Myocarditis pathophysiology

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.

Myocarditis is a continuum of three phases of the disease processes with each one evolving into the next.^[1]

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.

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.

• Cytokines, which are produced in reaction to infection and cell death, are a leading cause of dilated cardiomyopathy.
• Matrix metalloproteinases, such as gelatinase, collagenases, and elastases may also be activated by cytokines during the autoimmune phase.^[2][3]
• Protease produced by coxsackie virus can modify the sarcoglycan complex in myocytes leading to ventricular dilation.^[4]

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.^[5][6] 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.

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.^[7]

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