Can myocardial infarction (MI) lead to raised aspartate transaminase (AST) levels?

Can Myocardial Infarction Lead to Raised AST?

Yes, myocardial infarction routinely causes elevated AST levels, with approximately 80-86% of MI patients demonstrating AST elevations above the upper limit of normal. 1, 2

Mechanism and Frequency of AST Elevation in MI

AST elevation in MI occurs due to myocyte necrosis and release of intracellular enzymes into the bloodstream, though AST is no longer recommended for diagnosing MI because it lacks cardiac specificity. 3

• AST elevations occur in 80-86% of acute MI patients, making it a common but non-specific finding 1, 2
• ALT elevations are less frequent, occurring in approximately 47-48% of MI patients 1, 2
• The De-Ritis ratio (AST/ALT) is characteristically elevated in MI, with AST concentrations consistently higher than ALT at all time points 1

Correlation with Infarct Size

The magnitude of AST elevation correlates directly with the extent of myocardial damage:

• Approximately 93% of patients with large infarctions demonstrate AST levels >3× the upper limit of normal 1
• 43% of all MI patients reach AST concentrations >3× ULN at some point during their acute event 1
• Maximum AST levels show strong correlation with CK-MB area under the curve (r=0.727), confirming the relationship between AST elevation and infarct size 2

Current Diagnostic Standards

Cardiac troponin (I or T) has replaced AST as the preferred biomarker for MI diagnosis because of its superior myocardial tissue specificity and sensitivity. 3

The 2012 Third Universal Definition of MI explicitly states that:

• Glutamic-oxaloacetic transaminase (ASAT/AST) should NOT be used to diagnose cardiac damage 3
• Cardiac troponin exceeding the 99th percentile is the diagnostic standard for MI 3
• CK-MB is the best alternative when troponin assays are unavailable, but total CK and transaminases are not recommended 3

Clinical Pitfalls

Elevated AST in the setting of suspected MI requires careful interpretation:

• AST can remain elevated for days after MI, complicating the timing of the event 3
• AST elevation is not specific to cardiac injury—liver disease, skeletal muscle injury, hemolysis, and other conditions can elevate AST 3
• Some hearts contain unexpectedly high baseline ALT activity (mean 21 U/g vs 7.7 U/g in controls), which may reflect increased amino acid metabolism in energy-depleted myocardium 4
• Secondary hepatic congestion from heart failure or cardiogenic shock can further elevate transaminases, confounding interpretation 1

Prognostic Implications

Despite being non-diagnostic, AST elevation carries independent prognostic significance:

• Both AST and ALT elevations independently predict worse mortality and clinical outcomes in STEMI, even after adjusting for CK-MB 2
• AST elevation is associated with increased all-cause mortality (HR 1.12,95% CI 1.05-1.19) and composite endpoints of death, heart failure, shock, or stroke (HR 1.08,95% CI 1.02-1.13) 2
• ALT ≥2× ULN carries an adjusted odds ratio of 2.24 (95% CI 1.33-3.77) for in-hospital mortality in AMI patients 5

Clinical Trial Considerations

Current transaminase exclusion criteria in clinical trials (typically >3× ULN) may inappropriately exclude patients with larger infarcts:

• 93% of patients with large infarctions present AST >3× ULN, meaning these patients—who might benefit most from novel therapies—are systematically excluded from trials 1
• This represents a significant selection bias that may limit the generalizability of trial results to real-world MI populations 1