AST and ALT are common enzymes measured in the blood, typically indicating liver health. They are released into the bloodstream when cells are damaged, causing levels to rise following a liver injury. Elevated AST and, less commonly, ALT are also significant findings in heart disease. Their measurement offers important insights into the extent of cardiac injury and the patient’s overall outlook. Understanding the dual nature of these biomarkers is key to interpreting their meaning in a cardiovascular context.
The Biological Function and Sources of AST and ALT
AST and ALT are aminotransferases that play a role in amino acid metabolism within cells. They help convert amino acids into energy, a process fundamental for cellular operation. Alanine Aminotransferase (ALT) is highly concentrated within the liver, making it a specific marker for liver cell damage.
Aspartate Aminotransferase (AST) is found in the liver, but is also present in other tissues, including skeletal muscle, kidneys, red blood cells, and the heart muscle (myocardium). This wider distribution explains why elevated AST is less specific for the liver than ALT. The presence of AST in the myocardium makes it a relevant marker when heart tissue is injured.
Due to this difference, cardiac injury is more likely to cause a pronounced increase in AST than in ALT. When AST levels rise substantially higher than ALT levels, it suggests the enzyme source is outside of the liver. The heart’s high metabolic activity means its cells are rich in AST, which is released upon damage.
Mechanism of Enzyme Elevation Following Cardiac Damage
The primary mechanism for elevated AST and ALT following a cardiac event is the loss of cell membrane integrity. When heart muscle cells (myocytes) are subjected to severe stress like lack of oxygen (ischemia), they undergo injury and death (necrosis). This cellular breakdown causes the cell contents, including the aminotransferases, to leak directly into the circulating blood.
This process is most dramatically seen during an acute myocardial infarction (heart attack), where a blockage starves the heart muscle of blood. The enzymes begin to rise in the bloodstream approximately six to eight hours after symptom onset. They typically reach their peak concentration around 24 to 36 hours before returning to normal levels within three to seven days.
AST was historically the first biochemical test used to diagnose acute myocardial infarction. While it has been largely replaced by the more sensitive cardiac troponin tests, its appearance in the blood remains a clear indicator of tissue damage. The magnitude and timing of the enzyme release correlate with the extent of the myocardial damage.
Specific Cardiovascular Conditions Linked to Elevated Enzymes
The elevation of AST and ALT in cardiovascular disease is not limited to acute events. These enzymes can also rise in chronic conditions, reflecting systemic stress or secondary organ damage. Acute coronary syndromes, such as a heart attack, cause a direct release of AST from necrotic heart muscle cells. This primary injury releases the enzymes stored within the heart.
A distinct mechanism occurs in chronic conditions like congestive heart failure, which can lead to cardiac hepatopathy, or “shock liver.” When the heart fails to pump blood effectively, blood backs up and causes passive congestion in the liver. This congestion and resulting low blood flow (hypoperfusion) cause damage to the liver tissue.
The resulting liver injury leads to a substantial release of both AST and ALT, often due to the liver’s large size. Inflammatory conditions affecting the heart, such as myocarditis (inflamed heart muscle), can also cause the release of these enzymes. Elevated levels in these cases signal widespread inflammation and cellular injury within the heart.
Understanding Test Results and Prognostic Value
Clinicians interpret AST and ALT results by considering the degree of elevation, the time course of the peak, and the relationship between the two enzymes. An extremely high elevation often suggests a large area of tissue damage, either in the heart or the liver. The pattern of the enzyme rise and fall helps distinguish an acute event from a chronic condition.
The ratio of AST to ALT, called the De Ritis ratio, is a helpful tool in differentiating the source of the injury. Since ALT is highly liver-specific, a disproportionately high AST level (a high AST/ALT ratio) strongly suggests a non-liver source, such as the heart or skeletal muscle. Conversely, in many types of liver disease, the ALT level is often higher than AST.
A persistently elevated AST/ALT ratio following acute myocardial infarction is associated with a less favorable long-term outlook. Studies show that a high De Ritis ratio following a heart attack is independently associated with increased cardiovascular mortality. The magnitude and ratio of these blood enzymes provide physicians with valuable information about the patient’s health trajectory following a cardiac event.