Myocarditis is collection of diseases of infectious, toxic, and autoimmune etiologies characterized by inflammation of the heart. Subsequent myocardial destruction can lead to dilated cardiomyopathy.

Causes:

  • Amongst the infectious causes, viral acute myocarditis is by far the most common. Identification of the coxsackie-adenovirus.
  • Other viruses implicated in myocarditis include influenza virus, echovirus, herpes simplex virus, varicella-zoster virus, hepatitis, Epstein-Barr virus, and cytomegalovirus.
  • Human immunodeficiency virus (HIV).
  • Amongst the infectious causes, viral acute myocarditis is by far the most common. Identification of the coxsackie-adenovirus.
  • Other viruses implicated in myocarditis include influenza virus, echovirus, herpes simplex virus, varicella-zoster virus, hepatitis, Epstein-Barr virus, and cytomegalovirus.
  • Human immunodeficiency virus (HIV).

Acute Myocarditis

Non Viral infectious causes are numerous and varied;

Bacteria: Chlamydia (C. pneumonia/psittacosis) haemophilus influence, legionella, pneumophilia, brucella clostridium, francisella tularensis, neisseria meningitis, mycobacterium (tuberculosis), salmonella, staphylococcus, streptococcus A, S. pneumonia, tularemia, tetanus, syphilis, Vibrio cholera.

Spirocheta: Borrelia recurrentis, leptospira, Treponema pallidum.

Reckettsia: Coxiella burnetii, R. rickettsii/prowazekii.

Protozoa: Entamoeba histolytica, leishmania, Plasmodium falciparum,Trypanosoma cruzi, Trypanosoma brucei, Toxoplasma gondii — Helmintic: ascaris, Echinococcus granulosus, Schistosoma, Trichinella spiralis,Wuchereria bancrofti.

  • Toxic myocarditis has a number of etiologies including both medical agents and environmental agents.
  • Numerous medications (eg, lithium, doxorubicin, cocaine, numerous catecholamines, acetaminophen).
  • Among the most common drugs that cause hypersensitivity reactions are penicillin, ampicillin, hydrochlorothiazide, methyldopa, and sulfonamide drugs.
  • Environmental toxins include lead, arsenic, and carbon monoxide.
  • Wasp, scorpion, and spider stings.
  • Radiation therapy may cause a myocarditis with the development of a dilated cardiomyopathy.

abnormal signal

Immunologic etiologies of myocarditis encompass a number of clinical syndromes and include the following: 

  • Connective tissue disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis, and dermatomyositis. 
  • Rejection of the post-transplant heart may present as inflammatory myocarditis.

Pathophysiology

Several mechanisms of myocardial damage:

  1. Direct injury of myocytes by the  infectious agent.
  2. Myocyte injury caused by a toxin such as that from Corynebacterium diphtheriae.
  3. Myocyte injury as a result of infection-induced immune reaction or autoimmunity.

Tri phasic Disease Process:

Acute Phase: Characterized by direct infiltration of cardio tropic virus into myo cyte. There is no histological evidence of myocarditis at this point.

Sub acute Phase: Host attempts to clear the virus.  Natural Killer cells, Macrophages, and Lymphocytes infiltrate infected heart tissue. The is subsequent pro inflammatory cytokine release, NO production, antibody secretion, and up regulation of MHC.

Chronic Myocarditis:  Dilated heart with evidence of fibrrosis.

Phase I: Viral Infection and Replication.

Phase 2: Autoimmunity and injury.

Phase 3: Dilated Cardiomyopathy.

Symptoms and Signs:

Patients(59%) frequently present days to weeks after an acute febrile illness, particularly a flu-like syndrome.

Myocarditis is most commonly asymptomatic, with no evidence of left ventricular dysfunction –  fever, malaise, fatigue, arthralgias, myalgias, and skin rash.

Cardiac symptoms may result from systolic or diastolic left ventricular dysfunction or from tachyarrhythmias or bradyarrhythmias (dyspnea, fatigue, decreased exercise tolerance, palpitations).

In cases where a dilated cardiomyopathy has developed, signs of peripheral or pulmonary thromboembolism may be found.

Diffuse inflammation may develop leading to pericardial effusion, without tamponade, and pericardial and pleural friction rub as the inflammatory process involves surrounding structures.

normal myocarditis

Clinical Findings:

Physical Examination: Tachycardia, hypotension, fever and tachycardia may be disproportionate to the degree of fever.

  • Bradycardia is seen rarely, and a narrow pulse pressure is occasionally detected.
  • Murmurs of mitral or tricuspid regurgitation are common , S3 and S4 gallops may also be heard. 
  • Distended neck veins, pulmonary rales, wheezes, gallops, and peripheral edema may be detected.

Diagnostic Studies

Electrocardiography:

  • The most common abnormality is sinus tachycardia.
  • May show ventricular arrhythmias or heart block, or it may mimic the findings in acute myocardial infarction or pericarditis with ST segment elevation, ST segment depression, PR segment depression, and pathological Q-waves.
  • Relations between these clinical and laboratory findings.
  • Echocardiography – to exclude other causes of heart failure and identify ventricular thrombi.
  • There are no specific echocardiographic features of myocarditis.
  • Segmental or global wall motion abnormalities can mimic myocardial infarction.
  • Patients with fulminant myocarditis tend to present with more normal cardiac chamber dimensions and thickened walls, compared with patients with less acute myocarditis who have greater left ventricular dilation and normal wall thickness.
  • Right ventricular dysfunction is an uncommon but important predictor of death or cardiac transplantation.
  • Chest radiography.
  • MRI is capable of showing abnormal signal intensity in the affected myocardium.

Imaging Studies:

  • Chest radiography.
  • MRI is capable of showing abnormal signal intensity in the affected myocardium.

Cardiac Catheterization:

  • Elevated left ventricular end-diastolic pressure, a depressed cardiac output, and increased ventricular volumes.
  • Coronary angiogram typically demonstrates normal coronary arteries.

Endomyocardial Biopsy:

  • Gold standard for the diagnosis of myocarditis.
  • Dallas criteria (an inflammatory infiltrate of the  myocardium +injury to the adjacent myocytes). 
  • Borderline myocarditis is made when the infiltrate is not accompanied by myocyte injury.

Laboratory Studies:

  • Cardiac troponin I may be more sensitive because it is present for longer periods after myocardial damage from any cause.
  • Erythrocyte sedimentation rate (ESR) is elevated in 60% of patients with acute myocarditis.
  • Leukocytosis is present in 25% of cases.

Other Studies:

If a systemic disorder (eg, SLE) is suspected, antinuclear antibody (ANA) and other collagen vascular disorder laboratory investigations may be useful.

Differential Diagnosis:

  • Dilative cardiomyopathy.
  • Secondary cardiomyopathy.
  • Electrolyte disturbanc.

Non Pharmacological Treatment:

  • Bed rest.
  • Reducing salt and liquids intake.
  • No training for athletes – 6 months.

Therapeutic Options:

  • Treatment of heart failure.
  • Treatment of arrhythmias.
  • Treatment of conduction abnormalities – heart blocks.

Intravenous gamma – globulin in children:

  • Antibiotics in bacterial myocarditis.
  • Anti-lymphocyte monoclonal antibodies.
  • Alfa and beta interferon (positive viral PCR reaction).
  • Immunosupresion in giant cell myocarditis and autoimmune myocarditis.
  • Glucocorticoids and azathioprine – debatable (negative viral PCR reaction).
  • NSAIDs are contraindicated in the ACUTE PHASE (increase cardiomyocyte lesion and necrosis).

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