Myocarditis pathophysiology

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 pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Google Images

American Roentgen Ray Society Images of Myocarditis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Myocarditis pathophysiology

CDC on Myocarditis pathophysiology

Myocarditis pathophysiology in the news

Blogs on Myocarditis pathophysiology

Directions to Hospitals Treating Type page name here

Risk calculators and risk factors for Myocarditis pathophysiology

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

During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction. Histopathological features include abundant edema in the myocardial interstitium and an inflammatory infiltrate which is rich in lymphocytes and macrophages. Focal destruction of myocytes as a result of the inflammatory process results in left ventricular dysfunction.[1]

Pathogenesis

Myocarditis is a continuum of three phases of the disease processes with each one evolving into the next.[2]

Phase I: Viral Infection and Replication

Viruses such as coxsackie and enterovirus, get internalized in peripheral tissues and activate the immune system. A few of these viral genomes attach to the immunologic cells which circulate throughout the body and lodge in other organs such as the heart where they further replicate and cause localized tissue destruction.

Phase II: Autoimmune Injury

After the host immune system eliminates the viral genomes from the body, the immune system may remains activated in patients who develop myocarditis. This leads to the development of an autoimmune reaction where T-cells and cytokines target the host tissue such as the myocardium which causes further myocyte damage.

Phase III: Dilated Cardiomyopathy

Eosinophilic and hypersensitive myocarditis may occur secondary to parasitic infections, drug hypersensitivity or hypereosinophilic syndrome. Eosinophilic infiltration in myocardium lead to release of eosinophilic proteins which increase cellular membrane permeability which in turn leads to cell death.[6][7] The pathogenesis of this hypersensitivity reaction include either an immediate reaction which involves the degranulation of mast cells and basophils mediated by IgE, or a delayed reaction involving the activation of helper T-cells and interleukin-5.

Microscopic Pathology

Histopathological features include abundant edema in the myocardial interstitium and an inflammatory infiltrate which is rich in lymphocytes and macrophages. Focal destruction of myocytes as a result of the inflammatory process results in left ventricular dysfunction.[1]

The Heart in Toxoplasma gondii Myocarditis

The Heart in Coxsackie B2 Myocarditis

References

  1. 1.0 1.1 Feldman AM, McNamara D (2000). "Myocarditis.". N Engl J Med. 343 (19): 1388–98. PMID 11070105. doi:10.1056/NEJM200011093431908. 
  2. Liu PP, Mason JW (2001). "Advances in the understanding of myocarditis.". Circulation. 104 (9): 1076–82. PMID 11524405. 
  3. Ono K, Matsumori A, Shioi T, Furukawa Y, Sasayama S (1998). "Cytokine gene expression after myocardial infarction in rat hearts: possible implication in left ventricular remodeling.". Circulation. 98 (2): 149–56. PMID 9679721. 
  4. Lee JK, Zaidi SH, Liu P, Dawood F, Cheah AY, Wen WH; et al. (1998). "A serine elastase inhibitor reduces inflammation and fibrosis and preserves cardiac function after experimentally-induced murine myocarditis.". Nat Med. 4 (12): 1383–91. PMID 9846575. doi:10.1038/3973. 
  5. Badorff C, Lee GH, Lamphear BJ, Martone ME, Campbell KP, Rhoads RE; et al. (1999). "Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy.". Nat Med. 5 (3): 320–6. PMID 10086389. doi:10.1038/6543. 
  6. Ginsberg F, Parrillo JE (2005). "Eosinophilic myocarditis.". Heart Fail Clin. 1 (3): 419–29. PMID 17386864. doi:10.1016/j.hfc.2005.06.013. 
  7. Amini R, Nielsen C (2010). "Eosinophilic myocarditis mimicking acute coronary syndrome secondary to idiopathic hypereosinophilic syndrome: a case report.". J Med Case Reports. 4: 40. PMC 2830978Freely accessible. PMID 20181108. doi:10.1186/1752-1947-4-40. 



Linked-in.jpg