Myocarditis laboratory findings: Difference between revisions
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{{Myocarditis}} | {{Myocarditis}} | ||
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Varun Kumar|Varun Kumar, M.B.B.S.]] | {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Varun Kumar|Varun Kumar, M.B.B.S.]] | ||
==Overview== | |||
Myocardial inflammation can be suspected on the basis of elevated [[C-reactive protein]], [[Erythrocyte sedimentation rate|ESR]] and antibodies against viruses known to affect the [[myocardium]]. Markers of myocardial damage such as [[troponin]] or [[creatine kinase]] are often elevated.<ref name="pmid11070105">{{cite journal| author=Feldman AM, McNamara D| title=Myocarditis. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 19 | pages= 1388-98 | pmid=11070105 | doi=10.1056/NEJM200011093431908 | pmc= | url= }} </ref> | |||
==Inflammatory Markers== | ==Inflammatory Markers== | ||
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**'''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>. | **'''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>. | **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>. | ||
*'''Viral antibody titers''' for [[coxsackie B virus]], human immunodeficiency virus ([[HIV]]), [[cytomegalovirus]], [[Ebstein-Barr virus]], [[hepatitis virus]] family, and [[influenza virus]] assist in recognizing the causative organism. However, the management of myocarditis of viral etiology seldom differ with the virus and hence, antibody titers are rarely indicated in the diagnosis. | |||
*'''Auto antibodies''' such as [[ANA]], [[rheumatoid factor]], and [[anti-topoisomerase antibodies]] help in determining the etiology of [[myocarditis]] and thus help in effective management of the condition with immunosuppressants if needed. | |||
*'''Polymerase chain reaction (PCR)''' may be used in detection and identification of viral infections from [[myocardial biopsy]], pericardial fluid or other body fluids. Persistence of viral genome is indicative of poor prognosis<ref name="pmid16172268">{{cite journal| author=Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W et al.| title=Viral persistence in the myocardium is associated with progressive cardiac dysfunction. | journal=Circulation | year= 2005 | volume= 112 | issue= 13 | pages= 1965-70 | pmid=16172268 | doi=10.1161/CIRCULATIONAHA.105.548156 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16172268 }} </ref>. | |||
==References== | ==References== | ||
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[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Laboratory Test]] | [[Category:Laboratory Test]] | ||
[[Category:Up to date]] | |||
[[Category:Up to date cardiology]] | |||
{{WS}} | {{WS}} | ||
{{WH}} | {{WH}} | ||
Revision as of 21:26, 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.
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 often elevated.[1]
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[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 necrosis. Cardiac enzymes may also be useful in differentiating myocarditis from dilated cardiomyopathy as demonstrated in a series in Thailand[4]. 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[5].
- Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis[6].
- 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[7].
- Viral antibody titers for coxsackie B virus, human immunodeficiency virus (HIV), cytomegalovirus, Ebstein-Barr virus, hepatitis virus family, and influenza virus assist in recognizing the causative organism. However, the management of myocarditis of viral etiology seldom differ with the virus and hence, antibody titers are rarely indicated in the diagnosis.
- Auto antibodies such as ANA, rheumatoid factor, and anti-topoisomerase antibodies help in determining the etiology of myocarditis and thus help in effective management of the condition with immunosuppressants if needed.
- Polymerase chain reaction (PCR) may be used in detection and identification of viral infections from myocardial biopsy, pericardial fluid or other body fluids. Persistence of viral genome is indicative of poor prognosis[8].
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.
- ↑ 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.