Myocarditis overview: Difference between revisions
(/* The AHA/ACCF/ESC Scientific Statement: The role of Endomyocardial Biopsy in fourteen clinical scenarios{{cite journal| author=Cooper LT, Baughman KL, Feldman AM, Frustaci A, Jessup M, Kuhl U et al.| title=The role of endomyocardial biopsy in th...) |
(/* The AHA/ACCF/ESC Scientific Statement: The role of Endomyocardial Biopsy in fourteen clinical scenarios (DO NOT EDIT) {{cite journal| author=Cooper LT, Baughman KL, Feldman AM, Frustaci A, Jessup M, Kuhl U et al.| title=The role of endomyocardi...) |
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| colspan="1" style="text-align:center; background:LemonChiffon"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIb]] | |||
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|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' New-onset [[heart failure]] of 2 weeks’ to 3 months’ duration associated with a dilated left ventricle, without new [[ventricular arrhythmias]] or [[second degree heart block|second-]] or [[third degree heart block|third-degree heart block]], that responds to usual care within 1 to 2 weeks. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki> | |||
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|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''2.''' [[Heart failure]] of >3 months’ duration associated with a dilated [[left ventricle]], without new [[ventricular arrhythmias]] or [[second degree heart block|second-]] or [[third degree heart block|third-degree heart block]], that responds to usual care within 1 to 2 weeks. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki> | |||
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|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''3.''' Heart failure associated with unexplained [[HCM]]. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki> | |||
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|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''4.''' Suspected [[ARVD/C]]. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki> | |||
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|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''5.''' Unexplained ventricular arrhythmias. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki> | |||
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|colspan="1" style="text-align:center; background:LightCoral"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class III]] (Harm) | |||
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|bgcolor="LightCoral"|<nowiki>"</nowiki>'''1.''' Unexplained [[atrial fibrillation]]. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki> | |||
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==Complications of Endomyocardial Biopsy<ref name="pmid17959655">{{cite journal| author=Cooper LT, Baughman KL, Feldman AM, Frustaci A, Jessup M, Kuhl U et al.| title=The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. | journal=Circulation | year= 2007 | volume= 116 | issue= 19 | pages= 2216-33 | pmid=17959655 | doi=10.1161/CIRCULATIONAHA.107.186093 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17959655 }} </ref><ref name="pmid20713901">{{cite journal| author=Yilmaz A, Kindermann I, Kindermann M, Mahfoud F, Ukena C, Athanasiadis A et al.| title=Comparative evaluation of left and right ventricular endomyocardial biopsy: differences in complication rate and diagnostic performance. | journal=Circulation | year= 2010 | volume= 122 | issue= 9 | pages= 900-9 | pmid=20713901 | doi=10.1161/CIRCULATIONAHA.109.924167 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20713901 }} </ref>== | ==Complications of Endomyocardial Biopsy<ref name="pmid17959655">{{cite journal| author=Cooper LT, Baughman KL, Feldman AM, Frustaci A, Jessup M, Kuhl U et al.| title=The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. | journal=Circulation | year= 2007 | volume= 116 | issue= 19 | pages= 2216-33 | pmid=17959655 | doi=10.1161/CIRCULATIONAHA.107.186093 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17959655 }} </ref><ref name="pmid20713901">{{cite journal| author=Yilmaz A, Kindermann I, Kindermann M, Mahfoud F, Ukena C, Athanasiadis A et al.| title=Comparative evaluation of left and right ventricular endomyocardial biopsy: differences in complication rate and diagnostic performance. | journal=Circulation | year= 2010 | volume= 122 | issue= 9 | pages= 900-9 | pmid=20713901 | doi=10.1161/CIRCULATIONAHA.109.924167 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20713901 }} </ref>== | ||
Revision as of 12:32, 30 October 2012
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Myocarditis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Myocarditis overview On the Web |
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American Roentgen Ray Society Images of Myocarditis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Varun Kumar, M.B.B.S.
Overview
Myocarditis is inflammation of the myocardium. It may present with chest pain, ST segment elevation, elevated biomarkers of myonecrosis, heart failure, and / or sudden death.
Pathophysiology
During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction. Myocarditis is a continuum of three phases of the disease processes with each one evolving into the next:[1]
Phase I: Viral Infection and Replication
Viruses such as coxsackie and enterovirus, get internalized in peripheral tissues and activate the immune system. A few of these viral genomes attach to the immunologic cells which circulate throughout the body and lodge in other organs such as the heart where they further replicate and cause localized tissue destruction.
Phase II: Autoimmune Injury
After the host immune system eliminates the viral genomes from the body, the immune system may remains activated in patients who develop myocarditis. This leads to the development of an autoimmune reaction where T-cells and cytokines target the host tissue such as the myocardium which causes further myocyte damage.
Phase III: Dilated Cardiomyopathy
Cytokines, which are produced in reaction to infection and cell death, are a leading cause of dilated cardiomyopathy. Matrix metalloproteinases, such as gelatinase, collagenases, and elastases may also be activated by cytokines during the autoimmune phase.[2][3] Protease produced by coxsackie virus can also modify the sarcoglycan complex in myocytes[4] leading to ventricular dilation.
Eosinophilic and hypersensitive myocarditis may occur secondary to parasitic infections, drug hypersensitivity or hypereosinophilic syndrome. Eosinophilic infiltration in myocardium lead to release of eosinophilic proteins which increase cellular membrane permeability which in turn leads to cell death.[5][6]
Epidemiology and Demographics
In developed countries, myocarditis is generally due to viral infections such as coxsackie B, enterovirus,adenovirus, parvovirus B19, hepatitis C, and herpes virus 6. In developing countries, myocarditis is generally due to HIV and rheumatic heart disease. In routine autopsies, 1-9% of all patients had evidence of myocardial inflammation. In young adults, up to 20% of all cases of sudden death are due to myocarditis. There is a male predominance.
Natural History, Complications and Prognosis
Myocarditis is usually self limiting and is associated with a good prognosis especially if it is secondary to a viral infection. Patients rarely develop cardiac failure, pulmonary edema, arrhythmias or cardiogenic shock. In some instances, myocarditis may be associated with sudden death. Patients with fulminant myocarditis have a good long term prognosis if they survive the acute phase of the disease.[7] The prognosis of fulminant myocarditis is better than that of either acute myocarditis or giant cell myocarditis.
The presence of left bundle branch block, q waves, AV block, syncope and a left ventricular ejection fraction < 40% are associated with sudden death and cardiac transplantation.[8]
Clinicopathological classification[9]
- Fulminant myocarditis - Fulminant myocarditis occurs following a viral prodrome. Fulminant myocarditis presents as acute severe cardiovascular compromise with ventricular dysfunction. The prognosis is good if the patient survives the acute illness.[7] On endomyocardial biopsy, there are multiple focci of inflammation. Fulminant myocarditis is associated with a non-dilated hypocontractile left ventricle with thick interventricular septum while acute myocarditis (see below) is associated with a dilated hypocontractile left ventricle with normal interventricular septum.[10]
- Acute myocarditis - Acute myocarditis presents with a less distinct onset of the illness. When the patient does present, there is already a decline in left ventricular dysfunction. Acute myocarditis may progress to dilated cardiomyopathy.
- Chronic active myocarditis Chronic active myocarditis has a less distinct onset of the illness. There are clinical and histologic relapses and the development of ventricular dysfunction. Histologically, chronic inflammatory changes with mild to moderate fibrosis may be present.
- Chronic persistent myocarditis - Chronic persistent myocarditis has a less distinct onset ff the illness. Histologically it is characterized by persistent infiltration and myocyte necrosis. Despite the presence of symptoms, ventricular dysfunction is absent.
Differential Diagnosis of the Underlying Causes of Myocarditis
(By organ system)
Diagnosis
Symptoms
The symptoms and the intensity of symptoms associated with myocarditis are variable. Myocarditis may be associated with no symptoms. If symptoms are present,they may be similar to the flu. Patients may present with chest pain as a result of the inflammatory process involving the myocardium or with symptoms of congestive heart failure. Patients may complain of palpitations, a racing heart or syncope. In fulminant myocarditis, patients present with the abrupt onset of flu-like symptoms and the abrupt onset of heart failure symptoms. In chronic and acute myocarditis, the onset of symptoms may be more insidious. Symptoms may include:
- Palpitations
- Chest pain
- Fatigue
- Fever and other signs of infection including headache, muscle aches, sore throat, diarrhea, or rashes
- Joint pain or swelling
- Pedal edema
- Shortness of breath
- Fainting, often related to irregular heart rhythms
- Low urine output
Physical examination
Physical examination in patients with myocarditis may reveal tachycardia, a cardiac gallop, mitral regurgitation and pulmonary edema suggestive of cardiac failure. A pericardial friction rub may be noted in presence of concomitant pericarditis, a condition sometimes referred to as myopericarditis.
Electrocardiographic Findings
The ECG findings in myocarditis are similar to those in pericarditis and myocardial infarction.[30][31] Myocarditis should be suspected in patients who are at low risk for ischemic heart disease and MI and in those patients with normal coronary arteries on coronary angiography.
The ECG findings most commonly seen in myocarditis are:[32]
- Sinus tachycardia
- Diffuse T wave inversions
- ST segment elevation without reciprocal depression. This helps in differentiating myocarditis from infarction particularly when EKG changes are diffuse.
- Low voltage of the QRS complexes may be observed.
- Arrhythmias such as atrial and ventricular ectopic beats, atrial and ventricular tachycardias and atrial fibrillation may also be present and are common in Chagas heart disease.
- Heart block is frequently observed in giant cell myocarditis and cardiac sarcoidosis.
These EKG changes may persist for several months before they resolve spontaneously.
The presence of ST segment elevation in patients with myocarditis can mimic pericarditis and myocardial infarction. Arrhythmias and heart blocks may also be observed in myocarditis patients. Myocarditis can be distinguished from pericarditis by the presence of PR depression in the patient with pericarditis.
Echocardiography
Echocardiography in patients with myocarditis allows for serial assessment of left ventricular dysfunction,[10] and can be used to distinguish fulminant (non-dilated hypocontractile left ventricle with thick interventricular septum) from acute myocarditis (dilated hypocontractile left ventricle with normal interventricular septum).[10]
Echocardiographic findings in myocardits include:
- Wall motion abnormalities[33]
- Systolic dysfunction[33][34]
- Diastolic dysfunction[35]
- Changes in image texture on echocardiogram, i.e. increase in brightness, heterogeneity, and contrast[36]
- Pericardial effusion
- Functional regurgitation through the AV valves may be noted due to ventricular dilation
In general, left ventricular function improves in fulminant myocarditis over a course of approximately 6 months.[10]
Endomyocardial Biopsy
Endomyocardial biopsy remains the gold standard test to evaluate for the presence of and to subclassify the type of myocarditis. A small tissue sample of the endocardium and myocardium is obtained via right sided cardiac catheterization. The sample is then evaluated by a pathologist using immunochemistry and special staining techniques as necessary. Histopathological features include abundant edema in the myocardial interstitium and an inflammatory infiltrate which is rich in lymphocytes and macrophages. Focal destruction of myocytes as a result of the inflammatory process results in left ventricular dysfunction.[32] Endomyocardial biopsy is recommended when the results would identify an underlying disease that is amenable to therapy. Routine performance of endomyocardial biopsy is not recommended in all patients with myocarditis.
2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults[37]
Endomyocardial Biopsy
| Class III (Harm) |
| "1. Endomyocardial biopsy should not be performed in the routine evaluation of patients with heart failure.[38] (Level of Evidence: C) " |
| Class IIa |
| "1. Endomyocardial biopsy can be useful in patients presenting with heart failure when a specific diagnosis is suspected that would influence therapy.[38] (Level of Evidence: C) " |
The AHA/ACCF/ESC Scientific Statement: The role of Endomyocardial Biopsy in fourteen clinical scenarios (DO NOT EDIT) [38]
| Class I |
| "1. New-onset heart failure of <2 weeks’ duration associated with a normal-sized or dilated left ventricle and hemodynamic compromise. (Level of Evidence: B) " |
| "2. New-onset heart failure of 2 weeks’ to 3 months’ duration associated with a dilated left ventricle and new ventricular arrhythmias, second- or third-degree heart block, or failure to respond to usual care within 1 to 2 weeks. (Level of Evidence: B) " |
| Class IIa |
| "1. Heart failure of >3 months’ duration associated with a dilated left ventricle and new ventricular arrhythmias, second- or third-degree heart block, or failure to respond to usual care within 1 to 2 weeks. (Level of Evidence: C) " |
| "2. Heart failure associated with a DCM of any duration associated with suspected allergic reaction and/or eosinophilia. (Level of Evidence: C) " |
| "3. Heart failure associated with suspected anthracycline cardiomyopathy. (Level of Evidence: C) " |
| "4. Heart failure associated with unexplained restrictive cardiomyopathy. (Level of Evidence: C) " |
| "5. Suspected cardiac tumors. (Level of Evidence: C) " |
| "6. Unexplained cardiomyopathy in children. (Level of Evidence: C) " |
| Class IIb |
| "1. New-onset heart failure of 2 weeks’ to 3 months’ duration associated with a dilated left ventricle, without new ventricular arrhythmias or second- or third-degree heart block, that responds to usual care within 1 to 2 weeks. (Level of Evidence: B) " |
| "2. Heart failure of >3 months’ duration associated with a dilated left ventricle, without new ventricular arrhythmias or second- or third-degree heart block, that responds to usual care within 1 to 2 weeks. (Level of Evidence: C) " |
| "3. Heart failure associated with unexplained HCM. (Level of Evidence: C) " |
| "4. Suspected ARVD/C. (Level of Evidence: C) " |
| "5. Unexplained ventricular arrhythmias. (Level of Evidence: C) " |
| Class III (Harm) |
| "1. Unexplained atrial fibrillation. (Level of Evidence: C) " |
Complications of Endomyocardial Biopsy[38][39]
Complications may be as high as 6% as observed in a series where 546 patients with cardiomyopathy underwent right ventricular endomyocardial biopsy.[40] Several other studies reported the incidence of complications to be 0.5 to 1.5%.[39][41]
- Myocardial perforation leading to pericardial tamponade
- Heart block
- Pulmonary embolization
- Pneumothorax
- Nerve injury
- Hematoma
- Tricuspid valve damage
- Arteriovenous fistula
- Deep venous thrombosis
- Bleeding at the puncture site (venous/arterial due to accidental arterial puncture)
- Arrhythmias (supraventricular tachycardia/ventricular tachycardia/complete heart block)
- Tricuspid valve damage
- Coronary artery to right ventricle fistula
Coronary Angiography
Coronary angiography may be helpful in excluding either myocardial ischemia or infarction as the cause of ST segment elevation, elevated cardiac biomarkers, or left ventricular dysfunction.
Cardiac Magnetic Resonance Imaging
Cardiac MRI findings associated with myocarditis include myocardial inflammation, myocardial edema, capillary leak, and reduced left ventricular function. While the cMRI pattern of gadolinium hyperenhancement in ST segment elevation myocardial infarction is transmural and extends from the endocardium to the epicardium, the patchy, non-segmental hyperenhancement pattern in myocarditis in contrast involves the epicardium and spares the subendocardium.[42][43]
Laboratory Findings
Myocardial inflammation can be suspected on the basis of the clinical history along with elevations of:[32]
- Biomarkers of myocardial damage such as troponin or creatine kinase
- Antibodies against viruses known to affect the myocardium and cause myocarditis
- ESR
- C-reactive protein
- Auto antibodies such as ANA and rheumatoid factor
Differentiating Myocarditis from Pericarditis and Myocardial Infarction
Myocarditis presents with chest pain and ST segment elevation. Myocarditis must be distinguished from pericarditis and the life threatening condition of ST elevation myocardial infarction.
Differentiating Myocarditis from ST Segment Elevation Myocardial Infarction
Both diseases present with chest pain, elevated cardiac biomarkers, and focal left ventricular dysfunction. There are two studies that can be used to distinguish the two syndromes:
Coronary Angiography
Coronary angiography can be performed to distinguish myocarditis from ST segment elevation myocardial infarction. ST segment elevation myocardial infarction is associated with either complete or subtotal occlusion of an epicardial coronary artery on coronary angiography.
Cardiac Magnetic Resonance Imaging
Cardiac magnetic resonance imaging is also useful in distinguishing between the two syndromes as well. On cardiac MRI, myocarditis is associated with patchy, non-sentimental, hyperenhancement which is confined to the epicardial layer of the myocardium. In contrast, in ST segment elevation myocardial infarction there is confluent hyperenhancement extending from the endocardium in a distribution that mimics the distribution of the epicardial coronary arteries.
Differentiating Myocarditis from Pericarditis
Both diseases present with chest pain and ST segment elevation. The two conditions can be distinguished by the following studies:
Electrocardiogram
While both disorders are associated with ST segment elevation, pericarditis is also associated with PR segment depression.
Cardiac Biomarkers
Myocarditis is associated with elevations of the CK-MB and the troponin, while pericarditis is not. If pericarditis is associated with underlying inflammation of the myocardium, then this is called myopericarditis. If there is concomitant involvement of both the pericardium and myocardium in myopericarditis, then there are elevations of the cardiac biomarkers.
Echocardiography
In patients with myocarditis there will be a focal wall motion abnormalities, while these will be absent in the patient with pericarditis.
Treatment
Insofar as most viral infections cannot be treated with directed therapy, symptomatic treatment is the mainstay of therapy for patients with viral myocarditis. Supportive therapy includes diuretics and inotropes for left ventricular failure. ACE inhibitor therapy may aid in left ventricular remodeling after the inflammation has begun to resolve. in patients with fulminant myocarditis, placement of an intra-aortic balloon pump or a left ventricular assist device may be necessary as bridge to recovery.
According to 2010 HFSA guidelines,[44] routine use of immunosuppressive therapies in management of myocarditis is not recommended (Strength of Evidence A). Immunotherapy is beneficial in giant cell myocarditis.
Cardiac transplantation is sometimes required to treat refractory giant cell myocarditis. However, the condition can recur in post-transplant patients. Recurrence of biopsy proven giant cell myocarditis between 3 weeks to 9 years was observed in 9 of 34 cardiac transplant patients.[45]
Bacterial infections are treated with antibiotics the selection of which is based upon the nature of the pathogen and its sensitivity to antibiotics.
References
- ↑ Liu PP, Mason JW (2001). "Advances in the understanding of myocarditis". Circulation. 104 (9): 1076–82. PMID 11524405.
- ↑ Ono K, Matsumori A, Shioi T, Furukawa Y, Sasayama S (1998). "Cytokine gene expression after myocardial infarction in rat hearts: possible implication in left ventricular remodeling". Circulation. 98 (2): 149–56. PMID 9679721.
- ↑ Lee JK, Zaidi SH, Liu P, Dawood F, Cheah AY, Wen WH; et al. (1998). "A serine elastase inhibitor reduces inflammation and fibrosis and preserves cardiac function after experimentally-induced murine myocarditis". Nat Med. 4 (12): 1383–91. doi:10.1038/3973. PMID 9846575.
- ↑ Badorff C, Lee GH, Lamphear BJ, Martone ME, Campbell KP, Rhoads RE; et al. (1999). "Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy". Nat Med. 5 (3): 320–6. doi:10.1038/6543. PMID 10086389.
- ↑ Ginsberg F, Parrillo JE (2005). "Eosinophilic myocarditis". Heart Fail Clin. 1 (3): 419–29. doi:10.1016/j.hfc.2005.06.013. PMID 17386864.
- ↑ Amini R, Nielsen C (2010). "Eosinophilic myocarditis mimicking acute coronary syndrome secondary to idiopathic hypereosinophilic syndrome: a case report". J Med Case Reports. 4: 40. doi:10.1186/1752-1947-4-40. PMC 2830978. PMID 20181108.
- ↑ 7.0 7.1 McCarthy RE, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Hare JM; et al. (2000). "Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis". N Engl J Med. 342 (10): 690–5. doi:10.1056/NEJM200003093421003. PMID 10706898.
- ↑ Scartazzini R, Schneider P, Bickel H (1975). "[New beta-lactam antibiotics. Functionalisation of the cephem 3-position with sulfur or nitrogen bearing substituents (author's transl)]". Helv Chim Acta. 58 (8): 2437–50. doi:10.1002/hlca.19750580824. PMID 1194054.
- ↑ Lieberman EB, Hutchins GM, Herskowitz A, Rose NR, Baughman KL (1991). "Clinicopathologic description of myocarditis". J Am Coll Cardiol. 18 (7): 1617–26. PMID 1960305.
- ↑ 10.0 10.1 10.2 10.3 Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL; et al. (2000). "Echocardiographic findings in fulminant and acute myocarditis". J Am Coll Cardiol. 36 (1): 227–32. PMID 10898439.
- ↑ Pursnani A, Yee H, Slater W, Sarswat N (2009). "Hypersensitivity myocarditis associated with azithromycin exposure". Ann Intern Med. 150 (3): 225–6. PMID 19189924.
- ↑ Taliercio CP, Olney BA, Lie JT (1985). "Myocarditis related to drug hypersensitivity". Mayo Clin Proc. 60 (7): 463–8. PMID 4010343.
- ↑ Ben m'rad M, Leclerc-Mercier S, Blanche P, Franck N, Rozenberg F, Fulla Y; et al. (2009). "Drug-induced hypersensitivity syndrome: clinical and biologic disease patterns in 24 patients". Medicine (Baltimore). 88 (3): 131–40. doi:10.1097/MD.0b013e3181a4d1a1. PMID 19440116.
- ↑ Haas SJ, Hill R, Krum H, Liew D, Tonkin A, Demos L; et al. (2007). "Clozapine-associated myocarditis: a review of 116 cases of suspected myocarditis associated with the use of clozapine in Australia during 1993-2003". Drug Saf. 30 (1): 47–57. PMID 17194170.
- ↑ Spear GS (1995). "Eosinophilic explant carditis with eosinophilia: ?Hypersensitivity to dobutamine infusion". J Heart Lung Transplant. 14 (4): 755–60. PMID 7578186.
- ↑ Johnson MR (2004). "Eosinophilic myocarditis in the explanted hearts of cardiac transplant recipients: Interesting pathologic finding or pathophysiologic entity of clinical significance?". Crit Care Med. 32 (3): 888–90. PMID 15090985.
- ↑ Frustaci A, Cuoco L, Chimenti C, Pieroni M, Fioravanti G, Gentiloni N; et al. (2002). "Celiac disease associated with autoimmune myocarditis". Circulation. 105 (22): 2611–8. PMID 12045166.
- ↑ Kühl U, Pauschinger M, Noutsias M, Seeberg B, Bock T, Lassner D; et al. (2005). "High prevalence of viral genomes and multiple viral infections in the myocardium of adults with "idiopathic" left ventricular dysfunction". Circulation. 111 (7): 887–93. doi:10.1161/01.CIR.0000155616.07901.35. PMID 15699250.
- ↑ 19.0 19.1 19.2 19.3 19.4 Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R; et al. (2003). "Detection of viruses in myocardial tissues by polymerase chain reaction. evidence of adenovirus as a common cause of myocarditis in children and adults". J Am Coll Cardiol. 42 (3): 466–72. PMID 12906974.
- ↑ Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W; et al. (2005). "Viral persistence in the myocardium is associated with progressive cardiac dysfunction". Circulation. 112 (13): 1965–70. doi:10.1161/CIRCULATIONAHA.105.548156. PMID 16172268.
- ↑ Rose NR, Neumann DA, Herskowitz A (1992). "Coxsackievirus myocarditis". Adv Intern Med. 37: 411–29. PMID 1558005.
- ↑ Grist NR, Bell EJ (1969). "Coxsackie viruses and the heart". Am Heart J. 77 (3): 295–300. PMID 4887187.
- ↑ Cohen JI, Corey GR (1985). "Cytomegalovirus infection in the normal host". Medicine (Baltimore). 64 (2): 100–14. PMID 2983175.
- ↑ Chimenti C, Russo A, Pieroni M, Calabrese F, Verardo R, Thiene G; et al. (2004). "Intramyocyte detection of Epstein-Barr virus genome by laser capture microdissection in patients with inflammatory cardiomyopathy". Circulation. 110 (23): 3534–9. doi:10.1161/01.CIR.0000148823.08092.0E. PMID 15557377.
- ↑ Matsumori A, Yutani C, Ikeda Y, Kawai S, Sasayama S (2000). "Hepatitis C virus from the hearts of patients with myocarditis and cardiomyopathy". Lab Invest. 80 (7): 1137–42. PMID 10908160.
- ↑ Breinholt JP, Moulik M, Dreyer WJ, Denfield SW, Kim JJ, Jefferies JL; et al. (2010). "Viral epidemiologic shift in inflammatory heart disease: the increasing involvement of parvovirus B19 in the myocardium of pediatric cardiac transplant patients". J Heart Lung Transplant. 29 (7): 739–46. doi:10.1016/j.healun.2010.03.003. PMC 2902647. PMID 20456978.
- ↑ Pankuweit S, Moll R, Baandrup U, Portig I, Hufnagel G, Maisch B (2003). "Prevalence of the parvovirus B19 genome in endomyocardial biopsy specimens". Hum Pathol. 34 (5): 497–503. PMID 12792925.
- ↑ Cassimatis DC, Atwood JE, Engler RM, Linz PE, Grabenstein JD, Vernalis MN (2004). "Smallpox vaccination and myopericarditis: a clinical review". J Am Coll Cardiol. 43 (9): 1503–10. doi:10.1016/j.jacc.2003.11.053. PMID 15120802.
- ↑ Cooper LT, Hare JM, Tazelaar HD, Edwards WD, Starling RC, Deng MC; et al. (2008). "Usefulness of immunosuppression for giant cell myocarditis". Am J Cardiol. 102 (11): 1535–9. doi:10.1016/j.amjcard.2008.07.041. PMC 2613862. PMID 19026310.
- ↑ Miklozek CL, Crumpacker CS, Royal HD, Come PC, Sullivan JL, Abelmann WH (1988). "Myocarditis presenting as acute myocardial infarction". Am Heart J. 115 (4): 768–76. PMID 3354405.
- ↑ Wang K, Asinger RW, Marriott HJ (2003). "ST-segment elevation in conditions other than acute myocardial infarction". N Engl J Med. 349 (22): 2128–35. doi:10.1056/NEJMra022580. PMID 14645641.
- ↑ 32.0 32.1 32.2 Feldman AM, McNamara D (2000). "Myocarditis". N Engl J Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105.
- ↑ 33.0 33.1 Pinamonti B, Alberti E, Cigalotto A, Dreas L, Salvi A, Silvestri F; et al. (1988). "Echocardiographic findings in myocarditis". Am J Cardiol. 62 (4): 285–91. PMID 3400607.
- ↑ Nieminen MS, Heikkilä J, Karjalainen J (1984). "Echocardiography in acute infectious myocarditis: relation to clinical and electrocardiographic findings". Am J Cardiol. 53 (9): 1331–7. PMID 6711435.
- ↑ James KB, Lee K, Thomas JD, Hobbs RE, Rincon G, Bott-Silverman C; et al. (1994). "Left ventricular diastolic dysfunction in lymphocytic myocarditis as assessed by Doppler echocardiography". Am J Cardiol. 73 (4): 282–5. PMID 8296760.
- ↑ Lieback E, Hardouin I, Meyer R, Bellach J, Hetzer R (1996). "Clinical value of echocardiographic tissue characterization in the diagnosis of myocarditis". Eur Heart J. 17 (1): 135–42. PMID 8682119.
- ↑ Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG; et al. (2009). "2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation". Circulation. 119 (14): e391–479. doi:10.1161/CIRCULATIONAHA.109.192065. PMID 19324966.
- ↑ 38.0 38.1 38.2 38.3 Cooper LT, Baughman KL, Feldman AM, Frustaci A, Jessup M, Kuhl U; et al. (2007). "The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology". Circulation. 116 (19): 2216–33. doi:10.1161/CIRCULATIONAHA.107.186093. PMID 17959655.
- ↑ 39.0 39.1 Yilmaz A, Kindermann I, Kindermann M, Mahfoud F, Ukena C, Athanasiadis A; et al. (2010). "Comparative evaluation of left and right ventricular endomyocardial biopsy: differences in complication rate and diagnostic performance". Circulation. 122 (9): 900–9. doi:10.1161/CIRCULATIONAHA.109.924167. PMID 20713901.
- ↑ Deckers JW, Hare JM, Baughman KL (1992). "Complications of transvenous right ventricular endomyocardial biopsy in adult patients with cardiomyopathy: a seven-year survey of 546 consecutive diagnostic procedures in a tertiary referral center". J Am Coll Cardiol. 19 (1): 43–7. PMID 1729344.
- ↑ Holzmann M, Nicko A, Kühl U, Noutsias M, Poller W, Hoffmann W; et al. (2008). "Complication rate of right ventricular endomyocardial biopsy via the femoral approach: a retrospective and prospective study analyzing 3048 diagnostic procedures over an 11-year period". Circulation. 118 (17): 1722–8. doi:10.1161/CIRCULATIONAHA.107.743427. PMID 18838566.
- ↑ Skouri HN, Dec GW, Friedrich MG, Cooper LT (2006). "Noninvasive imaging in myocarditis". J. Am. Coll. Cardiol. 48 (10): 2085–93. doi:10.1016/j.jacc.2006.08.017. PMID 17112998.
- ↑ Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, Alakija P, Cooper LT; et al. (2009). "Cardiovascular magnetic resonance in myocarditis: A JACC White Paper". J Am Coll Cardiol. 53 (17): 1475–87. doi:10.1016/j.jacc.2009.02.007. PMC 2743893. PMID 19389557.
- ↑ Heart Failure Society of America. Lindenfeld J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA; et al. (2010). "HFSA 2010 Comprehensive Heart Failure Practice Guideline". J Card Fail. 16 (6): e1–194. doi:10.1016/j.cardfail.2010.04.004. PMID 20610207.
- ↑ Cooper LT, Berry GJ, Shabetai R (1997). "Idiopathic giant-cell myocarditis--natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators". N Engl J Med. 336 (26): 1860–6. doi:10.1056/NEJM199706263362603. PMID 9197214.