Myocarditis

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Pericarditis is an inflammation of the pericardium.

Myocarditis – inflammation of the myocardium.

Pericarditis is often accompanied by some degree of myocarditis.[1] Pericarditis and myocarditis may at times coexist and share the same etiologic agents.

Cardiothropic viruses are the most common cause of pericarditis and myocarditis

Table: Etiology of Myopericarditis/Perimyocarditis:[1][2]
1. Infectious (2/3 of cases)
Viral (common): Enteroviruses (Coxsackie A and B, Echoviruses), Epstein-Barr virus (EBV), Cytomegalovirus (CMV), Human Herpes Virus 6 (HHV6), Adenoviruses, Influenza A and B, Parvovirus B19, Hepatitis B a,d C, HIV, Varicella, Mumps, Rubeola Rubella, Poliomyelitis, Rhinoviruses, Vaccinia.

Bacterial (most common): tuberculeous (4-5%), Coxiella burnetti; other bacteria (rare): pneumococci, meningococci, staphylococci, haemophilus, Chlamydia, mycoplasma, legionella, leptospira, listeria,

Fungi rare: histoplasma (immunocompetent), aspergillosis, blastomycosis, candida (immunosupressed) Parasitic very rare: echinococci, toxoplasma

2. Non infectious (1/3 of cases)
Autoimmune pericarditis (<10%)

Post-myocardial/pericardial injury syndromes: post-myocardial infarction, Rheumatoid arthritis, Sarcoidosis, Churg-Strauss syndrome, Acute rheumatic fever, Sjogren's syndrome, systemic sclerosis, Bechchet syndrome, Familial Mediterranean fever) Inflammatory bowel diseases (Crohn's disease, ulcerative colitis)

Neoplastic pericarditis (5-7%) Primary tumors (rare, pericardial mesothelioma) Secondary metastatic tumors (common; lung and breast cancer, lymphoma)

Metabolic pericarditis (common; uremia, myxedema) Post-irradiation drugs (rare): Procainamide, Hydralazine, isoniazid, Phenytoin (lupus-like syndrome), penicillines (hypersensitivity percarditis with eosinophilia), Doxorubicin, Daunorubicin, Methyldopa, Methysergide, Sulphonamides, Sytosine Arabinoside, Phenylbutazone, Cocaine)


Direct damage of the heart by the viruses results in release of the intracellular proteins and induces immune response. This mechanism results in damage of the myocardium and pericardium because of viral infection, connective tissue diseases, inflammatory bowel diseases, post irradiation exposure or due to drugs.[1][2]

Clinical presentation: typical viral infection with fever, systemic symptoms, myalgia, sore throat, diarrhea, vomiting; followed by pleuritic chest pain, aggravating with inspirium and supine position, intolerance to exercise, palpitations. Typical chest pain reflects involvement of the pericardium [pericarditis], while systemic symptoms: fatigue, palpitations and tachycardia are more characteristic of myocardial involvement [myocarditis].

In most patients with pericarditis, there is some involvement of the myocardium.[2] Regional wall motion abnormalities on echocardiography and elevation of cardiac enzymes [especially cardiac troponin T and/or I] are characteristic of myocardial involvement.

Pericarditis includes a wide range of symptoms from the pure pericardial involvement to cases of pure myocarditis with significant LV dysfunction. In most cases, though, pericarditis and myocarditis coexist: perimyocarditis / myopericarditis.[1][2]

Electrocardiographic changes

Electrocardiographic changes typically include 4 stages:

Stage 1. The first hours- days: Diffuse ST elevation and PR depression, prominent in leads V5 and V6

ECG in Acute Pericarditis.

Stage 2. Normalization of ST and PR

Stage 3. Inversion of T waves after normalization of ST segment

Stage 4. Normalization of the electroardiogram or persistence of residual T wave changes

Electrocardiographic changes are not always classic. Often electrocardiographic changes are less typical and when associated with significant chest pain may simulate acute coronary syndrome. Physical examination can reveal pericardial friction rub, often detectable during sitting or during expirium [in this conditions the heart is in close proximity to the chest wall]. Pericardial friction rub can be found while the amount of the pericardial fluid is small or minimal. When the amount of the pericardial fluid increases, pericardial friction rub disappears. In patients with large pericardial effusion, heart sounds are muffled and fast, atrial fibrillation may occur, low blood pressure and right side failure may develop. In some cases ventricular arrhythmias can complicate the course and continuous monitoring is obligatory preferrably in intensive/intermediate cardiac units.

In cases of very large pericardial effusion, or when the fluid accumulates rapidly, right heart chambers may become compressed and affect diastolic filling of the right ventricle/right atrium. This results in hemodynamic compromise and cardiac tamponade , a dangerous situation requiring immediate evacuation of the the fluid by pericardiocentesis or by surgical intervention. Before decision on percardiocentesis is established, careful evaluation of the amount of pericardial fluid from the subcostal view is obligatory. If there is not enough fluid anteriorly to the right ventricle during diastole , pericardiocentesis may be risky and perhaps should be avoided. In these cases surgical evacuation of the pericardial fluid in the operating theater is recommended.

In addition to cardiac enzymes (Troponins and CPK) reflecting myocardial damage, inflammatory markers: CRP and ESR usually increase in inflammatory pericardial and myocardial diseases, however, there are rare cases of pericarditis with notmal CRP level.

Echocardiography

Echocardiography exam: In most patients with pericardial inflammatory syndromes, global LV function is preserved. Regional wall motion abnormalities most often occur in the inferior and postero-lateral wall [3]. According to clinical and echocardiographic presentations patients can be classified as pure percarditis, predominant pericarditis, predominant myocarditis and pure myocarditis. Pericardial effusion can often be found, in most cases in small-moderate amount, but can accumulate to a large amount and cause pressure on the cardiac chambers (see above). Absense of pericardial fluid does not exclude percarditis.

Cardiac MRI

Cardiac MRI,[4] can reveal typical findings characteristic of Myocarditis/ Perimyocarditis. During MRI examination, contrast Dotarem , a derivate of gadolinium, is used. Dotarem distributes through blood vessels but cannot penetrate into the cells.

When myocardial cells are damaged as a result of inflammation, contrast cell’s membranes are not intact and contrast dotarem can reach them slowly, with delay,[4] about 10 minutes after the intravenous injection: delayed enhancement can be observed on MRI exam.

In myocarditis, delayed enhancement occurs in the epicardium and in mid-layer but not in the endocardium. This feature is useful in differentiation from ischemic heart disease, where delayed enhancement occurs primarily in the endocardium. Cardiothropic viruses damage first the pericardial layer and then may reach the myocardial tissue, thus regions of delayed enhancement are seen usually in mid-layer and in epicardium. Wall motion abnormalities can be observed in the regions of delayed enhancement.

Cardiothropic viruses are prone to damage specific territories of the heart,[5] that can change the couse of the disease: patients with parvovirus B 19 infection usually ask medical help earlier due to chest pain, have preserved LV function or mild LV dysfunction and delayed enhancement on MRI focused mainly in the epicardial layer of the lateral wall.

In infection with Herpes virus HHV6, clinical picture is usually different, part of the patients present with heart failure and LV dysfunction, delayed enhancement on MRI is located in the antero-septal region more often in the mid-layer.

In mixed infection with Parvovirus B19 and HHV6, patients suffer from heart failure, severe LV dysfunction, and delayed enhancement over the septum.[5]

Biopsy.

Myocardial biopsy for diagnosis of myocarditis was used previously quite often, but today it is seldom in use due to the invasive nature of the procedure, complications, and low diagnostic yield. Since cardiac MRI is available, this is the preferrable procedure for the diagnosis of myocarditis.

Patients presented with less typical chest pain and electrocardiographic changes may require evaluation with cardiac CT or coronary angiography to rule out significant coronary artery disease.

After the basic evaluation [physical examination, electrocardiogram, chest X-ray, echo exam, blood tests for CRP or ESR, Troponin level], in some cases it is necessary to rule out Tuberculosis, underlying malignancy or other systemic diseases.

Identification of an etiologic viral agent is not a routine test. Blood cultures help to diagnose purulent pericarditis, which is usually a severe illness, or other bacterial infections accompanied with pericardial effusion.

Therapy

Patients with suspected pericarditis / myocarditis should be admitted for clinical evaluation, observation and monitoring. Pharmacological management of acute pericarditis is based on anti-inflammatory therapy: NSAIDS, Colchicine, steroids, the specific doses and regimens for each drug, specific indications are summarized.[2][6] Treatment should be planned until complete normalization of CRP. The choice of anti-inflammatory drugs is based on clinical experience, success of the drug in a previous episode of pericarditis, coexistence of coronary artery disease, underlying pathology, and clinical presentation.

In patients with LV dysfunction, ACE inhibitors and beta-blockers should be considered. These patients should be followed with serial echo exams and Holter or continuous monitoring. Physical exercise should be avoided in patients with perimyocarditis for at least 6 weeks and until 6 months according to the clinical course, presentation and LV function.[2] It is highly recommended that atients with pericarditis / myocarditis would be evaluated and treated by cardiologists.


References:

  1. 1.0 1.1 1.2 1.3 Imazio M, Trinchero R: Myopericarditis: Etiology, management, and prognosis. International Journal of Cardiology 127 (2008) 17–26
  2. 2.0 2.1 2.2 2.3 2.4 2.5 Imazio M, Spodick DH, Brucato A, Trinchero R, Adler Y: Controversial Issues in the Management of Pericardial Diseases. Circulation 2010;121;916-928
  3. Leitman M, Tyomkin V, Peleg E, Copel L, Vered Z.Left ventricular function in acute inflammatory peri-myocardial diseases -- new insights and long-term follow-up. Cardiovasc Ultrasound. 2012 Nov 5;10(1):42
  4. 4.0 4.1 Mahrholdt H, Goedecke C, Wagner A, et al. Cardiovascular Magnetic Resonance Assessment of Human Myocarditis: A Comparison to Histology and Molecular Pathology. Circulation 2004;109;1250-1258
  5. 5.0 5.1 Mahrholdt H, Wagner A, Deluigi CC, et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation. 2006;114(15):1581-90.
  6. Maisch B, Seferovic PM, Ristic AD, Erbel R, Rienmuller R, Adler Y, Tomkowski WZ, Thiene G, Yacoub MH, for the Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology. Guidelines on the diagnosis and management of pericardial diseases. Eur Heart J. 2004;25:587– 610.
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