Myocarditis laboratory findings: Difference between revisions
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==Markers of Myonecrosis== | ==Markers of Myonecrosis== | ||
The following markers of myonecrosis is often elevated in myocarditis: | The following markers of myonecrosis is often elevated in myocarditis: | ||
*[[Creatine Kinase]] (CK-MB) | *'''[[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<ref name="pmid8994432">{{cite journal| author=Smith SC, Ladenson JH, Mason JW, Jaffe AS| title=Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 163-8 | pmid=8994432 | doi= | pmc= | url= }} </ref><ref name="pmid9350939">{{cite journal| author=Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE et al.| title=Cardiac troponin T in patients with clinically suspected myocarditis. | journal=J Am Coll Cardiol | year= 1997 | volume= 30 | issue= 5 | pages= 1354-9 | pmid=9350939 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9350939 }} </ref>. cTnI is elevated early in the course and is suggestive of acute myocarditis<ref name="pmid8994432">{{cite journal| author=Smith SC, Ladenson JH, Mason JW, Jaffe AS| title=Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 163-8 | pmid=8994432 | doi= | pmc= | url= }} </ref>. 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<ref name="pmid12211203">{{cite journal| author=Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D et al.| title=Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children. | journal=Pediatr Cardiol | year= 2002 | volume= 23 | issue= 5 | pages= 531-5 | pmid=12211203 | doi= | pmc= | url= }} </ref>. CK-MB and cTnT levels were found to be higher in myocarditis than dilated cardiomyopathy. | *'''Cardiac [[troponin]] I (cTnI) or T (cTnT''') are elevated more frequently than CK-MB (34-53% versus 2-6 %) as reported in two series<ref name="pmid8994432">{{cite journal| author=Smith SC, Ladenson JH, Mason JW, Jaffe AS| title=Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 163-8 | pmid=8994432 | doi= | pmc= | url= }} </ref><ref name="pmid9350939">{{cite journal| author=Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE et al.| title=Cardiac troponin T in patients with clinically suspected myocarditis. | journal=J Am Coll Cardiol | year= 1997 | volume= 30 | issue= 5 | pages= 1354-9 | pmid=9350939 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9350939 }} </ref>. cTnI is elevated early in the course and is suggestive of acute myocarditis<ref name="pmid8994432">{{cite journal| author=Smith SC, Ladenson JH, Mason JW, Jaffe AS| title=Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 163-8 | pmid=8994432 | doi= | pmc= | url= }} </ref>. | ||
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<ref name="pmid12211203">{{cite journal| author=Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D et al.| title=Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children. | journal=Pediatr Cardiol | year= 2002 | volume= 23 | issue= 5 | pages= 531-5 | pmid=12211203 | doi= | pmc= | url= }} </ref>. 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<ref name="pmid16168288">{{cite journal| author=Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R et al.| title=Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy. | journal=J Am Coll Cardiol | year= 2005 | volume= 46 | issue= 6 | pages= 1036-42 | pmid=16168288 | doi=10.1016/j.jacc.2005.05.067 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16168288 }} </ref>. | |||
**'''Antimyosin autoantibodies''' are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis<ref name="pmid10636253">{{cite journal| author=Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP| title=Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 35 | issue= 1 | pages= 11-8 | pmid=10636253 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10636253 }} </ref>. | |||
**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<ref name="pmid15364334">{{cite journal| author=Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T et al.| title=Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis. | journal=J Am Coll Cardiol | year= 2004 | volume= 44 | issue= 6 | pages= 1292-7 | pmid=15364334 | doi=10.1016/j.jacc.2004.01.055 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15364334 }} </ref>. | |||
==References== | ==References== | ||
Revision as of 19:49, 25 August 2011
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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.