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Acute Myocarditis

Dr. Khalid is a health researcher and science writer with a Ph.D. in clinical research.

Myocyte Damage in Acute Myocarditis

Myocyte Damage in Acute Myocarditis

What is Acute Myocarditis?

The progressive inflammation of the myocardium at any age manifests with myocyte deterioration. The viral illnesses usually trigger acute myocarditis in teenagers, infants, adults, and elderly individuals. Some of the potential causes of acute myocarditis include hepatitis C, adenoviruses, and the human immunodeficiency virus (1). The disease also progresses due to non-infectious conditions including, dermatomyositis, polymyositis, eosinophilic myocarditis, systemic lupus erythematosus, and granulomatous inflammatory diseases like giant cell myocarditis and sarcoidosis (2).

Clinical History

Acute myocarditis progresses with edema, paroxysmal nocturnal dyspnea, orthopnea, shortness of breath, and acute onset dyspnea (3). Patients with atrioventricular block and ventricular arrhythmia often experience syncope and palpitations. The acute onset of heart failure manifests with the symptoms (of chest discomfort, malaise, palpitations, dyspnea, and fatigue). Viral myocarditis often develops due to gastrointestinal infections and upper respiratory tract infections. The exertional dyspnea or dyspnea at rest is the most prominent symptom that corresponds to the progression of heart failure. Some acute myocarditis patients report fever with chills and sweating with or without chest pain that develops due to myocardial inflammation (4). The patients with drug-induced myocarditis develop a generalized or maculopapular skin rash with or without pruritus. The acute myocarditis also progresses following the ingestion of drugs including, antiepileptics and phenothiazines. The atrioventricular block and ventricular arrhythmias also trigger sudden cardiac deaths in rare scenarios. The first five months after delivery or the third trimester of pregnancy (in some scenarios) attribute to the development of postpartum myocarditis (5).

Clinical Examination

The clinical examination of the patients suspected of acute myocarditis may reveal one or more of the following outcomes (6).

  1. Murmur indicating mitral regurgitation
  2. Diffuse pulmonary crackles indicative of pulmonary edema
  3. Diminishment of the first heart sound and the appearance of third heart sound
  4. The giant cell myocarditis manifests with sustained ventricular tachycardia
  5. Arrhythmia
  6. The sarcoid myocarditis progresses with lymphadenopathy
  7. The drug-induced myocarditis progresses with maculopapular rash
  8. Myocarditis with pericarditis triggers pericardial rub
  9. Dependent and peripheral edema indicative of heart failure

Differential Assessment/Diagnoses (As Applicable)

  1. The manifestations of Chagas disease include cardiac arrest, altered heart rhythm/rate, heart failure, and cardiomyopathy
  2. A pre-existing systemic disease may also trigger cardiomyopathy and its clinical manifestations
  3. The symptoms including, palpitations and dyspnea with chest pain may trigger sudden cardiac death
  4. The progressive deterioration of lung tissue due to age-related pulmonary fibrosis triggers dyspnea or shortness of breath
  5. The cardiogenic pulmonary edema develops due to acute-on-chronic heart failure/acute left heart failure or myocardial infarction
  6. The chest pain emanating from acute coronary syndrome (ACS) radiates to the jaw/left arm.
  7. The ACS patients also report pain and constriction on the left side of their chest

Diagnostic Investigations (As Applicable)

  1. The physician needs to rule out post-viral myocarditis (if suspected) via viral antibody titers
  2. The causative factors for myocarditis (requiring investigation) also include viral hepatitis, Ebstein-Barr virus, cytomegalovirus, human immunodeficiency virus, parvovirus B19, and group B coxsackievirus
  3. Assessment of viral myocarditis
  4. Cardiac troponins/creatine kinase to rule out cardiac myonecrosis
  5. Chest X-ray to rule out pleural effusions, upper lobe diversion, Kerley B lines, and pulmonary edema
  6. ECG (electrocardiogram) to investigate ST-segment elevation, PQ segment depression, non-specific ST/T-wave changes, ventricular arrhythmia, and tachycardia
  7. CRP (C-reactive protein) elevation and ESR (erythrocyte sedimentation rate) assessment to rule out inflammation
  8. CBC (Complete blood count) to rule out inflammation/leukocytosis
  9. Cardiac myosin heavy chain antibody assessment
  10. Cardiac MRI (magnetic resonance imaging) to investigate inflammation
  11. Gadolinium scan to evaluate cellular edema and inflammation
  12. Echocardiography to evaluate pericardial effusion, diastolic dysfunction, left ventricle enlargement, and abnormal wall motions
  13. Dallas criteria to investigate myocyte necrosis and inflammatory infiltrate
  14. Assessment of lymphocyte infiltration
  15. An endomyocardial biopsy followed by viral PCR (polymerase chain reaction) to evaluate viral genomes

Medical Management (As Applicable)

  1. Administration of antiarrhythmics
  2. Therapeutic management of underlying infection
  3. Cessation of the drug that triggered myocarditis
  4. Complete bed rest and avoidance of strenuous activities
  5. Fluid restriction to minimize fluid overload
  6. Compliance with a low sodium diet
  7. Influenza/poliomyelitis/mumps/rubella/measles vaccination to prevent infective myocarditis
  8. Oxygen management after assessing circulation and breathing patterns (as needed)
  9. Regular cardiac monitoring
  10. Intravenous fluid administration as per medical necessity
  11. Mechanical cardiac support for patients with cardiogenic shock and severe cardiac failure
  12. Tachyarrhythmia management via antiarrhythmics (to control ventricular tachycardia and atrial tachycardia)
  13. AICD (automatic implantable cardioverter-defibrillator) or permanent pacer/temporary pacemaker for treating complete/Mobitz type-II (2nd degree AV [atrioventricular]) heart block
  14. Immune modulation/suppression via corticosteroids to treat autoimmune myocarditis
  15. Heart failure management via milrinone/dobutamine (inotropic medications), ACE (angiotensin-converting enzyme) inhibitors, beta-blockers, and diuretics
  16. Conservative/supportive management for post viral myocarditis
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1. Al-Akchar, M.; Kiel, J. Acute myocarditis. In StatPearls;, 2021.

2. Cooper-Jr, L. T. Myocarditis. N Engl J Med 2009, 360 (15), 1526–1538.

3. Hall, W. H. K.; Hurst, J. W. Dyspnea, Orthopnea, and Paroxysmal Nocturnal Dyspnea. In Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition; Butterworths, 1990.

4. Smid, J.; Scherner, M.; Wolfram, O.; Groscheck, T.; Wippermann, J.; Braun-Dullaeus, R. C. Cardiogenic Causes of Fever. Dtsch Arztebl Int 2018, 115 (12), 193-199.

5. Kim, M. J.; Shin, M. S. Practical management of peripartum cardiomyopathy. Korean J Intern Med 2017, 32 (3), 393–403.

6. Blauwet , L. A.; Cooper, L. T. Myocarditis. Prog Cardiovasc Dis 2010, 52 (4), 274-288.

This content is for informational purposes only and does not substitute for formal and individualized diagnosis, prognosis, treatment, prescription, and/or dietary advice from a licensed medical professional. Do not stop or alter your current course of treatment. If pregnant or nursing, consult with a qualified provider on an individual basis. Seek immediate help if you are experiencing a medical emergency.

© 2021 Dr Khalid Rahman

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