The parasite is transferred by biting insect from Reduviidae family [26]. Afterward, it infects primarily muscle cells (of the myocardium, smooth and skeletal muscles) and ganglionic cells [92], damaged by the parasite´s activity.

The active phase of the disease comes 1 to 2 weeks after the exposure to the transmitter. The course is mostly asymptomatic or mild manifesting with fever, Romanov syndrome (one-sided oedema in eye socket area at the seat of attachment of a transmitter) and lymphadenopathy [93]. The symptoms disappear spontaneously in up to 90 % of patients [92, 93]. The mortality rate in this disease stage is 5 to 10 % as a result of myocarditis or meningoencephalitis [26, 94]. In 30 to 40 % of infected people, the disease progresses in chronic phase what may happen even decades after the contact with the transmitter [26, 92]. In the rest of the patients, the disease progresses in the latent phase with normal cardiological finding [92].

In chronic phase, impairment of the cardiovascular system is the most frequent, but even GIT and urogenital systems may be affected [94]. In case of chronic cardiovascular impairment, the disease progresses in so-called Chagas cardiomyopathy when references describe extensive changes in heart structure and function – myocardial fibrosis, the direct damage of the heart electrical system, ventricular dilatation, production of thrombus and aneurysms of the left ventricular apex [26, 92, 94]. The clinical picture of patients is very variable. Besides above-mentioned changes, there are described even ECG changes like ventricular arrhythmias, AV block of the 1^st degree, ventricular tachycardia, ST and PQ segment changes etc. [92, 93 ,94]. Bilateral heart failure with the predominance of the right-heart failure symptoms is an often complication and sudden cardiac death is also not an exception [92]. Therapy consists primarily of anti-parasitic treatment and therapy of heart failure (ACE inhibitors, beta blockers, diuretics, amiodaron, ICD etc.) and of thromboembolism, [92, 93]. Prognosis is variable and is based on the extent of cardiovascular damage, which is the main cause of mortality in infected patients [93, 95].

Author of the opening picture: Public domain

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References:

26) COOPER L. T., JR., KNOWLTON K. U. Chapter 67: Myocarditis. In.: D.P., ZIPES, MANN D.L., LIBBY P., BONOW R.O. a BRAUNWALD E. (eds.). Braunwald´s Heart Disease: A Textbook of Cardiovascular medic Tenth edition. Philadelphia: Elsevier Saunders, 2015. pp. 1589–1602. ISBN 978-1-4557-5133-4.

91) What is Chagas disease? WHO [online]. -: -, 2016 [cit. 2017-02-09].

92) JR., RASSI a et al. Chagas disease. Lancet. 2010, 375(-), 1388-1402.

93) H., MALIK a et al. The Epidemiology, Clinical Manifestations, and Management of Chagas Heart Disease. Clin. Cardiol. 2015, 38(9), 565-569.

94) BYSTRIANSKY. Kardiovaskulárne postihnutie pri Chagasovej chorobe. Očkování a cestovní medicína. 2015, 6(-), 35-38.

95) -X., LESCURE a et al. Chagas disease: changes in knowledge and management. Lancet Infect Dis. 2010, 10(-), 556-570.

Příspěvek Chagas disease pochází z Myokarditida

Systematic lupus erythematosus (SLE) is a multiorgan systematic disease affecting skin, lungs and cardiovascular and other systems. Cardiac manifestation is present in 50 % of patients and myocarditis specifically in approximately 10 % [75, 76]. Manifestation and symptoms are similar to other myocarditis types. Signs of heart failure may be observed. Similarly, resources describe even non-specific repolarization changes on ECG together with sinus tachycardia and the presence of segmental or global left ventricular hypokinesis, ventricular dilatation, pericardial effusion and decreased EF [75, 77]. According to the references, CMRI proves besides the above-mentioned findings even myocardial fibrosis. Opinions differ in the question of the benefit of EMB [75]. SLE myocarditis is mostly treated with standard heart failure therapy and with immunosuppressive therapy including corticosteroids [76, 77]. In a Chinese study of 25 patients, hospital mortality was 4 % [77].

Inflammatory intestinal diseases (ulcerative colitis and Crohn´s disease) are rarely complicated by myocarditis. Ulcerative colitis and Crohn´s disease are, in some cases, put in association with GCM (see chapter GCM). Their aetiology may include even mesalamine [78] and lack of selenium [79]. Manifestation, diagnosis algorithm, and the findings are similar to those in other types of myocarditis. They may present even under the picture of a cardiogenic shock [78]. No specific therapy is known. Heart failure therapy is administered if necessary, alternatively, in some cases, symptoms may improve after the discontinuing of mesalamine [78, 80].

Coeliac disease is a chronic inflammatory disease of the small intestine. Its sizeable prevalence was detected in both myocarditis (4,4 %,) [81] and idiopathic DCMP (5,7 %), [82]. Pathogenesis of myocarditis in patients with coeliac disease is unclear. Involvement of autoimmune mechanism is described what was proved even by results of an Italian study [81] when in all patients with myocarditis and coeliac disease cardiac auto-antibodies were detected. There are also speculations about the role of other antibodies which are produced in patients with coeliac disease and the changes of intestinal permeability and so influencing of levels of substances involved in the metabolism of cardiomyocytes could also play an important role [81, 83]. Manifestation is variable. Even the death of patients was described in some cases [84]. In the Italian study [81], 5 patients presented with heart failure resisted to standard pharmacotherapy and 4 with ventricular arrhythmias without syncope. In all patients, the gluten-free diet was applied and in patients with heart failure even immunosuppressive therapy because all patients had no infectious agent in the myocardium according to EMB. The therapy led to the improvement in the heart function and general state of health.

Rheumatic fever is a disease affecting different organs (joints, heart, central nervous system), arising on the autoimmune bases after untreated streptococcus infection [76, 88]. Its prevalence is often primarily in developing countries with the prevalence up to 100 cases per 100 000 inhabitants per year [88]. Cardiac impairment is present in up to 50 % of cases [76, 88] including impairment of valves, coronary arteries and carditis when the pericardium, myocardium (presence of Aschoff bodies, [38]) and endocardium are affected to varying degrees and which is also the most severe complication of rheumatic fever [88]. The prevalence of rheumatic heart disease was in 2015 almost 35 million cases [89]. Pathogenesis according to the resources lies primarily in the production of auto-antibodies against myosin and sarcolemma components [88]. The existence of rheumatic myocarditis was questioned several times already [90] because of the absence of well-marked troponin elevation and ECHO parameters changes, but the diagnosis was not completely rejected. Diagnosis of rheumatic myocarditis is thus highly challenging. Patients with rheumatic carditis may manifest even with heart failure or arrhythmias [88]. Therapy includes corticosteroids, salicylates, Penicillium, alternatively heart failure therapy [88]. The issue of rheumatic fever and carditis is far extensive. This chapter summarized only some pieces of knowledge.

Author of the opening picture: Lennart81

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References:

75) MASON J. C. Chapter 84: Rheumatic Diseases and the Cardiovascular System. In.: D.P., ZIPES, MANN D.L., LIBBY P., BONOW R.O. a BRAUNWALD E. (eds.). Braunwald´s Heart Disease: A Textbook of Cardiovascular medicine. Tenth edition. Philadelphia: Elsevier Saunders, 2015. pp. 1843–1862. ISBN 978-1-4557-5133-4.

76) Srdce a systémová onemocnění. ECardio.cz [online]. -: -, – [cit. 2017-02-05].

77) ZHANG a et al. Lupus Myocarditis: A Case–Control Study from China. Chin Med J (Engl) [online]. 2015, 128(19), 2588-2594 [cit. 2017-02-05].

78) Recurrent lymphocytic myocarditis in a young male with ulcerative colitis. Varnavas, Varnavas C et al. “Recurrent Lymphocytic Myocarditis in a Young Male with Ulcerative Colitis.” European Journal of Medical Research 19.1 (2014): 11. PMC. Web. 5 Feb. 2017. [online]. 2014, 19(1), – [cit. 2017-02-05].

79) H., KATSANOS a et al. The heart in inflammatory bowel disease. ANNALS OF GASTROENTEROLOGY. 2002, 15(2), 124-133.

80) ROCZEK a et al. Myopericarditis in a patient with ulcerative colitis treated with mesalamine—Case report and review of the literature. Journal of Cardiology Cases [online]. 2014, 10(-), 104-107 [cit. 2017-02-05].

81) FRUSTACI a et al. Celiac Disease Associated With Autoimmune Myocarditis. Circulation [online]. 2002, 105(22), 2611-2618 [cit. 2017-02-05].

82) ZAHMATKESHAN a et al. Prevalence of coeliac disease in idiopathic dilated cardiomyopathy. Iran J Pediatr [online]. 2014, 24(5), 587-592 [cit. 2017-02-05].

83) ROMAGNOLI a et al. Association between celiac disease and idiopathic dilated cardiomyopathy: a case report. Internal and Emergency Medicine [online]. 2011, 6(2), 125-128 [cit. 2017-02-05].

84) BOSKOVIC a et al. Cardiomyopathy Associated with Celiac Disease in Childhood. Case Rep Gastrointest Med [online]. 2012, 2012(-), – [cit. 2017-02-05].

88) HROBOŇOVÁ V. Kapitola 58: Revmatická horečka In V., CHALOUPECKÝ a et al. Dětská kardiologie. Praha: Galén, 2006. pp. 335-339 ISBN 80-7262-406-5.

89) GLOBAL BURDEN OF DISEASE STUDY 2015. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. 2016, 388(-), 1546-1602, konkrétně 1563.

90) KAMBLOCK a et al. Does rheumatic myocarditis really exists? Systematic study with echocardiography and cardiac troponin I blood levels. European Heart Journal. 2003, 24(-), 855-862.

Příspěvek Myocarditis connected with autoimmune diseases pochází z Myokarditida

Aetiology of myocarditis in HIV positive patients is unclear. Besides a direct viral infection with HIV, myocarditis could be caused by different infections in association with immunosuppression of the immune system (Toxoplasma gondii, Mycobacterium tuberculosis, EBV, Coxsackie B, CMV etc.), [63, 64], autoimmune mechanisms (auto-antibodies production), [65], drug toxicity, nutritive conditions (for example lack of selenium), [66] and mitochondrial dysfunction as a result of viral activity [69]. Even higher levels of TNF alpha, IL-6, and other cytokines were observed in patients.

Manifestation and clinical picture of HIV positive patients with myocarditis are similar to other myocarditis types and also include a wide spectrum from asymptomatic individuals to cases presenting as a sudden death [70].

Treatment of myocarditis in HIV positive individuals is still not standardized including heart failure management, however, still standard heart failure therapy (ACE inhibitors, beta blocker, alternatively other therapeutic options) is recommended, [67, 68]. Some resources state that opportunist infection should be treated aggressively [34]. The role of antiretroviral therapy in the therapy of myocarditis in HIV positive individuals is uncertain. Rather its protective effect is described [66, 67]. Immunological therapy is also not standardized, even though in HIV positive children, therapy with IVIG was connected with the heart function improvement [71]. Controversial is treatment with mechanical supports and with heart transplant [67]. When nutritional deficit occurs, use of selenium, multivitamins and other substances is recommended [34].

Prognosis of patients is generally unclear and often unfavorable. There is a worse prognosis primarily in patients with the development of heart failure [34]. In a study including even 45 patients with HIV induced cardiomyopathy, this group belonged to groups with the worst prognosis and 5-year survival rate of 25 % [72]. Other study described the median of the survival in patients with AIDS and cardiomyopathy 101 days in comparison with 472 days in patients without cardiac manifestation [73]. In a study of HIV positive children, the better prognosis was described [74]. 5-year mortality based on the left ventricular FS score varied between 15 and 55 %.

Author of the opening picture: BruceBlaus

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References:

33) CAMBREA S. C. Chapter 8: Myocarditis in HIV Positive Patients. In: WILSON J. Clinical Handbook of Myocarditis. New Jersey: Foster Academics, 2015. pp. 165-182. ISBN: 978-1-63242-083-1.

34) FISHER S. D., LIPSHULTZ S. E. Cardiovascular Abnormalities in HIV-Infected Individuals.: D.P., ZIPES, MANN D.L., LIBBY P., BONOW R.O. a BRAUNWALD E. (eds.). Braunwald´s Heart Disease: A Textbook of Cardiovascular medicine. Tenth edition. Philadelphia: Elsevier Saunders, 2015. pp. 1624–1635. ISBN 978-1-4557-5133-4.

63) SHIRANI a et al. CARDIOVASCULAR IMAGING IN CLINICAL AND EXPERIMENTAL ACUTE INFECTIOUS MYOCARDITIS. Frontiers in Bioscience. 2003, 8(-), e323 – e336.

64) Cardiac Involvement in the Acquired Immunodeficiency Syndrome: A Multicenter Clinical-Pathological Study. Mary Ann Liebert, Inc. publishers [online]. USA: Mary Ann Liebert, Inc. publishers, 2009 [cit. 2017-02-05].

65) F., CURRIE a et al. Cardiac autoimmunity in HIV related heart muscle disease. Heart [online]. 1998, 79(-), 599-604 [cit. 2017-02-05].

66) H., LUMSDEN a et al. The Causes of HIV-Associated Cardiomyopathy: A Tale of Two Worlds. BioMed Research International [online]. 2016, 2016(-), 9 stránek [cit. 2017-02-05].

67) REMICK a et al. Heart Failure in Patients With Human Immunodeficiency Virus Infection. Circulation [online]. 2014, 129(17), 1781-1789 [cit. 2017-02-05].

68) OLSON L. J. Chapter 22: Myocarditis Associated With Human Immunodeficiency Virus Infection and Acquired Immunodeficiency Syndrome. In: L.T., JR., COOPER, ed. Myocarditis: From Bench to Bedside. USA: Humana Press, 2003. pp. 545–558. ISBN 1-58829-112-X.

69) S., BLOOMFIELD a et al. Human Immunodeficiency Virus and Heart Failure in Low-and Middle-Income Countries. JACC: Heart Failure. 2015, 3(8), 579–590.

70) KISELNIK a et al. Acute Myocarditis and Myopathy as Presenting Manifestations of Human Immunodeficiency Virus Infection. IMAJ [online]. 2015, 17(-), 524-525 [cit. 2017-02-05].

71) E., LIPSHULTZ a et al. Immunoglobulins and Left Ventricular Structure and Function in Pediatric HIV Infection. Circulation [online]. 1995, 92(8), 2220-2225 [cit. 2017-02-05].

72) M., FELKER a et al. Underlying Causes and Long-Term Survival in Patients with Initially Unexplained Cardiomyopathy. The New England Journal of Medicine [online]. 2000, 342(-), 1077-1084 [cit. 2017-02-05].

73) F., CURRIE a et al. Heart muscle disease related to HIV infection: prognostic implications. BMJ [online]. 1994, 309(1605), – [cit. 2017-02-05].

74) D., FISHER a et al. Mild dilated cardiomyopathy and increased left ventricular mass predict mortality: The Prospective P2C2 HIV Multicenter Study. America Heart Journal [online]. 2005, 150(3), 439–447 [cit. 2017-02-05].

Příspěvek Myocarditis in HIV positive patients pochází z Myokarditida

Clinical manifestation of cardiac sarcoidosis is varied. It presents with heart failure under the picture of dilated or restrictive cardiomyopathy and with arrhythmias [50]. In the Finnish study published in 2014 [60], 44 % of patients with cardiac sarcoidosis presented with AV block, 33 % with ventricular tachycardia or fibrillation and 18 % with heart failure. The same study evaluated even ECG, ECHO, CMRI and PET findings, treatment results and mortality. A very often ECG finding was AV block of the 2^nd or 3^rd degree (45 %), RBBB (37 %) and LBBB (21 %). During ECHO examinations, except decreased left ventricular EF in approximately 50 % of patients, even left ventricular dilatation and changes in the dimensions of the interventricular septum were described. There were even some findings of the right ventricular aneurysm [50].

CMRI has an important role in the diagnosis of cardiac sarcoidosis where except above-mentioned findings, even LGE is presented in the most of patients with the localization in basal segments of the interventricular septum and lateral wall of the LV in the epicardium and the middle layer of the myocardium [50]. PET examination is also used when inflammatory activity is detected by 18F-FDG (fluorodeoxyglucose), [50]. The sensitivity of EMB in cardiac sarcoidosis is 20 to 25 % [50]. The sensitivity was in one Canadian patient increased with the previous electroanatomic mapping of the heart ventricle [61].

Like in eosinophilic and giant-cell myocarditis, even in cardiac sarcoidosis, the main therapeutic method is immunosuppressive therapy. This treatment is usually administered in monotherapy or in combination with other immunosuppressive drugs, primarily methotrexate. In the treatment of arrhythmias and prevention of sudden cardiac death, implantation of a permanent pacemaker or ICD is considered [62]. ACE inhibitors, beta-blockers and alternatively diuretics are recommended in heart failure treatment. Digoxin is not commonly recommended [58]. Primarily in patients with advanced heart failure, the heart transplant is sometimes necessary [50]. Prognosis varies in different studies. According to the Finnish study [60], 10-year survival rate including patient without the necessity of heart transplant was 83 % (for comparison with the study from 2003 – 5-year survival rate was 70 %), [49]. Worse prognosis is in patients with an isolated form of cardiac sarcoidosis with an initial manifestation with heart failure with the 10-year survival rate of 52 %.

Author of the opening picture: Yale Rosen from USA

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References:

49) OKURA a et al. A clinical and histopathologic comparison of cardiac sarcoidosis and idiopathic giant cell myocarditis. Journal of the American College of Cardiology [online]. 2003, 41(2), 322 [cit. 2017-02-05].

50) KUBÁNEK a VOSKA L. Obrovskobuněčná myokarditida a sarkoidóza srdce – update 2015. Kardiologická revue – Interní medicína. 17(4), 295-299.

58) T., JR., COOPER. Chapter 18: Cardiac Sarcoidosis. In: L.T., JR., COOPER, ed. Myocarditis: From Bench to Bedside. USA: Humana Press, 2003. pp. 421-436. ISBN 1-58829-112-X.

59) MORIMOTO a et al. Epidemiology of sarcoidosis in Japan. European Respiratory Journal [online]. 2008, 31(-), 372-379 [cit. 2017-02-07].

60) KANDOLIN. Cardiac Sarcoidosis: Epidemiology, Characteristics and Outcome over 25 Years in a Nationwide Study. Circulation [online]. 2014, 2014(-), 1-35 [cit. 2017-02-05].

61) B., NERY a et al. Isolated Cardiac Sarcoidosis: Establishing the Diagnosis With Electroanatomic Mapping-Guided Endomyocardial Biopsy. Canadian Journal of Cardiology. 2013, 2013(29), 1015.e1 – 1015.e3.

62) H., BIRNIE a et al. HRS Expert Consensus Statement on the Diagnosis and Management of Arrhythmias Associated With Cardiac Sarcoidosis. Heart Rhythm. 2014, 11(7), 1304–1323.

Příspěvek Cardiac sarcoidosis pochází z Myokarditida

GCM is characterized by the histopathological finding of giant multinuclear cells, infiltration with eosinophils and T lymphocytes and necrosis of cardiomyocytes.

Giant cells are localized primarily at the edge of the myocardial necrosis [48]. In contrast to sarcoidosis, in GCM there are observed smaller fibrous changes and a minimal number of irregularly shaped granulomas [49, 50]. The presence of bordered granulomas confirms rather the diagnosis of sarcoidosis [51]. These changes do not have to in some cases affect just the ventricular myocardium, but also the myocardium of atriums [48]. GCM is definitively confirmed just with EMB.

GCM prevalence is very low. In the USA, the disease is even written in the list of rare disease [52]. In a retrospective study of patients who underwent EMB, GCM was confirmed just in 4 from 851 performed biopsies [53]. Specifically, in children, its prevalence is even lower. Up to the year 2006, there were just 14 documented cases [54] with the prevalence of females.

Pathogenesis of GCM in not still quite clear. Most likely, it arises on the basis of autoimmune disorder [50]. Up to 20 % of patients had a simultaneous presence of an autoimmune disease (for example Crohn´s disease, ulcerative colitis, autoimmune thyroiditis or myasthenia), [55, 56].

It is often a fatal disease presenting in fulminant form and even with a transition to the cardiogenic shock. In the research of GCM from 1997, 75 % of patients presented with heart failure, 14 % with ventricular tachycardia and 5 % with complete AV block [55]. Simultaneously, the effectiveness of immunosuppressants and corticosteroids therapy, which remain the main therapy of GCM up to the present, was researched. A prolongation of the median of the survival was described in patients with this therapy (12,3 months) in comparison with patients treated just with the heart failure therapy (3 months). The mortality rate of patients or the necessity of heart transplant was even up to 89 % [55]. Similar results were observed even in a study from 2003 with the 5-year survival rate of 22 % including patients without the necessity of the heart transplant [49].

In the Finnish study published in 2012, the 5-year survival rate was 52 % also including patients without the necessity of heart transplant [56].

The relapse of GCM was recorded in 20 to 25 % of patients after the heart transplant. It was mostly suppressed by higher doses of immunosuppressive drugs [54, 57].

Combined immunosuppressive therapy includes according to the resources usually the combination of corticosteroids with azathioprine or mycophenolate and cyclosporine. In the most of patients, ICD is indicated because of a high risk of death due to malignant arrhythmias [56, 57]. There are also many patients where the heart transplant is the only therapeutic option even though there are described some cases when patients were stabilized just with the immunosuppressive and heart failure therapy [57].

Author of the opening picture: Gregory Marcus, MD, MAS, FACC

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References:

48) J., DAVIES a et al. Idiopathic giant cell myocarditis-a distinctive clinico-pathological entity. British Heart Journal [online]. 1975, 1975(37), 192-195 [cit. 2017-02-05].

49) OKURA a et al. A clinical and histopathologic comparison of cardiac sarcoidosis and idiopathic giant cell myocarditis. Journal of the American College of Cardiology [online]. 2003, 41(2), 322 [cit. 2017-02-05].

50) KUBÁNEK a VOSKA L. Obrovskobuněčná myokarditida a sarkoidóza srdce – update 2015. Kardiologická revue – Interní medicína. 17(4), 295-299.

51) T., JR., COOPER. Chapter 17: Idiopathic Giant Cell Myocarditis. In: L.T., JR., COOPER, ed. Myocarditis: From Bench to Bedside. USA: Humana Press, 2003. pp. 405-420. ISBN 1-58829-112-X.

52) Giant Cell Myocarditis. National Organization for Rare Disorders [online]. USA: -, 2006 [cit. 2017-02-07].

53) K., BENNETT a et al. Evaluation of the Role of Endomyocardial Biopsy in 851 Patients With Unexplained Heart Failure From 2000–2009. Circulation: Heart Failure [online]. 2013, 2013(6), 676-684 [cit. 2017-02-05].

54) D., BINHUTI a et al. Cardiac Transplantation for Pediatric Giant Cell Myocarditis. Journal of Heart Lung Transplant. 2006, 2006(25), 474-478.

55) T., JR., COOPER a et al. IDIOPATHIC GIANT-CELL MYOCARDITIS — NATURAL HISTORY AND TREATMENT. The New England Journal of Medicine. 1997, 1997(336), 1860-1866.

56) KANDOLIN a et al. Diagnosis, Treatment, and Outcome of Giant-Cell Myocarditis in the Era of Combined Immunosuppression. Circulation: Heart Failure [online]. 2013, 2013(6), 15-22 [cit. 2017-02-05].

57) A., CHAUDHRY a et al. Modern day management of giant cell myocarditis. International Journal of Cardiology. 2015, 2015(178), 82-84.

Příspěvek Giant-cell myocarditis pochází z Myokarditida

The basic characteristic of the disease in a finding of eosinophilia in blood. Its severity is assessed by the absolute number of eosinophils per mm³. Aetiology of eosinophilic myocarditis includes various agents – antibiotics (penicillin, sulfonamides, cephalosporine etc.), antipsychotics (clozapine), non-steroidal anti-inflammatory drugs (indomethacin), diuretics, some ACE-inhibitors (captopril and enalapril), digoxin, dobutamine, small-pox vaccine and others. Non-pharmacological causes of the eosinophilic heart impairment are parasitic infections, some systematic disorders (primarily Churg Strauss syndrome) and hematological diseases, various malignant diseases and idiopathic hypereosinophilic syndromes [44, 45].

Clinical manifestation and laboratory and imaging methods results are varied and may even detect no pathologies. In most of the patients, peripheral eosinophilia is present, however, its presence is not necessary for the diagnosis. The definitive diagnosis is confirmed by EMB findings [46]. A curiosity of LGE during CMRI examination in eosinophilic myocarditis is its localization in the subendocardial layer. In contrast to ischemic heart disease, the myocardial damage is not limited just in the areas supplied by coronary arteries [47].

Some authors set aside, in addition, acute eosinophilic necrotizing myocarditis accompanied by a distinct eosinophilia, necrosis and oedema of the myocardium and manifesting as fulminant myocarditis [25].

The most important therapeutic measure in patients with eosinophilic myocarditis is the removal of the agent if it is known. In most of the patients with non-infectious type of this myocarditis, immunosuppressive therapy consisting primarily from corticosteroids is indicated [46].

Author of the opening picture: Blausen Medical

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References:

16) KUBÁNEK M., Kapitola 8.2.: Myokarditidy. In: KAUTZNER J., MELENOVSKÝ V., et al. Srdeční selhání – aktuality pro klinickou praxi. Praha: Mladá fronta a.s., 2015. pp. 147–157. ISBN: 978-80-204-3573-6.

25) ABDULLAH, M.A.A., L.P. STRAATMAN a et al. Eosinophilic myocarditis: Case series and review of literature. Canadian Journal of Cardiology. 2006, 22(14), 1233–1237.

44) BAANDRUP. Eosinophilic myocarditis. Herz. 2012, 2012(37), 849-853.

45) E., ECKART a et al. Incidence and Follow-Up of Inflammatory Cardiac Complications After Smallpox Vaccination. Journal of the American College of Cardiology. 2004, 44(1), 201-205.

46) KUCHYNKA a et al. Current Diagnostic and Therapeutic Aspects of Eosinophilic Myocarditis. BioMed Research International [online]. 2016, 2016(-), 6 stran [cit. 2017-02-05].

47) E., PETERSEN a et al. Subendocardial and papillary muscle involvement in a patient with Churg-Strauss syndrome, detected by contrast enhanced cardiovascular magnetic resonance. Heart [online]. 2005, 91(1), e9 [cit. 2017-02-07].

Příspěvek Eosinophilic myocarditis pochází z Myokarditida

It is an uncommon form of myocarditis which is characterized by a fast progression of the disease. Usually in the term of just several days, often one or two, before the first manifestation of the disease, prodrome of a viral infection is quite frequent (fever, myalgia, arthralgia etc.). Patients present with acute heart failure and sometimes even with cardiogenic shock and a rapid decrease of the left ventricular ejection fraction may be observed [16]. Frequent ECHO finding is non-enlarged left ventricle with thickening of its walls [16]. In fulminant myocarditis, it is recommended to exclude giant cell and eosinophilic myocarditis as the cause of the disease, because they require specific therapy (see other chapters). If patients do not respond to the pharmacological treatment and/or their state of health deteriorates rapidly, mechanical cardiac support, including ECMO, is often necessary what then serves either as “bridge to recovery” or “bridge to transplant” [96]. When patients survive the acute stage of heart failure, their prognosis is usually favorable [16, 87]. According to the research from 2000 including 147 patients with myocarditis (14 of them with the fulminant form of myocarditis), the long-term prognosis of patients with fulminant myocarditis is even better than in patients with “classical” acute form. After 11 years, 93 % of patients with fulminant myocarditis (including patients without heart transplant) survived, compared to the group of patients with acute myocarditis with the survival rate of 45 % [87].

Acute myocarditis

Acute myocarditis is a “classical” form of myocarditis which differs from fulminant myocarditis in the milder initial course of the disease and often in the slower manifestation of symptoms. Symptoms of a viral infection (primarily of the respiratory and gastrointestinal system) may be observed in patients even several weeks before the cardiac manifestation. The myocarditis itself usually manifests according to the resources with heart failure, arrhythmias or chest pain mimicking acute coronary syndrome [16, 86].

Chronic myocarditis

It is a long-term damage to the myocardium with inflammatory processes. In the case that this process is connected with the systolic dysfunction and dilatation of the left ventricle, it is called ICMP. Earlier, chronic myocarditis was classified in chronic active form (repeated relapses of acute myocarditis connected with chronic inflammatory changes of the myocardium and with the fibrosis and left ventricular dysfunction) and chronic persisting form (presence of the persisting inflammatory infiltrate and necrosis of cardiomyocytes, however, without signs of the left ventricular dysfunction), [4, 43].

Authors of the opening picture: Video file from Bogabathina H, Olson P, Rathi V, Biederman R (2012). “Cardiac Sarcoidosis or Giant Cell Myocarditis? On Treatment Improvement of Fulminant Myocarditis as Demonstrated by Cardiovascular Magnetic Resonance Imaging”. Case Reports in Cardiology. DOI:10.1155/2012/647041. PMID 24826266. PMC: 4008442.

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References:

4) AL-AQEEDI R.F., Chapter 2: Clinical Presentation. In: WILSON J. Clinical Handbook of Myocarditis. New Jersey: Foster Academics, 2015. pp. 33–69. ISBN: 978-1-63242-083-1.

16) KUBÁNEK M., Kapitola 8.2.: Myokarditidy. In: KAUTZNER J., MELENOVSKÝ V., et al. Srdeční selhání – aktuality pro klinickou praxi. Praha: Mladá fronta a.s., 2015. pp. 147–157. ISBN: 978-80-204-3573-6.

43) M, HOLICKÁ a ŠPINAR J. Myokarditidy. ACTA MEDICINAE. 2013, 2013(7), 68-74.

86) E., AMM a COOPER L.T., JR. Management of myocarditis. Heart Metab. 2014, 62(2014), 8-12.

87) E., MCCARTHY a et al. Long-Term Outcome of Fulminant Myocarditis as Compared with Acute (Nonfulminant) Myocarditis. The New England Journal of Medicine [online]. 2000, 342(-), 690-695 [cit. 2017-02-07].

96) Onemocnění myokardu: Myokarditida, zánětlivá kardiomyopatie. ECardio.cz [online]. -: -, – [cit. 2017-01-30].

Příspěvek Fulminant, acute and chronic myocarditis pochází z Myokarditida

It may be classified based on the aetiology (infectious or non-infectious), further according to the histopathological finding (eosinophilic, lymphocytic, granulomatous, giant-cell), based on the clinical picture and manifestation (for example myocarditis connected with heart failure, arrhythmias etc.), [16, 22, 38]. The most commonly used classification is so-called clinical-pathological evaluation combining histopathological findings with the clinical course of the disease. According to the duration, myocarditis is usually classified in acute and chronic form, however, some authors replaced term chronic myocarditis with the term ICMP [8].

Perimyocarditis is a term used for myocarditis connected with the inflammation of the pericardium.

ICMP itself does not have any specific classification. It is mostly classified on the grounds of the EMB results, thus according to the presence or absence of the agent and inflammation [23, 29].

In the following chapters, there are mentioned “basic” and even rare or in other ways “unique” forms of myocarditis (eosinophilic and giant-cell myocarditis, myocarditis in HIV positive patients etc.). Due to the clear arrangement of the chapters about rare forms of myocarditis, these chapters contain even a brief description of the pathogenesis, if it is known, further the description of the clinical course, diagnostical and therapeutic methods and prognostic data. The aim of these chapters is to point at the heterogeneity of myocarditis.

Author of the opening picture: KGH

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References:

8) ZEMÁNEK D. Kapitola 15: Zánětlivé onemocnění myokardu. In: VESELKA, J. a V.ROHN. Kardiovaskulární medicína [online]. 1. vydání. Brno: Fasta Medica, 2015. ISBN 978-80-88056-00-3.

16) KUBÁNEK M., Kapitola 8.2.: Myokarditidy. In: KAUTZNER J., MELENOVSKÝ V., et al. Srdeční selhání – aktuality pro klinickou praxi. Praha: Mladá fronta a.s., 2015. pp. 147–157. ISBN: 978-80-204-3573-6.

22) SAGAR, Sandeep, Peter P. LIU a Leslie T. COOPER, JR. Myocarditis. Lancet. 2012,379(-), 738–747.

23) SCHULTHEISS, Heinz-Peter, Uwe KÜHL a Leslie T. COOPER, JR. The management of myocarditis. European Heart Journal. 2011, 32(-), 2616–2625.

29 KUCHYNKA, P. Nové diagnostické a terapeutické aspekty zánětlivé kardiomyopatie. Praha, 2011. Disertační práce. 1. LF UK.

38) ŠTEINER, I. Kardiopatologie: pro patology i kardiology. Praha: Galén, 2010. ISBN 978-80-7262-672-4.

Příspěvek Classification of myocarditis and ICMP pochází z Myokarditida