Myocarditis laboratory findings
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S.
Overview
Myocardial inflammation can be suspected on the basis of elevated C-reactive protein, ESR and antibodies against viruses known to affect the myocardium. Markers of myocardial damage such as troponin or creatine kinase are elevated, particularly early on in the course of the disease.[1] Other auto-antibodies such as ANA and rheumatoid factor may also be detected.
Laboratory Findings
Markers of Myonecrosis
The following markers of myonecrosis are often elevated in myocarditis, particularly early on in the course of the disease:
- 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.[2][3] cTnI is elevated early in the course and is suggestive of acute myocarditis[2]. 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.[4]
- Lactate dehydrogenase (LDH)
- Alanine transaminase (ALT)
- Aspartate transaminase (AST)
- AST is considered to be the most sensitive marker of myocarditis with the sensitivity of 85%.[5] 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.[6]
Inflammatory Markers
The following inflammatory markers are often elevated:
- CBC: Leukocytosis or eosinophilia in hypersensitive myocarditis.
- C-reactive protein
- Erythrocyte sedimentation rate (ESR)
Other Biomarkers
- Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis.
- Fas and Fas ligand are markers of cell death (apoptosis) and are associated with cardiac dysfunction. A study evaluating the role of gene expression for predicting myocardial recovery in recent-onset cardiomyopathy, reported that patients in the highest tertile of Fas expression had minimal improvement at six months when compared with the intermediate and lowest tertiles[7].
- Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis[8].
- 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[9].
- 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 diagnosing 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[10].
References
- ↑ Feldman AM, McNamara D (2000). "Myocarditis". N Engl J Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105.
- ↑ 2.0 2.1 Smith SC, Ladenson JH, Mason JW, Jaffe AS (1997). "Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates". Circulation. 95 (1): 163–8. PMID 8994432.
- ↑ Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE; et al. (1997). "Cardiac troponin T in patients with clinically suspected myocarditis". J Am Coll Cardiol. 30 (5): 1354–9. PMID 9350939.
- ↑ Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D; et al. (2002). "Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children". Pediatr Cardiol. 23 (5): 531–5. PMID 12211203.
- ↑ Freedman SB, Haladyn JK, Floh A, Kirsh JA, Taylor G, Thull-Freedman J (2007). "Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation". Pediatrics. 120 (6): 1278–85. doi:10.1542/peds.2007-1073. PMID 18055677.
- ↑ Lippi G, Salvagno GL, Guidi GC (2008). "Cardiac troponins in pediatric myocarditis". Pediatrics. 121 (4): 864, author reply 864-5. doi:10.1542/peds.2008-0031. PMID 18381554.
- ↑ Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R; et al. (2005). "Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy". J Am Coll Cardiol. 46 (6): 1036–42. doi:10.1016/j.jacc.2005.05.067. PMID 16168288.
- ↑ Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP (2000). "Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis". J Am Coll Cardiol. 35 (1): 11–8. PMID 10636253.
- ↑ Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T; et al. (2004). "Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis". J Am Coll Cardiol. 44 (6): 1292–7. doi:10.1016/j.jacc.2004.01.055. PMID 15364334.
- ↑ Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W; et al. (2005). "Viral persistence in the myocardium is associated with progressive cardiac dysfunction". Circulation. 112 (13): 1965–70. doi:10.1161/CIRCULATIONAHA.105.548156. PMID 16172268.