion of CK, and even CK-MB is higher than CK. It is common in brain tissue, gastrointestinal and uterine smooth muscle damage, and malignant tumors. This is because when the immunosuppressive method is used to measure CK-MB, it is interfered by elevated CK-BB and giant CK.
1) Elevated troponin but low CK-MB: It may be that myocardial infarction is outside the CK-MB time window, the infarct size is small, or troponin is increased non-specifically.
2) CK-MB is elevated, troponin is not high, it does not indicate myocardial infarction, it can be seen in skeletal muscle damage, malignant tumors, etc.
(source:internet, reference only)
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