Cardiac injury can be defined as the disruption of normal cardiac myocyte membrane integrity resulting in the loss into the extracellular space (including blood) of intracellular constituents including detectable levels of a variety of biologically active cytosolic and structural proteins such as troponin, creatine kinase, myoglobin, heart-type fatty acid binding protein, and lactate dehydrogenase. Injury is usually considered irreversible (cell death), but definitive proof that cell death is an inevitable consequence of the process is not available.
Causes of cardiac injury include trauma, toxins, and viral infection, but ischemia or infarction consequent to an imbalance between the supply and demand of oxygen (and nutrients) is the most common cause.
When a sufficient number of myocytes have died (myocyte necrosis) or lost function, acute clinical disease is apparent; examples include myocardial infarction (MI) or myocarditis. (See "Criteria for the diagnosis of acute myocardial infarction" and "Clinical manifestations and diagnosis of myocarditis in adults".)
The biochemical characteristics and utility of myoglobin, fatty acid binding protein, and lactate dehydrogenase for the diagnosis of and prognosis after acute myocardial infarction (MI) will be reviewed here. Troponins and creatine kinase, which are the preferred biomarkers for diagnosis and prognosis, are discussed separately. (See "Troponins and creatine kinase as biomarkers of cardiac injury".)
Copeptin, which is not released from myocardial cells, but rather the pituitary gland, is also discussed.