Myocarditis

from Wikipedia, the free encyclopedia
Classification according to ICD-10
I09.0 Rheumatic myocarditis
I40 Acute myocarditis
ICD-10 online (WHO version 2019)

Myocarditis ( inflammation of the heart muscle ) is a collective term for inflammatory diseases of the heart muscle with different causes. A distinction is made between acute and chronic forms of myocardial inflammation, whereby acute myocarditis can turn into chronic. Many inflammations of the heart muscles (myocarditis) are symptom-free; However, myocarditis can also trigger life-threatening cardiac arrhythmias and lead to sudden cardiac death . If the inner lining of the heart (endocardium) and the heart cover (epicardium) are also affected, it is called pancarditis .

Epidemiology

The epidemiology of myocarditis is largely unknown because of the variable symptoms. In the United States, the incidence is estimated at 1–10 / 100,000 population per year. Myocardial involvement is assumed in 1–5% of patients with a viral infection.

causes

Infectious forms

Histopathology of viral myocarditis

Myocarditis can be caused by bacteria, fungi, parasites, and viruses. In Europe and the USA, enteroviruses , especially Coxsackie viruses B1-B5, are responsible for myocarditis in over 50% of cases . A causal relationship has also been shown in some serotypes of the Coxsackie A viruses and the ECHO viruses . In other cases, parvovirus B19 , adenoviruses , influenza viruses and mumps viruses could be isolated from the myocardium.

Bacterial pathogens, including Brucella , Campylobacter species, pneumoniae Chlamydia and Chlamydophila psittaci , clostridial , Corynebacterium diphtheriae , Coxiella burnetii , Ehrlichia , Legionella , monocytogenes Listeria , tuberculosis Mycobacterium , pneumoniae Mycoplasma , Neisseria meningitidis , Pneumococcus , Salmonella , Shigella species, Staphylococcus , Streptococcus pyogenes , Tropheryma whipplei, and Vibrio cholerae , are rare in patients with an intact immune system.

The protozoon Trypanosoma cruzi , the causative agent of Chagas disease , is the main pathogen of myocarditis in South America, but does not play a role in Europe.

Further pathogens are spirochetes ( Borrelia burgdorferi and Leptospira ), rickettsiae , parasites ( Leishmania , Toxoplasma gondii and Toxoplasma canis as well as Trichinae ) and fungi ( Aspergillus , Candida ).

Occasionally, a viral infection of the mother during pregnancy can cause myocarditis in the child, who is then born with heart failure .

Toxic forms

These include myocarditis caused by alcohol consumption (most common) and heavy metals . Other cases are attributed to the toxic effects of drugs, especially chemotherapeutic agents ( anthracyclines , cyclophosphamide , fluorouracil ), as well as barbiturates and antipsychotics .

Autoimmune forms

After the acute phase, which is caused by the immediate cytopathic effects of the virus, a small proportion of patients develop autoimmune-mediated , chronic myocarditis. The form of myocarditis is characterized by circulating autoantibodies that are directed against cardiac myosin and other cardiac antigens. In some cases, this can lead to heart failure and death after developing dilated cardiomyopathy (DCM).

Symptoms

There is no specific key symptom . Many myocarditis remain asymptomatic during the course of the disease. In the other patients, unspecific symptoms such as tiredness , general malaise, palpitations , fever and shortness of breath are in the foreground. Up to 60% of them are preceded by a flu-like infection , mostly of the upper airways.

Acute chest pain occurs in 10–30% of symptomatic patients and cannot be distinguished from acute coronary syndrome . In 5–15% of patients the disease manifests itself in the form of cardiac arrhythmias , in 60–70% as heart failure and in 5–10% as cardiogenic shock . Other heart diseases with the same clinical picture should therefore be excluded from the diagnosis.

Diagnosis

The x-ray only shows an enlarged heart if the course is fulminant. The electrocardiogram often shows first-degree AV blockages , rarely higher ones; Supraventricular and ventricular arrhythmias come in all forms, including life-threatening ventricular tachycardia . Furthermore, ST / T changes and cardiac enzyme courses can resemble those of an acute myocardial infarction .

Echocardiography often shows diastolic dysfunction and, in 20% of patients, mostly a small pericardial effusion . The size of the ventricle only increases rapidly in severe forms. In the case of viral myocarditis, antimyolemmal and / or antisarcolemmal antibodies can be detected in the serum . The myocardial scintigraphy and magnetic resonance imaging of the heart make it possible to detect myocardial necrosis with high sensitivity. Using magnetic resonance imaging mapping procedures, diffuse changes in the myocardium, such as B. fibrosis ( T1-mapping ) or edema ( T2-mapping ) to be recorded exactly. This allows the severity and course to be estimated.

The coronary angiography is, in patients who present themselves as acute coronary syndrome to rule out coronary artery disease carried out on an emergency basis. It is also indicated in patients with significantly reduced left ventricular pump function and is necessary for performing a myocardial biopsy . Myocardial biopsy is the gold standard in diagnosing myocarditis. Because only through a myocardial biopsy can the cause of myocarditis be confirmed and appropriate, personalized therapy initiated. This of course means that the myocardial biopsy should be examined for all possible causes of myocarditis. This includes a histological (what does the tissue look like), immunohistological (which cells are involved? Are there signs of autoimmune genesis) and molecular biological (e.g. PCR methods for analyzing which viruses are involved) examination of the myocardial biopsy. Recently, microRNAs and gene expression profiles have also been used for diagnostics.

course

The mechanisms of the different courses of myocarditis are only partially understood. In half to two thirds of cases, the disease heals spontaneously and no symptoms remain. The assumption that acute myocarditis turns into dilated cardiomyopathy is supported by several studies, but the definitive proof of this is still pending. A favorable prognosis is that of acute coronary syndrome . In terms of mortality, however, the first manifestation as syncope , signs of advanced heart failure or significantly reduced left ventricular function are unfavorable .

therapy

Viral myocarditis

Since viral myocarditis on the one hand often heals spontaneously, on the other hand it can lead to sudden cardiac death within a very short time, strict physical restraint and rhythm monitoring are in the foreground in the acute phase. If heart failure develops , it should be treated appropriately. If inflammatory cardiomyopathy develops ( dilated cardiomyopathy on the basis of myocarditis), after detection of viruses, therapy with interferon- β can be attempted. In the first studies, it was possible to achieve complete virus elimination and an improvement in cardiac output; a standard cannot yet be derived from this.

Arrhythmias that occur during myocarditis rarely require long-term treatment.

Acute non-viral myocarditis

Therapy is carried out according to the antibiogram . If this is not the case or not yet available, so-called calculated antimicrobial therapy is started, for example by administering ceftriaxone and doxycycline .

Chronic myocarditis

For the treatment of chronic myocarditis, ACE inhibitors , AT1 antagonists , diuretics , cardiac glycosides and beta-blockers are used. More specific therapeutic approaches with administration of immunosuppressants such as prednisolone or azathioprine are discussed.

Intravenous administration of immunoglobulins showed no improvement in long-term survival in a study with 62 patients.

See also

literature

  • S2k guidelines for myocarditis of the German Society for Pediatric Cardiology (DGPK). In: AWMF online (as of 2013)
  • BE Strauer, et al .: [Update 2001. Myocarditis-cardiomyopathy]. In: Medical Clinic. Volume 96, Number 10, October 2001, pp. 608-625, ISSN  0723-5003 . PMID 11715333 .
  • MC Savoia, MN Oxanan: Myocarditis and Pericarditis. In: Mandell, Douglas, and Bennett's Principle and Practice of Infectious Diseases. 6th edition 2005.
  • JW Magnani, GW Dec: Myocarditis, current trends in diagnosis and treatment. In: Circulation. Volume 116, 2006, pp. 876-890.
  • U. Kühl, H.-P. Schultheiss: Myocarditis: Early biopsy enables differentiated regenerative therapy . In: Dtsch Arztebl Int . No. 109 (20) , 2012, p. 361-368 ( review article ).
  • Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , p. 33 ( spectrum of pathogens and calculated antimicrobial therapy ).

Web links

Wiktionary: Myocarditis  - explanations of meanings, word origins, synonyms, translations

Individual evidence

  1. ↑ Barbara Naegeli: Myocarditis: Diagnosis and course. In: Cardiovascular Medicine. 2004, 7, pp. 248-257, cardiovascmed.ch ( Memento of the original from November 7, 2017 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. (PDF) @1@ 2Template: Webachiv / IABot / cardiovascmed.ch
  2. ^ NR Rose, A. Herskowitz u. a .: Autoimmune myocarditis: a paradigm of post-infection autoimmune disease. In: Immunology today. Volume 9, Number 4, April 1988, pp. 117-120, doi : 10.1016 / 0167-5699 (88) 91282-0 , PMID 3076766 (Review).
  3. ↑ HS Li, DL Ligon, NR Rose: Genetic complexity of autoimmune myocarditis. In: Autoimmunity Reviews . Volume 7, number 3, January 2008, pp. 168-173, doi : 10.1016 / j.autrev.2007.11.010 , PMID 18190873 , PMC 2233796 (free full text) (review).
  4. ^ NR Rose: Myocarditis: infection versus autoimmunity. In: Journal of clinical immunology. Volume 29, Number 6, November 2009, pp. 730-737, doi : 10.1007 / s10875-009-9339-z , PMID 19826933 (review).
  5. ^ A. Salvi et al .: Clinical presentation and evolution in treated and untreated myocarditis. In: G. Baroldi, F. Camerini, JF Goodwin (Eds.): Advances in cardiomyopathies . Springer, Berlin 1990, ISBN 0-387-51068-0 , pp. 316-324.
  6. ↑ J. Narula et al .: Recognition of acute myocarditis masquerading as acute myocardial infarction. In: N Engl J Med . 1993 Jan 14; 328 (2), pp. 100-104, PMID 8416421
  7. ↑ CL Miklozek et al .: Myocarditis presenting as acute myocardial infarction. In: Am Heart J . 1988 Apr, 115 (4), pp. 768-776, PMID 3354405
  8. ↑ Rocio Hinojar, Lucy Foote, Eduardo Arroyo Ucar, Thomas Jackson, Andrew Jabbour: Native T1 in Discrimination of Acute and Convalescent Stages in Patients With Clinical Diagnosis of Myocarditis: A Proposed Diagnostic Algorithm Using CMR . In: JACC: Cardiovascular Imaging . tape 8 , no. 1 , January 1, 2015, ISSN  1936-878X , p. 37-46 , doi : 10.1016 / j.jcmg.2014.07.016 ( sciencedirect.com [accessed July 28, 2020]).
  9. Jump up ↑ A. D'Ambrosio, G. Patti, A. Manzoli, G. Sinagra, A. Di Lenarda, F. Silvestri, G. Di Sciascio: The fate of acute myocarditis between spontaneous improvement and evolution to dilated cardiomyopathy: a review. In: Heart . 2001 May, 85 (5), pp. 499-504, PMID 11302994 .
  10. ^ A b G. Sinagra, P. Maras, A. D'Ambrosio, D. Gregori, R. Bussani, F. Silvestri et al .: Polimorfismo clinico di presentazione e storia naturale della miocardite attiva: sperienza su 60 casi. In: G Ital Cardiol. 1997, 27, pp. 758-774, PMID 9312504 .
  11. ↑ P. Ammann, B. Naegeli, E. Schuiki, R. Mury, J. Frielingsdorf, O. Bertel: Long-term outcome of acute myocarditis is independent of initial cardiac enzyme release. In: Int J Cardiol 2003, 89, pp 217-222, PMID 12767545 .
  12. ^ A b L. R. Goldberg, J. Suk, KK Patton, MJ Semigran, GW Dec, TG Di Salvo: Predictors of adverse outcome in biopsy-proven myocarditis (abstract). In: J Am Coll Cardiol . 1999, 33 (suppl A), p. 505 A.
  13. ↑ Mewis, Riessen, Spyridopoulos (ed.): Cardiology compact - Everything for ward and specialist examination . 2nd Edition. Thieme, Stuttgart / New York 2006, ISBN 3-13-130742-0 , pp. 413-421 ( Cardiology compact - books.google.de ).
  14. ↑ U. Kuhl, M. Pauschinger, PL Schwimmbeck, C. Lober, HP Schultheiss: Interferon-beta therapy in patients with enteroviral heart muscle disease. In: Zeitschrift für Kardiologie 2000, 89, p. 180.
  15. ↑ U. Kühl et al .: Interferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction . In: Circulation . tape 107 , no. 22 , June 10, 2003, p. 2793-2798 , PMID 12771005 ( circ.ahajournals.org [PDF]).
  16. ↑ N. Schauer: Myokarditis In: Jörg Draeger, Jürgen Kriebel (Ed.) Practical Aviation Medicine. P. 226 ( limited preview in Google Book search).
  17. ↑ DM Mc Namara, R. Holubkov, RC Starling, GW Dec, E. Loh, G. Torre-Amione et al .: Controlled trial of intravenous immune globulin in recent-onset dilated cardiomyopathy. In: IMAC Trial. Circulation. 2001, 103, pp. 2254-2259, PMID 11342473 .