Laboratory findings consistent with the diagnosis of myocarditis include elevated markers of myonecrosis, inflammatory markers, and other biomarkers. Markers of myonecrosis include creatine kinase (CK-MB), cardiac troponin I (cTnI) or T (cTnT), lactate dehydrogenase (LDH), alanine transaminase (ALT), and aspartate transaminase (AST). Elevated levels of C-reactive protein and erythrocyte sedimentation rate (ESR), and leukocytosis are suggestive of myocarditis. Serologic markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis. Other auto-antibodies such as ANA and rheumatoid factor may also be detected.

The following markers of myonecrosis are often elevated in myocarditis, particularly early on in the course of the disease:^{[1][2][3][4][5]}

• Creatine kinase (CK-MB)
• Cardiac troponin I (cTnI) or T (cTnT) are elevated more frequently than CK-MB (34-53% versus 2-6 %) as reported in two series. Cardiac troponin I is elevated early in the course and is suggestive of acute myocarditis. Persistently elevated cTnT or CK-MB is suggestive of ongoing myonecrosis. Cardiac enzymes may also be useful in differentiating myocarditis from dilated cardiomyopathy as CK-MB and cTnT levels are higher in myocarditis than dilated cardiomyopathy.

• Lactate dehydrogenase (LDH)
• Alanine transaminase (ALT)
• Aspartate transaminase (AST)

Note: AST is considered to be the most sensitive marker of myocarditis with the sensitivity of 85%. However, the specificities of AST and ALT are low in patients with myocarditis as they may be elevated secondary to other coexisting systemic or organ dysfunction.

The following inflammatory markers are often elevated:^[6][7]

• CBC: leukocytosis or eosinophilia in hypersensitive myocarditis.
• C-reactive protein
• Erythrocyte sedimentation rate (ESR)

• Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis. ^{[8][9][10][11]}
  • Fas and Fas ligand are markers of cell death (apoptosis) and are associated with cardiac dysfunction.
  • Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis.
  • High levels of interleukin-10 in fulminant myocarditis patients at admission may be predictive of subsequent development of cardiogenic shock (requiring mechanical cardiopulmonary support system) and mortality.
  • Viral antibody titers for coxsackie B virus, human immunodeficiency virus (HIV), cytomegalovirus, Ebstein-Barr virus, hepatitis virus family, and influenza virus may be useful in diagnosis the causative organism. However, the management of myocarditis due to a viral etiology seldom differs depending upon the virus, and therefore, antibody titers are rarely indicated in the diagnostic evaluation of myocarditis.

• Auto-antibodies such as ANA, rheumatoid factor, and anti-topoisomerase antibodies may identify conditions that respond to immunosuppressive therapy.

• Polymerase chain reaction (PCR) may be used in the detection of and identification of viral infections from myocardial biopsy, pericardial fluid or other body fluids. Persistence of a viral genome is indicative of a poor prognosis.