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.
Inflammatory Markers
The following inflammatory markers are often elevated:
- CBC: Leukocytosis or eosinophilia in hypersensitive myocarditis.
- C-reactive protein
- Erythrocyte sedimentation rate (ESR)
Markers of Myonecrosis
The following markers of myonecrosis is often elevated in myocarditis:
- 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[1][2]. cTnI is elevated early in the course and is suggestive of acute myocarditis[1].
Persistently elevated cTnT or CK-MB is suggestive of ongoing necrosis. Cardiac enzymes may also be useful in differentiating myocarditis from dilated cardiomyopathy as demonstrated in a series in Thailand[3]. CK-MB and cTnT levels were found to be higher in myocarditis than dilated cardiomyopathy.
Other Biomarkers
- Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis.
- Fas and Fas ligand can lead to apoptotic death of myocytes and thus causing 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[4].
- Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis[5].
- 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[6].
References
- ↑ 1.0 1.1 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.
- ↑ 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.