There are 6 possible reasons for elevated myocardial enzymes, in addition to myocardial infarction

Clinically, how to quickly determine whether the patient has a myocardial infarction based on the report, and when does it need to be reviewed again? All rely on the following "vomiting blood sorting"!

1. 3 enzymes and 2 proteins

The main markers of myocardial injury are myocardial enzymes and myocardial proteins. Its central muscle enzymes include serum aspartate aminotransferase, serum lactate dehydrogenase and its isoenzymes, serum creatine kinase and its isoenzymes; cardiomyocardial proteins include troponin, myoglobin and the like.

1. Aspartic acid aminotransferase (AST)

AST is also known as aspartate aminotransferase (GOT). AST is elevated 6 to 12 hours after the onset of acute myocardial infarction (AMI), peaks at 24 to 48 hours, lasts for 5 days or 1 week, and then decreases.

Due to its widespread presence, it is not tissue-specific. Sensitivity is not high, so elevated AST alone cannot diagnose myocardial injury.

2. Serum lactate dehydrogenase (LDH) and its isoenzymes

Lactate dehydrogenase and its isoenzyme LDH1 began to rise 8 to 12 hours after the onset of AMI, peaked at 48 to 72 hours, and returned to normal in 7 to 12 days.

Continuous determination of lactate dehydrogenase has certain reference value for patients with acute myocardial infarction who are late in seeking medical treatment and have returned to normal creatine kinase.

3. Serum creatine kinase (CK) and its isoenzymes

CK is an important energy regulatory enzyme in the heart muscle. CK has three isoenzymes, CK-BB (distributed in the brain), CK-MB (distributed in the myocardium), and CK-MM (distributed in skeletal muscle). The specificity and sensitivity of CK-MB are higher than CK, so CK-MB and CK are often measured at the same time.

CK-MB rises 3-8 hours after the onset of AMI, peaks at 24 hours, and returns to normal in 2-3 days.

CK and CK-MB have the following significance:

AMI is diagnosed earlier, estimated infarction range size or re-infarction.

CK-MB has a high sensitivity and specificity for AMI and is the best serum enzyme indicator for the diagnosis of AMI. Whether the peak time is advanced or not is helpful in judging whether the thrombolysis is successful.

Disadvantages: Compared with the specificity of myocardial troponin, it is difficult to distinguish from skeletal muscle disease and injury, and it is insensitive to minor injuries to myocardium.

4. Cardiac troponin (cTn)

cTn is composed of three subunits (cTnT, cTnI, cTnC) with different structure and function, cTnT and cTnI are specific to cardiomyocytes, and cTnC is not specific to myocardial tissue.

Therefore, cTnT and cTnI are currently clinically used as the biomarkers of choice for monitoring myocardial injury.

cTnT begins to rise 3 to 6 hours after the onset of AMI, peaks in 10 to 24 hours, and returns to normal in 10 to 15 days; cTnI begins to rise 3 to 6 hours after the onset of AMI, peaks at 14 to 20 hours, and returns to normal in 5 to 7 days.

cTn can not only be used for the diagnosis of acute myocardial infarction, but also for the judgment of reperfusion after thrombolysis, detection of minor injuries, determination of severity, and guidance of correct treatment.

5. Myoglobin (Mb)

Serum Mb is one of the earliest markers of AMI after the onset of AMI. Mb begins to rise at 1-4 hours of onset of AMI, peaks at 6-7 hours, and returns to normal at 24 hours. Mb elimination is very quick, which is a good indicator of re-infarction, but the specificity is poor.

Second, is elevated myocardial enzymes a myocardial infarction?

Is elevated myocardial enzymes a myocardial infarction? Of course not! Myocardial enzymes are not only present in cardiomyocytes, but also widely present in other tissues and organs, so the significance of their elevation lacks specificity, and elevated cardiac enzymes are seen in the following conditions in addition to AMI:

1. Acute heart failure

Acute heart failure also presents with elevated myocardial enzymes. Myocardial troponin is a specific marker of myocardial injury, and elevated troponin in patients with acute heart failure often indicates a poor prognosis.

2. Myocarditis

Elevated myocardial enzymes are also important markers of the diagnosis of myocarditis. However, due to the relatively slow onset of myocarditis, the time for troponin testing is relatively delayed, and most patients have fallen below the test range during testing.

3. Stress cardiomyopathy

Stress cardiomyopathy is a syndrome of acute reversible heart failure in which transient left ventricular dysfunction occurs under severe emotional, somatic stress, or disease-induced causes.

Uncoordinated range of ventricular wall movements and elevated levels of cTn are important clues to the diagnosis of stress cardiomyopathy, which usually presents with only a mild elevation. However, previous studies have also shown that elevated cTn is not associated with its prognosis.

4. Hypothyroidism

Hypothyroidism causes an increase in skeletal muscle volume, slowing muscle contraction and relaxation, and edema and hypertrophy of muscles leading to the spillage of muscle enzymes present in skeletal muscle from within cells.

Secondly, T3 can stimulate the clearance of CK, and when hypothyroidism, T3 decreases, and the decrease in CK clearance leads to an increase in serum CK. At the same time, when thyroid hormone synthesis and secretion decrease, capillary permeability increases, and the deposition of mucin, mucopolysaccharide and hyaluronic acid between myocardial cells leads to hypotonia, pericardial effusion, pseudoe hypertrophy of myocardium, and myocardial fiber interstitial myxedema, degeneration and necrosis, resulting in elevated myocardial enzymes in patients with hypothyroidism.

5. Other situations

Such as unstable angina, hepatitis, hepato parenchymal cell lesions, rhabdomyolysis, polymyositis. And also

Diabetes mellitus with ketoacidosis, lactic acidosis, or hypertonicity may be seen with increased myocardial enzymes. Electrolyte abnormalities (low potassium, low sodium, low calcium, etc.) can also lead to dysfunctional myocyte metabolism, and the release of intracellular muscle enzymes into the blood leads to increased myocardial enzymes.

Therefore, do not diagnose myocardial infarction at the first sight of elevated myocardial enzymes, but make a differential diagnosis based on the patient's symptoms and other laboratory indicators.

bibliography:

LI Hongwei, GAO Hongli. Correct interpretation of common auxiliary examination indicators in cardiology[J]. Journal of Cardiovascular and Vasculopathy, 2020(1):74-76.

Image source: 123RF

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