Can Heart Attacks Cause Elevated Liver Enzymes?
Yes, heart attacks (myocardial infarction) commonly cause elevated liver enzymes, particularly AST and ALT, with AST elevations occurring in approximately 85% of STEMI patients and ALT elevations in approximately 48% of patients. 1, 2
Mechanism and Pattern of Elevation
The elevation of liver enzymes following myocardial infarction occurs through multiple mechanisms:
Hepatic congestion from acute heart failure develops when reduced cardiac output and elevated right-sided pressures lead to passive hepatic congestion, causing hepatocyte injury and enzyme release 3, 4
Hypoperfusion injury (ischemic hepatitis) results from decreased hepatic blood flow during cardiogenic shock or severe hemodynamic compromise, leading to centrilobular hepatocyte necrosis 3, 1
AST release from cardiac myocytes contributes significantly, as AST is present in both cardiac muscle and liver tissue, making it less specific for hepatic injury compared to ALT 5, 6, 4
Characteristic Laboratory Pattern
The transaminase pattern in acute MI differs distinctly from primary liver disease:
AST elevates more prominently than ALT, with AST levels correlating strongly with CK-MB area under the curve (r=0.727), while ALT shows weaker correlation (r=0.456) 1
The De-Ritis ratio (AST/ALT) is typically elevated (>1) in cardiac injury, contrasting with the ratio <1 typically seen in non-alcoholic liver disease 7, 1, 2
Peak elevations occur within 24 hours of the acute event, with AST concentrations exceeding 3× upper limit of normal in approximately 43% of STEMI patients 1, 2
ALT elevations are generally milder, with only 8% of STEMI patients showing ALT >3× ULN, reflecting ALT's greater liver specificity 2
Clinical Significance and Prognostic Value
Elevated transaminases in acute MI carry important prognostic implications:
Both AST and ALT elevations independently predict worse outcomes, even after adjusting for CK-MB levels, with hazard ratios of 1.12 (95% CI 1.05-1.19) for AST and 1.15 (95% CI 1.04-1.27) for ALT regarding all-cause mortality 1
Transaminase levels correlate with infarct size and severity, showing significant associations with Killip classification (P<0.001), cardiac troponin I levels, and pre-TIMI flow 8
Patients with larger infarctions show more pronounced elevations, with approximately 93% of patients with "large infarction" presenting AST concentrations >3× ULN 2
Extremely elevated transaminases (≥95th percentile) predict both short- and long-term mortality, particularly when both AST and ALT are markedly elevated 8
Differential Diagnosis Considerations
When evaluating elevated liver enzymes in the context of suspected or confirmed MI:
AST lacks specificity for liver injury because it is present in cardiac muscle, skeletal muscle, kidneys, brain, and red blood cells, making isolated AST elevation common in cardiac events 5, 6, 4
ALT is more liver-specific with minimal presence in cardiac tissue, so significant ALT elevation (>3× ULN) in acute MI should prompt consideration of concomitant hepatic pathology 5, 6, 2
Cardiovascular diseases are recognized causes of elevated liver enzymes in patients with known or suspected cardiac disease, and sonography or liver histology may be needed if elevations persist 3
Important Clinical Pitfalls
Do not exclude acute MI patients from clinical trials based solely on transaminase elevations, as current thresholds for liver dysfunction (often 2-3× ULN) may lead to excessive and inappropriate exclusions of patients with larger infarcts who could benefit from study interventions 2
Transient elevations are expected and typically resolve within days to weeks following the acute event, so persistent elevations beyond 2-4 weeks warrant investigation for alternative hepatic pathology 5, 3
Do not attribute all transaminase elevation to cardiac injury alone when ALT significantly exceeds AST or when elevations persist, as this may indicate concurrent primary liver disease requiring separate evaluation 7, 4