Myocarditis laboratory findings

Jump to: navigation, search

Myocarditis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Adrenergic Myocarditis
Giant Cell Myocarditis

Causes

Differentiating Myocarditis from other Diseases

Epidemiology and Demographics

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Endomyocardial Biopsy

Chest X Ray

MRI

Echocardiography

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Canadian Guidelines

Cardiac Transplantation

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Myocarditis laboratory findings On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Google Images

American Roentgen Ray Society Images of Myocarditis laboratory findings

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Myocarditis laboratory findings

CDC on Myocarditis laboratory findings

Myocarditis laboratory findings in the news

Blogs on Myocarditis laboratory findings</small>

Directions to Hospitals Treating Type page name here

Risk calculators and risk factors for Myocarditis laboratory findings

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S., Maliha Shakil, M.D. [2]

Overview

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. Serological 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.

Laboratory Findings

Markers of Myonecrosis

The following markers of myonecrosis are often elevated in myocarditis, particularly early on in the course of the disease:

AST is considered to be the most sensitive marker of myocarditis with the sensitivity of 85%.[4] 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.[5]

Inflammatory Markers

The following inflammatory markers are often elevated:

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.[6]
    • Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis.[7]
    • 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.[8]
  • 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.
  • 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.[9]

References

  1. 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. 
  2. 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. 
  3. 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. 
  4. 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. PMID 18055677. doi:10.1542/peds.2007-1073. 
  5. Lippi G, Salvagno GL, Guidi GC (2008). "Cardiac troponins in pediatric myocarditis.". Pediatrics. 121 (4): 864; author reply 864–5. PMID 18381554. doi:10.1542/peds.2008-0031. 
  6. 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. PMID 16168288. doi:10.1016/j.jacc.2005.05.067. 
  7. 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. 
  8. 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. PMID 15364334. doi:10.1016/j.jacc.2004.01.055. 
  9. 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. PMID 16172268. doi:10.1161/CIRCULATIONAHA.105.548156. 

Linked-in.jpg