Enzymodiagnostics of myocardial infarction

Pathogenesis and differential diagnosis

Enzyme diagnostics is based on resorption-necrotic syndrome. When a vessel supplying the heart muscle is occluded, ischemia and subsequent destruction of cardiomyocytes occur. As a result, cell membranes lose their integrity, and enzymes flood into the blood, causing hyperenzymemia.

This laboratory tool is critically important when a patient presents with shortness of breath and a clinical picture suspicious for acute coronary pathology. Enzyme analysis helps perform differential diagnosis between true myocardial infarction and other life-threatening conditions, such as acute heart failure, unstable angina, or pulmonary embolism (PE).

Reference values and calculation algorithm

To confirm the diagnosis, it is necessary to compare the patient's indicators with normal (reference) values. Traditionally, enzyme activity is expressed in international units per liter (IU/L).

Normal values (upper limit):

• CK (Creatine kinase): less than 190 IU/L.
• AST (Aspartate aminotransferase): less than 47 IU/L.
• LDH (Lactate dehydrogenase): less than 250 IU/L.

Evaluation algorithm:

1. Record the patient's laboratory enzyme activity indicators.
2. Calculate the fold increase using the formula: `Patient value / Normal value`.
3. If the obtained figures for CK and AST significantly exceed the norm, the diagnosis of myocardial infarction is confirmed.

Hourly dynamics of enzyme activity

Each marker has its own kinetics, which allows tracking the stages of pathological development. Dynamics are typically divided into three key periods after occlusion:

1. Early period (12–24 hours):

• By 12 hours, levels already exceed the norm: CK reaches 380 IU/L, AST — 75 IU/L, and LDH — 500 IU/L.
• By 24 hours, the maximum peak value is observed for CK (570 IU/L). AST rises to 200 IU/L, and LDH to 1000 IU/L.

2. Intermediate period (48–72 hours):

• At the 48-hour mark, CK begins to decline (380 IU/L). At the same time, AST and LDH reach their absolute peaks: 330 IU/L and 2000 IU/L, respectively.
• By 72 hours, the activity of all enzymes begins to decline smoothly (CK — 285, AST — 190, LDH — 1750 IU/L).

3. Late period (96–120 hours):

• By 96 hours, CK approaches the upper limit of normal (200 IU/L), AST drops to 140 IU/L, and LDH decreases to 1500 IU/L.
• By 120 hours, CK completely returns to normal (190 IU/L), and AST is 70 IU/L. However, LDH remains colossally high (1250 IU/L), significantly exceeding the 250 IU/L threshold.

Interpretation of the enzymatic profile

Based on the kinetics, the classic enzymatic profile of myocardial infarction is constructed:

• Creatine kinase (CK): Characterized as a marker of early damage. Activity rises very rapidly (within 3–6 hours), peaks faster than all others by 24 hours, after which it drops relatively steeply and normalizes.
• Aspartate aminotransferase (AST): A marker of intermediate response speed. Begins to rise in 4–6 hours. Increases slower than CK, and its peak activity occurs at 48 hours, followed by a gradual decline.
• Lactate dehydrogenase (LDH): A marker for late detection and prolonged monitoring. Rises later than all others (in 24–48 hours) and increases more slowly. The peak in some cases coincides with AST (around 48 hours), but its main feature is that it remains elevated longer than all other markers.

Determining the age of infarction

A proper combination of tests for CK, AST, and LDH gives the clinician the ability to accurately determine the age of the ischemic event.

A high concentration of CK clearly indicates a "fresh" myocardial infarction that occurred within the last 1–2 days. Conversely, if the analysis reveals an isolated increase in LDH against normal CK values, this strongly indicates a past myocardial infarction that occurred several days ago, since the early fraction of enzymes has already been eliminated from the bloodstream.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Plotting graphs of the dynamics of CK, AST, and LDH activity changes.
• Abscissa and ordinate axes: calculating the fold change relative to time after occlusion.
• Mechanism of development of resorption-necrotic syndrome.
• Differential diagnosis of chest pain (pulmonary embolism, unstable angina).
• Tissue specificity of enzymes.

Other topics in the "Enzymology" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.