“Enzyme Tests in Determination of Myocardial Infarction”

Myocardial infarction (MI), commonly known as a heart attack, represents one of the leading causes of morbidity and mortality worldwide. It occurs when blood supply to the heart muscle is interrupted due to obstruction in coronary arteries, leading to ischemia and irreversible myocardial necrosis. Rapid and accurate diagnosis is essential for timely intervention and reduction of complications. Apart from clinical evaluation and electrocardiography, biochemical markers, particularly enzymes, have been invaluable in diagnosing and monitoring myocardial infarction.

The rationale for enzyme testing lies in the release of intracellular proteins and enzymes into the bloodstream following myocardial necrosis. The pattern of rise, peak, and normalization of these biomarkers provides important diagnostic and prognostic information. Historically, enzymes such as Aspartate Aminotransferase (AST), Lactate Dehydrogenase (LDH), and Creatine Kinase (CK) were used as primary indicators. AST was the earliest enzyme utilized; however, its lack of specificity limited its diagnostic role, since elevations are also seen in hepatic and muscular disorders. LDH offered a broader diagnostic window with its characteristic “LDH flip” (LDH-1 > LDH-2), but again suffered from limited specificity.

Creatine Kinase and particularly its myocardial-specific isoenzyme CK-MB brought greater accuracy to MI diagnosis. CK-MB rises within 4–6 hours, peaks at 18–24 hours, and normalizes in 2–3 days, making it useful not only for initial diagnosis but also for detecting reinfarction when other markers remain elevated. Myoglobin, although the earliest to rise (1–3 hours post-infarction), lacks specificity, but its combination with troponins improves early detection strategies.

The advent of cardiac troponins (cTnI, cTnT) revolutionized myocardial infarction diagnostics. These regulatory proteins are highly specific and sensitive for cardiac muscle injury. Troponins rise within 3–6 hours, peak at 12–24 hours, and remain elevated for up to 14 days, offering an extended diagnostic window. Troponin I is more specific, while Troponin T demonstrates higher sensitivity. Their use not only facilitates early and accurate detection but also provides prognostic value by correlating with infarct size and patient outcomes.

In summary, enzyme tests remain central to the biochemical evaluation of myocardial infarction. While traditional enzymes like AST, LDH, and CK-MB laid the foundation, troponins are now the gold standard for diagnosis. Their integration with clinical findings and ECG ensures a comprehensive and reliable approach to managing patients with suspected acute coronary syndrome.

1. Enzyme Tests in Determination
of Myocardial Infarction
Dr. Monisha Prasad

2. Introduction to Myocardial Infarction (MI)
commonly known as a heart attack, occurs when
blood flow decreases or stops in one of the
coronary arteries of the heart, causing infarction
(tissue death) to the heart muscle
The most common symptom is retrosternal chest
pain or discomfort that classically radiates to the left
shoulder, arm, or jaw.

The pain may occasionally feel like heartburn.This is
the dangerous type of acute coronary syndrome.

3. Introduction to Myocardial Infarction (MI)
Definition: Irreversible necrosis of heart muscle due to ischemia
Leading cause of morbidity and mortality worldwide
Diagnosis requires clinical evaluation, ECG, and biochemical
markers
Enzyme tests → crucial for early and accurate diagnosis

4. Rationale for Enzyme Testing

●Myocardial necrosis releases intracellular enzymes/proteins

●Blood levels rise in proportion to extent of injury

●Helps in:

○Early detection of MI

○Monitoring progression

○Assessing prognosis

○Detecting reinfarction

5. Biomarkers Overview

●Historically used: AST, LDH, CK

●Modern markers: CK-MB, Myoglobin, Troponins (gold
standard)

●Enzymes vary in specificity, sensitivity, and time course

6. Aspartate Aminotransferase (AST/SGOT)

●First enzyme marker used in MI diagnosis

●Rises: 6–12 h after MI

●Peaks: 24–36 h

●Returns to normal: 3–7 days

●Limitations: Not specific (also ↑ in liver, muscle diseases)

7. Lactate Dehydrogenase (LDH)

●Found in heart, liver, kidney, RBCs

●LDH-1 predominant in heart

●MI → “LDH flip” (LDH-1 > LDH-2)

●Rises: 8–12 h

●Peaks: 2–3 days

●Remains elevated: 10–14 days

●Limitation: Lack of specificity

8. LDH Isoenzymes

●5 isoenzymes: LDH-1 to LDH-5

●LDH-1 (heart, RBCs), LDH-2 (reticuloendothelial system)

●Diagnostic feature: LDH-1 > LDH-2 in MI

●Replaced by troponins in modern practice

9. Creatine Kinase (CK)

●Found in skeletal muscle, myocardium, brain

●Total CK not specific (↑ in trauma, exercise)

●MI diagnosis relies on CK-MB isoenzyme

10. CK-MB Isoenzyme


●More specific to myocardium (though ~20% in skeletal muscle)

●Rises: 4–6 h

●Peaks: 18–24 h

●Normalizes: 2–3 days

●Advantage: Detects reinfarction (new MI) when troponins
remain high

●Limitation: False positives in muscle injury

11. Myoglobin

●Oxygen-binding protein in cardiac + skeletal muscle

●Earliest marker: rises within 1–3 h

●Peaks: 6–12 h

●Returns to baseline: 24 h

●Very sensitive but not specific

●Best used with troponins for early detection

12. Cardiac Troponins (cTnI, cTnT)

●Regulatory proteins in cardiac muscle contraction

●Highly specific and sensitive to myocardial injury

●Rise: 3–6 h

●Peak: 12–24 h

●Elevated: 7–14 days

●Troponin I more specific; Troponin T more sensitive

●Gold standard biomarker

13. Advantages of Troponins

●High sensitivity (detects small infarcts)

●High specificity for cardiac tissue

●Wide diagnostic window (up to 2 weeks)

●Correlates with infarct size and prognosis