Myocarditis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]

Myocarditis is defined as inflammation of the myocardium. It may present with chest pain, ST segment elevation, elevated biomarkers of myonecrosis, heart failure, and/ or sudden death. Myocarditis can be classified clinicopathologically into fulminant myocarditis, acute myocarditis, chronic active myocarditis, and chronic persistent myocarditis. During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction. Life-threatening causes of myocarditis include carbon monoxide poisoning and Dengue fever. Common causes of myocarditis include infections, Lyme disease, and medications. Idiopathic myocarditis is the most common type of myocarditis and is often suspected to be secondary to a viral infection. Myocarditis must be distinguished from pericarditis and the life threatening condition of ST elevation myocardial infarction. In young adults, up to 20% of all cases of sudden death are due to myocarditis. Myocarditis is slightly more frequent among males than females. 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. 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. The physical examination in patients with myocarditis may reveal tachycardia, a cardiac gallop, mitral regurgitation due to left ventricular dilation, and pedal edema suggestive of cardiac failure. A pericardial friction rub may be noted in presence of concomitant pericarditis, a condition sometimes referred to as myopericarditis.

Myocarditis was first discovered by Jean Baptiste Senac, a French physician, in 1794. The term myocarditis was introduced by German physician Joseph Friedrich Sobernheim in 1837. In 1980s, the World Health Organization and the International Society and Federation of Cardiology were the first to differentiate between myocarditis and other cardiomyopathies. The Dallas criteria was published in 1986 as a guideline for classification of myocarditis.

Myocarditis can be classified based on the causative, histological, and clinicopathological criteria. Causative criteria include three main groups, as well as infectious, immune-mediated, and toxic myocarditis. Based on the type of infiltrating cells myocarditis divided in lymphocytic, eosinophilic, polymorphic, giant cell myocarditis, and cardiac sarcoidosis. Acute, fulminant, chronic active, and chronic persistent are subtypes of clinicopathopogical classification.

During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction.

Life-threatening causes of myocarditis include carbon monoxide poisoning and Dengue fever. Common causes of myocarditis include infections such as Lyme disease and medications. Idiopathic myocarditis is the most common type of myocarditis and is often suspected to be secondary to a viral infection.

Myocarditis must be distinguished from pericarditis and the life threatening condition of ST elevation myocardial infarction.

There are no established risk factors for myocarditis.

There is insufficient evidence to recommend routine screening for myocarditis.

The incidence of myocarditis is approximately 10 to 20 per 100,000 patients worldwide. It commonly affects younger individuals. Yong males are slightly more commonly affected by myocarditis than females. There is no racial predilection to myocarditis. Viral infections especially coxsackie B and enterovirus are the most common cause of myocarditis in developed countries. While, In South America, Chagas’ disease (caused by Trypanosoma cruzi) is the main cause of myocarditis.

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. The prognosis of fulminant myocarditis is better than that of either acute myocarditis or giant cell myocarditis. The presence of syncope, pulmonary hypertension, biventricular dysfunction, left bundle branch block, q waves, AV block, and a left ventricular ejection fraction < 40% are associated with sudden death and cardiac transplantation. Complications of myocarditis include chronic dilated cardiomyopathy, heart block, congestive heart failure, pericarditis, ventricular dysfunction, arrythmias, and sudden cardiac death.

Myocarditis should be suspected in a patient with acute decompensation of cardiac function who is at low risk of ischemic heart disease. A history of a recent (within the preceding 2-4 weeks) viral illness is often elicited in a large number of patients with myocarditis. Cardiac specific symptoms may become apparent usually in the subacute virus-clearing phase. In myocarditis due to drug hypersensitivity, patients may give a history of ingesting an offending drug. 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. Common symptoms of myocarditis include chest pain, pedal edema, palpitations, fever, and joint pains.

There are no specific findings for myocarditis. Patients with myocarditis usually show signs of cardiac dysfunction and underlying diseases. The physical examination in patients with myocarditis may reveal tachycardia, a cardiac gallop, mitral regurgitation due to left ventricular dilation, and pedal edema suggestive of cardiac failure. A pericardial friction rub may be noted in presence of concomitant pericarditis, a condition sometimes referred to as myopericarditis.

Laboratory findings consistent with the diagnosis of myocarditis include elevated markers of myonecrosis, inflammatory markers, and other biomarkers. Markers of myonecrosis include creatine kinase (CK-MB), cardiac troponin I (cTnI) or T (cTnT), lactate dehydrogenase (LDH), alanine transaminase (ALT), and aspartate transaminase (AST). Elevated levels of C-reactive protein and erythrocyte sedimentation rate (ESR), and leukocytosis are suggestive of myocarditis. Serologic markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis. Other auto-antibodies such as ANA and rheumatoid factor may also be detected.

The presence of ST segment elevation in patients with myocarditis can mimic pericarditis and myocardial infarction. Arrhythmias and heart block may also be observed in myocarditis patients. Myocarditis can be distinguished from pericarditis by the presence of PR depression in the patient with pericarditis.

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. 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.

Findings on chest x-ray suggestive of myocarditis include cardiomegaly, cephalization of the pulmonary vessels and, Kerley B-lines in presence of heart failure pericardial thickening in presence of pericarditis, pulmonary edema, and pleural effusion.

Echocardiography in patients with myocarditis allows for serial assessment of left ventricular dysfunction 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). Echocardiography may be helpful in the diagnosis of myocarditis. Findings on an echocardiography suggestive of myocarditis include wall motion abnormalities, systolic and diastolic dysfunction, changes in image texture, pericardial effusion, and functional regurgitation through the AV valves.

Cardiac CT scan may be helpful in the diagnosis of myocarditis. Cardiac CT scan can be used in diagnosis of acute myocarditis ( subepicardial late iodine enhancement), exclusion of acute coronary syndrome by CT angiography, and alternative diagnostic tool in patients with CMR contraindications.

Cardiac MRI is indicated in patients with new or persisting symptoms of chest pain and congestive heart failure, who have evidence of significant myocardial injury, in the absence of or in whom there is a low suspicion of coronary atherosclerosis. Cardiac MRI findings associated with myocarditis include myocardial inflammation, myocardial edema, capillary leak, and reduced left ventricular function. While the CMR 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. CMR has a sensitivity of 76%, specificity of 95.5%, and overall diagnostic accuracy of 85% when any-two of the following three sequences are used, focal and global T2 signal intensity, myocardial global relative enhancement, and delayed gadolinium enhancement.

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. Nuclear imaging may be useful in diagnosis of cardiac sarcoidosis.  

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. Among patients with fulminant myocarditis, placement of either an intra-aortic balloon pump or a left ventricular assist device may be necessary as bridge to recovery. Administration of antimicrobial therapy is recommended for bacterial myocarditis. Immunosuppressive therapy may be effective in the management of giant cell myocarditis, autoimmune myocarditis, and eosinophilic myocarditis. In patients with arrythmias, treatment should be initiated only if arrhythmias are symptomatic or sustained. Myocarditis patients presenting with conduction abnormalities, particularly Mobitz type II and complete heart block require temporary pacemaker usually during the acute phase.

Cardiac transplantation is sometimes required to treat refractory giant cell myocarditis. However, the condition can recur in post-transplant patients.

There are no established measures for the primary prevention of all types of myocarditis. Vaccination against measles, rubella, mumps, poliomyelitis, and influenza could prevent myocarditis secondary to these diseases.

Effective measures for the secondary prevention of myocarditis include, clinical evaluation, ECG, and echocardiography. CMR, cardiac CT scan, nuclear assessment in patients that echocardiography is undiagnostic. Patients should udergo cardiac function assessment at one and six months and yearly after that.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]

Cases of myocarditis have been documented as early as the 1600’s. The term myocarditis was introduced by German physician Joseph Friedrich Sobernheim in 1837.^[1] The Dallas criteria was published in 1986 as a guideline for classification of myocarditis.^[2]

• Cases of myocarditis have been documented as early as the 1600’s.^[1]
• The term myocarditis was introduced by German physician Joseph Friedrich Sobernheim in 1837.^[1]
• The Dallas criteria was published in 1986 as a guideline for classification of myocarditis.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]

Myocarditis can be classified based on the causative, histological, and clinicopathological criteria. Causative criteria include three main groups, as well as infectious, immune-mediated, and toxic myocarditis. Based on the type of infiltrating cells myocarditis divided in lymphocytic, eosinophilic, polymorphic, giant cell myocarditis, and cardiac sarcoidosis. Acute, fulminant, chronic active, and chronic persistent are subtypes of clinicopathopogical classification.

• Myocarditis can be classified based on the causative, histological, and clinicopathological criteria.
• Myocarditis may be classified according to causative criteria into three groups:^{[1][2][3][4][5][6][7][8][9]}
  • Infectious myocarditis
  • Immune-mediated myocarditis
  • Toxic myocarditis

• Myocarditis may be classified according to histological criteria into five groups:^[10][11][2]
  • Lymphatic myocarditis
  • Eosinophilic myocarditis
  • Polymorphic myocarditis
  • Giant cell myocarditis
  • Cardiac sarcoidosis

• Myocarditis may be classified according to clinicopathological four criteria into three groups:^[12][13][14]
  • Fulminant myocarditis
  • Acute myocarditis
  • Chronic active myocarditis
  • Chronic persistent myocarditis

• Myocarditis can be classified based on the causative criteria into immune-mediated myocarditis, infectious myocarditis and toxic myocarditis. bkjvskaljbkjbkjbakj

• Myocarditis can be classified based on the type of infiltrating cells in lymphocytic, eosinophilic, polymorphic, giant cell myocarditis, and cardiac sarcoidosis.

• Fulminant myocarditis: Fulminant myocarditis occurs following a viral prodrome. Fulminant myocarditis presents as acute severe cardiovascular compromise with ventricular dysfunction. On endomyocardial biopsy, there are multiple foci of inflammation.^[15][16]

• 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 develop after 2 to 4 years.

• Chronic persistent myocarditis: Chronic persistent myocarditis has a less distinct onset of the illness. Histologically it is characterized by persistent infiltration and myocyte necrosis. Despite the presence of symptoms, ventricular dysfunction is absent.^[14]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S., Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]

During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction. 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.

Myocarditis is a continuum of three phases of the disease processes with each one evolving into the next.^[1]

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.

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.

• 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 modify the sarcoglycan complex in myocytes leading to ventricular dilation.^[4]

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] The pathogenesis of this hypersensitivity reaction include either an immediate reaction which involves the degranulation of mast cells and basophils mediated by IgE, or a delayed reaction involving the activation of helper T-cells and interleukin-5.

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.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Ogheneochuko Ajari, MB.BS, MS [2] Homa Najafi, M.D.[3]

Life-threatening causes of myocarditis include carbon monoxide poisoning and Dengue fever. Common causes of myocarditis include bacterial infections, Lyme disease, and medications. Idiopathic myocarditis is the most common type of myocarditis and is often suspected to be secondary to a viral infection.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.^[1]

• Carbon monoxide poisoning
• Dengue fever

• Bacterial infections
• Lyme disease^[2]
• Medications
• Viral infections

Disease name] may be caused by [cause1], [cause2], or [cause3].

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Common causes of [disease] include [cause1], [cause2], and [cause3].

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The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].

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The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click here.

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of disease name, however complications resulting from untreated disease name is common.
• Life-threatening causes of [symptom/manifestation] include [cause1], [cause2], and [cause3].
• [Cause] is a life-threatening cause of [disease].

Common causes of [disease name] may include:

• [Cause1]
• [Cause2]
• [Cause3]

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• [Disease name] is caused by an infection with [pathogen name].
• [Pathogen name] is caused by [pathogen name].

Less common causes of [disease name] include:

• [Cause1]
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• [Disease name] is caused by a mutation in the [gene name] gene.

Causes of myocarditis:^{[22][23][24][25][26][27][28][29][30]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]

Myocarditis must be differentiated from other causes of chest pain such as ST elevation myocardial infarction, pericarditis, and unstable angina. Myocarditis must also be differentiated from pulmonary edema and alcoholic cardiomyopathy.

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 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. When used in conjunction with the findings on coronary angiography, cardiac MRI is useful in establishing the diagnosis of myocarditis.^[1]

Cardiac magnetic resonance imaging is also useful in distinguishing between the two diseases 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.

Both diseases present with chest pain and ST segment elevation. The two conditions can be distinguished by the following studies:

While both disorders are associated with ST segment elevation, pericarditis is also associated with PR segment depression.

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.

In patients with myocarditis there will be a focal wall motion abnormalities, while these will be absent in patients with pericarditis. There may be a pericardial effusion in the patient with pericarditis, while myocarditis is not associated with a pericardial effusion.

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].

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[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Varun Kumar, M.B.B.S., Cafer Zorkun, M.D., Ph.D. [2], Maliha Shakil, M.D. [3]

In young adults, up to 20% of all cases of sudden death are due to myocarditis. Myocarditis is slightly more frequent among males than females.^[1]

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.

Myocarditis is slightly more frequent among males than females. This may be due to protection conferred by the ovarian cycle.^[1]

No difference in frequency of myocarditis has been observed between various races.

• Viral infections are the most common cause of myocarditis in developed countries.
• Common viral causes include coxsackie B and enterovirus.
• The frequency of dilated cardiomyopathy secondary to myocarditis is 7.5-10 per 100,000 individuals with enterovirus infections, with the Coxsackie-B viruses being the most common cause.^[2]
• Recent studies show that adenovirus, parvovirus B19, hepatitis C, and human herpes virus 6 were the common causes for myocarditis.^[3][4]
• Myocarditis secondary to lyme disease should be suspected in people traveling to regions where it is endemic, particularly if there are associated conduction abnormalities of the heart.^[5]

In South America, Chagas’ disease (caused by Trypanosoma cruzi) is the main cause of myocarditis. Other causes in developing countries include rheumatic fever^[6] and HIV infection.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Varun Kumar M.B.B.S., Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]

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. The prognosis of fulminant myocarditis is better than that of either acute myocarditis or giant cell myocarditis. The presence of syncope, pulmonary hypertension, biventricular dysfunction, left bundle branch block, q waves, AV block, and a left ventricular ejection fraction < 40% are associated with sudden death and cardiac transplantation. Complications of myocarditis include chronic dilated cardiomyopathy, heart block, congestive heart failure, pericarditis, ventricular dysfunction, arrythmias, and sudden cardiac death.

• The course of viral myocarditis is usually benign and the majority of cases of Coxsackie B virus infection are subclinical.
• Patients presenting with mild ventricular dysfunction secondary to viral myocarditis typically improve within weeks to months and rarely progress to severe ventricular dysfunction, heart block, arrhythmias, or even sudden cardiac death.
• Among patients who present with more advanced left ventricular dysfunction; 50% of patients develop chronic ventricular dysfunction and 25% have spontaneous improvement in ventricular function while the remaining 25% progress to transplantation or death.^[1][2][3]

• Complications of myocarditis include:^[1][2][3]
  • Chronic dilated cardiomyopathy
  • Heart block
  • Congestive heart failure
  • Pericarditis
  • Ventricular dysfunction
  • Arrythmias
  • Sudden cardiac death

• An endomyocardial biopsy is usually obtained in patients presenting with advanced heart failure or arrhythmias. The endomyocardial biopsy can shed light on the prognosis by ascertaining the underlying cause and the histopathologic severity of the disease.

• The markers which can be associated with poor prognosis include:^{[4][5][6][7][8][9]}
  • Fas and Fas ligand (cell death receptors) are associated with apoptotic death of myocytes and are a marker of cardiac dysfunction.
  • Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis.
  • Persistence of the viral genome in the myocardium is associated with worsening of left ventricular ejection fraction.
  • Giant cell myocarditis (GCM) is a less common form of myocarditis which usually occurs in relatively young and healthy adults. It is associated with a poorer prognosis.
  • High levels of interleukin-10 in fulminant myocarditis patients at admission may be predictive of subsequent development of cardiogenic shock (requiring mechanical cardiopulmonary support system) and mortality.

• Despite its worrisome appearance, ST segment elevation suggestive of myocardial infarction is usually self-limited with no overt sequelae.^[10][11]
• In contrast, the presence of either left bundle branch block, q waves suggestive of old infarct or high degree AV block is associated with a poor long term prognosis, development of cardiac failure and the need for cardiac transplantation.

• The clinical manifestations which can associated with poor prognosis (associated with death or cardiac transplantation) include: ^[12][13]
  • Syncope
  • Bundle branch block
  • Ejection fraction <40%
  • Pulmonary hypertension
  • Biventricular dysfunction

• The prognosis in patients with new onset heart failure depends on the degree of ventricular dysfunction.^[1][14]
• The majority of myocarditis patients recover well with treatment. However, approximately 25% of patients develop chronic ventricular dysfunction and 25% of patients will continue to deteriorate.

• In a small series of 15 patients with fulminant myocarditis, 14(93%) survived for 11 years without the need for cardiac transplantation. This suggests that patients with fulminant myocarditis have a good long term prognosis if they survive the acute phase of the disease. In the same series, 132 patients met the criteria for acute myocarditis and 60(45%) of these patients were alive at the end of 11 years without having received a cardiac transplant.^[15]

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