{"product_id":"understanding-myocarditis-causes-symptoms-diagnosis-and-treatment","title":"Understanding Myocarditis: Causes, Symptoms, Diagnosis, and Treatment","description":"\u003cp\u003eMyocarditis is an inflammation of the heart muscle that ranges from a mild, self-limiting illness to a life-threatening emergency requiring mechanical heart support or transplantation. This patient-friendly guide, based on a comprehensive review published in the \u003cem\u003eNew England Journal of Medicine\u003c\/em\u003e, explains how doctors define, diagnose, and treat myocarditis—including the specific symptoms to watch for, the viruses and other triggers responsible, and what the latest research says about who recovers fully and who faces long-term complications like dilated cardiomyopathy and heart failure.\u003c\/p\u003e\n\n\u003ch1\u003eUnderstanding Myocarditis: Causes, Symptoms, Diagnosis, and Treatment\u003c\/h1\u003e\n\n\u003ch2\u003eTable of Contents\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\u003ca href=\"#ddn-key-points\"\u003eKey Points\u003c\/a\u003e\u003c\/li\u003e\n\n  \u003cli\u003e\u003ca href=\"#overview\"\u003eWhat Is Myocarditis?\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#definition\"\u003eHow Doctors Define Myocarditis\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#symptoms\"\u003eSymptoms and How Common Myocarditis Is\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#causes\"\u003eWhat Causes Myocarditis?\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#pathogenesis\"\u003eHow Myocarditis Damages the Heart\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#diagnosis\"\u003eHow Myocarditis Is Diagnosed\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#scenarios\"\u003eClinical Scenarios: A Guide to Diagnosis and Prognosis\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#implications\"\u003eWhat This Means for Patients\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#limitations\"\u003eStudy Limitations\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#recommendations\"\u003eRecommendations for Patients\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#ddn-faq\"\u003eFrequently Asked Questions\u003c\/a\u003e\u003c\/li\u003e\n\u003cli\u003e\u003ca href=\"#source\"\u003eSource Information\u003c\/a\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003c!-- ddn:keypoints:start --\u003e\n\u003ch2 id=\"ddn-key-points\"\u003eKey Points\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003eMyocarditis is heart muscle inflammation that can be mild or life-threatening, with symptoms ranging from fatigue to cardiogenic shock.\u003c\/li\u003e\n\u003cli\u003eViral infections like coxsackievirus B, adenovirus, and parvovirus B19 are major causes; nonviral causes include Lyme disease, Chagas, and HIV.\u003c\/li\u003e\n\u003cli\u003eDiagnosis often uses troponin I, ECG, MRI, and biopsy, but a normal troponin does not rule out myocarditis.\u003c\/li\u003e\n\u003cli\u003ePrognosis varies: fulminant lymphocytic myocarditis often has good recovery with support, but giant-cell myocarditis has poor outcomes.\u003c\/li\u003e\n\u003cli\u003eLong-term risks include dilated cardiomyopathy and heart failure, sometimes appearing years later, especially in children.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003c!-- ddn:keypoints:end --\u003e\n\n\n\u003ch2 id=\"overview\"\u003eWhat Is Myocarditis?\u003c\/h2\u003e\n\n\u003cp\u003eMyocarditis is an inflammatory condition of the heart muscle (the myocardium) that can affect people of all ages. It is a challenging diagnosis because it can look like many other heart conditions. In fact, the symptoms range from mild shortness of breath or chest pain that resolves on its own—without any specific treatment—all the way to cardiogenic shock (a condition where the heart cannot pump enough blood to meet the body's needs) and even death.\u003c\/p\u003e\n\n\u003cp\u003eThe most common long-term consequence of myocarditis is dilated cardiomyopathy with chronic heart failure. Dilated cardiomyopathy is a condition in which the heart's main pumping chamber (the left ventricle) becomes enlarged and weakened, making it harder for the heart to pump blood efficiently.\u003c\/p\u003e\n\n\u003cp\u003eThis review article was written by Dr. Leslie T. Cooper, Jr., from the Division of Cardiovascular Diseases at the Mayo Clinic in Rochester, Minnesota. It was published in the \u003cem\u003eNew England Journal of Medicine\u003c\/em\u003e on April 9, 2009, and it provides a practical, up-to-date approach to evaluating and treating patients with suspected myocarditis. As the author notes, the prognosis and treatment vary significantly depending on the underlying cause, and doctors often use clinical and hemodynamic (blood flow) data to decide when a patient should be referred to a specialist for an endomyocardial biopsy (a procedure in which a small sample of heart tissue is taken for examination).\u003c\/p\u003e\n\n\u003ch2 id=\"definition\"\u003eHow Doctors Define Myocarditis\u003c\/h2\u003e\n\n\u003cp\u003eThe traditional method for diagnosing myocarditis is called the \u003cstrong\u003eDallas pathological criteria\u003c\/strong\u003e. According to these criteria, myocarditis is present when a conventional stained heart-tissue sample shows an inflammatory cellular infiltrate (immune cells invading the heart tissue)—with or without associated myocyte necrosis (death of heart muscle cells).\u003c\/p\u003e\n\n\u003cp\u003eHowever, these Dallas criteria have important limitations:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eVariability in interpretation:\u003c\/strong\u003e Different pathologists may read the same sample differently.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eLack of prognostic value:\u003c\/strong\u003e The criteria do not reliably predict how well a patient will do.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eLow sensitivity:\u003c\/strong\u003e The test often misses cases of myocarditis—partly due to sampling error, since the biopsy needle may miss the inflamed areas of the heart.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eBecause of these limitations, researchers have developed alternative pathological classifications that rely on cell-specific immunoperoxidase stains for surface antigens, such as anti-CD3, anti-CD4, anti-CD20, anti-CD68, and anti–human leukocyte antigen. These are special staining techniques that label different types of immune cells (T lymphocytes, B lymphocytes, and macrophages) to make them visible under a microscope. Criteria based on immunoperoxidase staining have greater sensitivity than the Dallas criteria and may also carry prognostic value—meaning they can help predict patient outcomes.\u003c\/p\u003e\n\n\u003cp\u003eThere is also growing interest in noninvasive diagnostic methods. Preliminary studies suggest that \u003cstrong\u003ecardiac magnetic resonance imaging (MRI)\u003c\/strong\u003e may offer an alternative way to diagnose myocarditis without the risks of biopsy. Regions of myocarditis have been reported to correlate closely with regions of abnormal signal on cardiac MRI. However, there is not yet a consensus on how much value invasive studies such as endomyocardial biopsy provide.\u003c\/p\u003e\n\n\u003cp\u003eBecause the overall prognosis is generally good for patients with mild, acute dilated cardiomyopathy who have suspected myocarditis, recent recommendations have shifted. Instead of biopsying every patient, doctors are now advised to consider endomyocardial biopsy primarily when there is a likelihood of finding \u003cstrong\u003especific treatable disorders\u003c\/strong\u003e.\u003c\/p\u003e\n\n\u003cp\u003eOne of the most useful approaches combines clinical and pathological information. Using \u003cstrong\u003eclinicopathological criteria\u003c\/strong\u003e, doctors can distinguish between two distinct forms of lymphocytic myocarditis:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eFulminant lymphocytic myocarditis:\u003c\/strong\u003e This form has a distinct onset, usually with a viral prodrome (early symptoms like fever, muscle aches, or respiratory\/gastrointestinal symptoms) within 2 weeks before the onset of heart symptoms. It causes hemodynamic compromise (the heart struggles to pump blood), but—perhaps surprisingly—it generally has a good prognosis if the patient survives the acute phase with aggressive support.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eAcute lymphocytic myocarditis:\u003c\/strong\u003e This form often lacks a distinct onset and may or may not involve hemodynamic compromise. However, it more frequently results in death or the need for cardiac transplantation.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eTwo important caveats apply to these clinicopathological criteria. First, even though patients with fulminant lymphocytic myocarditis frequently recover, they are quite ill and typically need treatment with intravenous inotropic agents (medications that strengthen the heart's contractions) or mechanical circulatory support (devices like ventricular assist devices that help the heart pump). Second, because both forms of myocarditis are rare, the prognostic data on heart transplantation and survival are limited to relatively few patients.\u003c\/p\u003e\n\n\u003ch2 id=\"symptoms\"\u003eSymptoms and How Common Myocarditis Is\u003c\/h2\u003e\n\n\u003cp\u003eAcute myocarditis is frequently first diagnosed as nonischemic dilated cardiomyopathy—that is, an enlarged and weakened heart that is \u003cem\u003enot\u003c\/em\u003e caused by blocked coronary arteries. This diagnosis often comes after symptoms have been present for a few weeks to several months. But the manifestations of myocarditis are incredibly varied, ranging from subclinical disease (no noticeable symptoms at all) to sudden death.\u003c\/p\u003e\n\n\u003cp\u003eSome patients present with new-onset atrial or ventricular arrhythmias (irregular heart rhythms), complete heart block (a condition where the electrical signals between the upper and lower chambers of the heart are completely blocked), or an acute myocardial infarction–like syndrome (symptoms that mimic a heart attack, including chest pain and ECG changes, but without blocked arteries).\u003c\/p\u003e\n\n\u003cp\u003eCardiac symptoms are variable and may include:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eFatigue\u003c\/li\u003e\n  \u003cli\u003eDecreased exercise tolerance\u003c\/li\u003e\n  \u003cli\u003ePalpitations (feeling like your heart is racing or skipping beats)\u003c\/li\u003e\n  \u003cli\u003ePrecordial chest pain (pain in the front of the chest over the heart)\u003c\/li\u003e\n  \u003cli\u003eSyncope (fainting)\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eChest pain in acute myocarditis can result from an associated pericarditis (inflammation of the sac surrounding the heart) or, occasionally, from coronary-artery spasm (a temporary tightening of the arteries that supply blood to the heart muscle).\u003c\/p\u003e\n\n\u003cp\u003eAlthough a viral prodrome with fever, myalgia (muscle aches), and respiratory or gastrointestinal symptoms is classically associated with myocarditis, the reported symptoms are highly variable. In the \u003cstrong\u003eEuropean Study of the Epidemiology and Treatment of Inflammatory Heart Disease\u003c\/strong\u003e, researchers screened 3,055 patients with suspected acute or chronic myocarditis. Here is what they found:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003e72%\u003c\/strong\u003e had dyspnea (shortness of breath)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e32%\u003c\/strong\u003e had chest pain\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e18%\u003c\/strong\u003e had arrhythmias\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eMost studies of acute myocarditis report a slight preponderance in male patients. This may be due to a protective effect of natural hormone variations on immune responses in women. The clinical presentation in children differs from that in adults—children often have a more fulminant (sudden and severe) presentation.\u003c\/p\u003e\n\n\u003cp\u003eBecause of this wide spectrum of clinical presentations, doctors need to consider myocarditis in the differential diagnosis (the list of possible causes) for many cardiac syndromes. This is particularly important because most people who present with acute dilated cardiomyopathy and myocarditis have relatively mild disease that resolves with few short-term sequelae (after-effects). However, certain clinical clues point to a higher risk for a more difficult course. These include:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eRash, fever, peripheral eosinophilia\u003c\/strong\u003e (an elevated count of eosinophils, a type of white blood cell), or a \u003cstrong\u003etemporal relationship with recently initiated medications\u003c\/strong\u003e—these suggest a possible hypersensitivity myocarditis (an allergic-type reaction to a drug).\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eGiant-cell myocarditis\u003c\/strong\u003e should be considered in patients with acute dilated cardiomyopathy associated with thymoma (a tumor of the thymus gland), autoimmune disorders, ventricular tachycardia (a dangerously fast heart rhythm), or high-grade heart block.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eCardiac sarcoidosis\u003c\/strong\u003e should be suspected in patients with chronic heart failure, dilated cardiomyopathy plus new ventricular arrhythmias, second-degree or third-degree heart block, or who do not respond to standard care.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe true incidence of myocarditis in the community is unknown. Endomyocardial biopsy is used infrequently because of perceived risks and the lack of a widely accepted, sensitive histologic (tissue) standard. Seroepidemiologic data (studies of antibodies in populations) are difficult to interpret because of the heterotypic (cross-reactive) effect of enteroviruses, which may cause an amnestic antibody response to other coxsackievirus B strains—meaning a previous infection with one virus can falsely elevate antibody levels to a related virus.\u003c\/p\u003e\n\n\u003cp\u003eThat said, the observation that viral genomes (genetic material from viruses) are more common in cardiac tissue from patients with chronic dilated cardiomyopathy than in tissue from patients with valvular or ischemic cardiomyopathy supports the concept that viral myocarditis leads to a substantial disease burden in the community.\u003c\/p\u003e\n\n\u003cp\u003eMyocarditis is also an important cause of \u003cstrong\u003esudden death\u003c\/strong\u003e and of \u003cstrong\u003echildhood cardiomyopathy\u003c\/strong\u003e. A recent long-term study of pediatric myocarditis demonstrated that the greatest burden of the disease may not become apparent for \u003cstrong\u003e6 to 12 years after diagnosis\u003c\/strong\u003e, when children die or need to undergo cardiac transplantation for chronic dilated cardiomyopathy.\u003c\/p\u003e\n\n\u003ch2 id=\"causes\"\u003eWhat Causes Myocarditis?\u003c\/h2\u003e\n\n\u003ch3\u003eViral Infections\u003c\/h3\u003e\n\n\u003cp\u003eViral and postviral myocarditis remain major causes of acute and chronic dilated cardiomyopathy. Seroepidemiologic and molecular studies linked \u003cstrong\u003ecoxsackievirus B\u003c\/strong\u003e to outbreaks of myocarditis from the 1950s through the 1990s. The spectrum of viruses detected in endomyocardial biopsy samples has shifted over time:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eIn the late 1990s: \u003cstrong\u003ecoxsackievirus B → adenovirus\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eIn the past 5 years (relative to the 2009 publication): \u003cstrong\u003eparvovirus B19\u003c\/strong\u003e and other viruses, according to reports from the United States and Germany\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eIn Japan, and in a serologic study in the United States, \u003cstrong\u003ehepatitis C virus\u003c\/strong\u003e was also linked to myocarditis and dilated cardiomyopathy. Many other viruses have been associated less frequently with myocarditis, including:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eEpstein–Barr virus (the virus that causes mononucleosis)\u003c\/li\u003e\n  \u003cli\u003eCytomegalovirus\u003c\/li\u003e\n  \u003cli\u003eHuman herpesvirus 6\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe large number of observations linking viruses to myocarditis has led to ongoing treatment trials of antiviral therapy in patients with virus-associated cardiomyopathy.\u003c\/p\u003e\n\n\u003ch3\u003eOther Infectious Causes\u003c\/h3\u003e\n\n\u003cp\u003eBeyond viruses, several other infectious causes deserve consideration in patients with acute or chronic cardiomyopathy:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eBorrelia burgdorferi (Lyme disease):\u003c\/strong\u003e Myocarditis can result from this tick-borne infection. Patients with Lyme myocarditis are occasionally coinfected with ehrlichia or babesia (other tick-borne organisms). Lyme myocarditis should be suspected in patients with a history of travel to endemic regions or a tick bite, particularly if they also have atrioventricular conduction abnormalities (problems with the electrical system of the heart).\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eTrypanosoma cruzi (Chagas disease):\u003c\/strong\u003e In rural Central and South America, this parasitic infection can present as acute myocarditis or chronic cardiomyopathy, sometimes with right bundle-branch block or left anterior fascicular block (specific ECG abnormalities). Echocardiography or contrast ventriculography may reveal a left ventricular apical aneurysm (a bulge in the lower tip of the heart's pumping chamber), regional wall-motion abnormalities, or diffuse cardiomyopathy.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHIV (human immunodeficiency virus):\u003c\/strong\u003e Myocarditis is the most common cardiac pathological finding at autopsy of patients infected with HIV, with a prevalence of \u003cstrong\u003e50% or more\u003c\/strong\u003e. Cardiomyopathy in HIV patients may be caused by inhibition of cardiac contractility by HIV type 1 glycoprotein 120, coinfections, or antiviral medications.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch3\u003eDrug-Induced Hypersensitivity and Eosinophilic Myocarditis\u003c\/h3\u003e\n\n\u003cp\u003eDrug-induced hypersensitivity reactions and systemic hypereosinophilic syndromes (conditions with abnormally high levels of eosinophils) can cause a specific form of myocarditis. This often responds to withdrawal of the offending agent or to treatment of the underlying disorder, though adjuvant corticosteroid therapy is often required.\u003c\/p\u003e\n\n\u003cp\u003eNumerous medications have been implicated in hypersensitivity myocarditis, including:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eSome anticonvulsants (seizure medications)\u003c\/li\u003e\n  \u003cli\u003eSome antibiotics\u003c\/li\u003e\n  \u003cli\u003eSome antipsychotics\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003e\u003cstrong\u003eEosinophilic myocarditis\u003c\/strong\u003e is characterized by a predominantly eosinophilic infiltrate in the myocardium. It may occur in association with systemic diseases such as:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eThe hypereosinophilic syndrome\u003c\/li\u003e\n  \u003cli\u003eThe Churg–Strauss syndrome (a rare autoimmune condition causing inflammation of blood vessels)\u003c\/li\u003e\n  \u003cli\u003eLöffler's endomyocardial fibrosis (a condition causing thickening and scarring of the heart lining)\u003c\/li\u003e\n  \u003cli\u003eCancer\u003c\/li\u003e\n  \u003cli\u003eParasitic, helminthic (worm), or protozoal infections\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eEosinophilic myocarditis has also been reported after vaccination for several diseases, including smallpox. Clinical manifestations include congestive heart failure, endocardial and valvular fibrosis (scarring of the heart lining and valves), and endocardial thrombi (blood clots inside the heart).\u003c\/p\u003e\n\n\u003cp\u003eA rare disorder, \u003cstrong\u003eacute necrotizing eosinophilic myocarditis\u003c\/strong\u003e, is an aggressive form with an acute onset and a high death rate.\u003c\/p\u003e\n\n\u003ch3\u003eGiant-Cell Myocarditis and Cardiac Sarcoidosis\u003c\/h3\u003e\n\n\u003cp\u003eTwo idiopathic (of unknown cause) and histologically similar disorders—\u003cstrong\u003egiant-cell myocarditis\u003c\/strong\u003e and \u003cstrong\u003ecardiac sarcoidosis\u003c\/strong\u003e—are rare but important causes of cardiomyopathy.\u003c\/p\u003e\n\n\u003cp\u003eGiant-cell myocarditis is an acute disorder with a high risk of death or need for cardiac transplantation. It is considered primarily autoimmune in nature because of its association with a variety of autoimmune disorders, thymoma, and drug hypersensitivity. Giant-cell myocarditis is sometimes distinguished from the much more common postviral myocarditis by the presence of ventricular tachycardia, heart block, and a downhill clinical course despite optimal clinical care.\u003c\/p\u003e\n\n\u003cp\u003ePatients who present with apparently chronic dilated cardiomyopathy yet with \u003cstrong\u003enew ventricular arrhythmias\u003c\/strong\u003e, \u003cstrong\u003esecond-degree or third-degree heart block\u003c\/strong\u003e, or \u003cstrong\u003eno response to optimal care\u003c\/strong\u003e are more likely to have cardiac sarcoidosis—a granulomatous myocarditis (inflammation with formation of granulomas, which are clusters of immune cells).\u003c\/p\u003e\n\n\u003ch3\u003eMyocarditis Alongside Other Heart Conditions\u003c\/h3\u003e\n\n\u003cp\u003eMyocarditis can occur together with other cardiomyopathies and may worsen the clinical course. For example:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eThe prognosis in \u003cstrong\u003ecardiac amyloidosis\u003c\/strong\u003e (a condition where abnormal proteins build up in the heart) is much worse if histologic evidence of myocarditis is present.\u003c\/li\u003e\n  \u003cli\u003eMyocarditis has been associated with clinical deterioration in \u003cstrong\u003ehypertrophic cardiomyopathy\u003c\/strong\u003e (a condition where the heart muscle becomes abnormally thick), and in such cases, evidence of a persistent viral genome may be found in the myocardium.\u003c\/li\u003e\n  \u003cli\u003eA high percentage of patients with \u003cstrong\u003earrhythmogenic right ventricular cardiomyopathy or dysplasia\u003c\/strong\u003e (a genetic condition affecting the heart muscle) have associated myocarditis. Some of these cases are linked to viral infection, though the prognostic value of this is not known.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eResearchers have also reported that active coxsackievirus B infection was present in \u003cstrong\u003eup to 40%\u003c\/strong\u003e of patients who died of acute myocardial infarction (heart attack). In these patients, the involved cardiomyocytes showed evidence of cytoskeletal disruption (damage to the internal structure of heart muscle cells).\u003c\/p\u003e\n\n\u003ch2 id=\"pathogenesis\"\u003eHow Myocarditis Damages the Heart\u003c\/h2\u003e\n\n\u003cp\u003eMost of what we know about the molecular pathogenesis (the biological mechanisms by which the disease develops) of viral and autoimmune myocarditis comes from rodent models and isolated cell systems, rather than from studies of human tissue. In these models, viruses appear to enter cardiac myocytes (heart muscle cells) or macrophages through specific receptors and coreceptors.\u003c\/p\u003e\n\n\u003cp\u003eFor example, the receptor for coxsackievirus B and adenoviruses 2 and 5 is the \u003cstrong\u003ehuman Coxsackie adenovirus receptor\u003c\/strong\u003e. A coreceptor that plays a role in viral entry for serotypes B1, B2, and B5 is the \u003cstrong\u003ecoxsackievirus B coreceptor decay-accelerating factor\u003c\/strong\u003e—and it appears that differential binding to this coreceptor influences viral virulence (how aggressive the virus is).\u003c\/p\u003e\n\n\u003cp\u003eThe virulence of coxsackievirus B is also modified by:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eVariations in its viral genome\u003c\/li\u003e\n  \u003cli\u003eHost factors, such as \u003cstrong\u003eselenium deficiency\u003c\/strong\u003e and \u003cstrong\u003emercury exposure\u003c\/strong\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eA better understanding of the genetic and environmental determinants of virulence is needed to understand why the great majority of infections with \"cardiotropic\" (heart-preferring) viruses—including enterovirus, adenovirus, and parvovirus B19—do not cause cardiomyopathy.\u003c\/p\u003e\n\n\u003cp\u003eThe \u003cstrong\u003einnate immune response\u003c\/strong\u003e (the body's first-line, non-specific defense against infection) is essential early during an infection. Viruses, streptococcal M protein, and certain host proteins can trigger this response through several mechanisms involving toll-like receptors and pattern-recognition receptors in patients with tissue injury. The development of myocarditis requires \u003cstrong\u003eMyD88\u003c\/strong\u003e, a key protein in dendritic-cell toll-like receptor signaling. Coxsackievirus B infection:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eUp-regulates toll-like receptor 4 on macrophages\u003c\/li\u003e\n  \u003cli\u003eStimulates the maturation of antigen-presenting cells (cells that show foreign proteins to the immune system)\u003c\/li\u003e\n  \u003cli\u003eLeads to proinflammatory cytokine release\u003c\/li\u003e\n  \u003cli\u003eDecreases regulatory T-cell function\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe production of increased levels of type 1 helper T (Th1) and type 2 helper T (Th2) cytokines, which occurs \u003cstrong\u003e6 to 12 hours\u003c\/strong\u003e into the innate immune response, is associated with the development of cardiomyopathy. In other words, the \u003cem\u003enature\u003c\/em\u003e of the initial immune response can determine what happens later with the more specific T-cell and B-cell responses. It is not yet known whether an autoreactive immune response (where the immune system attacks the body's own tissues) will lead to viral clearance and normal heart function, or ultimately progress to chronic immune-mediated cardiomyopathy, in any given patient.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eCD4+ T lymphocytes\u003c\/strong\u003e (a type of white blood cell) are key mediators of cardiac damage in experimental autoimmune myocarditis. Circulating T cells that have a low avidity (weak attraction) for self-antigens are normally harmless, but they can cause immune-mediated heart disease if stimulated with large amounts of self-antigens. T-cell responses associated with the production of both Th1 and Th2 cytokines have been implicated in the pathogenesis of myocarditis after viral infection. More recently, a third T-helper subgroup—\u003cstrong\u003eTh17 cells\u003c\/strong\u003e, which produce \u003cstrong\u003einterleukin-17\u003c\/strong\u003e—has also been implicated in myocarditis. Both CD4+ and CD8+ T cells are important in a murine (mouse) model of coxsackievirus B myocarditis.\u003c\/p\u003e\n\n\u003cp\u003eThe prominent role of T lymphocytes in multiple models of experimental myocarditis supports the rationale for using \u003cstrong\u003eanti–T-cell therapy\u003c\/strong\u003e in severe human cardiomyopathy with prominent autoimmune features.\u003c\/p\u003e\n\n\u003cp\u003eCirculating CD4+ T cells are normally kept in check by at least one subgroup of regulatory T cells (T\u003csub\u003ereg\u003c\/sub\u003e). Research by Ono and colleagues demonstrated that a subgroup of regulatory T cells that express CD4, the transcription factor forkhead box p3 (FOXP3), and a high level of the corticosteroid-induced tumor necrosis factor receptor can influence the course of autoimmune myocarditis. \u003cstrong\u003eCD4+CD25+FOXp3+ T cells\u003c\/strong\u003e are also important negative regulators of inflammation in coxsackievirus B myocarditis. Notably, regulatory T-cell subgroups have not yet been studied in human myocarditis—this is a gap in our knowledge.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eAutoantibodies\u003c\/strong\u003e (antibodies that attack the body's own tissues) to a variety of cardiac antigens are common in suspected or histologically confirmed lymphocytic myocarditis and dilated cardiomyopathy. Streptococcal M protein and coxsackievirus B share epitopes (the specific parts of an antigen that antibodies recognize) with cardiac myosin, an intracellular protein in heart muscle cells. Cross-reactive antibodies may result in the production of autoantibodies through this \u003cstrong\u003eantigenic mimicry\u003c\/strong\u003e—the body mistakes its own proteins for the invader. After the virus is cleared, cardiac myosin may provide an endogenous (internal) source of antigen in chronic myocarditis and stimulate chronic inflammation through autoimmune mechanisms. Studies over the past decade have also described cross-reactivity between cardiac myosin and \u003cstrong\u003elaminin\u003c\/strong\u003e, a protein on the surface of human cells.\u003c\/p\u003e\n\n\u003ch2 id=\"diagnosis\"\u003eHow Myocarditis Is Diagnosed\u003c\/h2\u003e\n\n\u003ch3\u003eBiomarkers (Blood Tests)\u003c\/h3\u003e\n\n\u003cp\u003eBiomarkers of cardiac injury are elevated in a minority of patients with acute myocarditis but may help confirm the diagnosis. \u003cstrong\u003eTroponin I\u003c\/strong\u003e—a protein released into the blood when heart muscle is damaged—has high specificity (\u003cstrong\u003e89%\u003c\/strong\u003e) but limited sensitivity (\u003cstrong\u003e34%\u003c\/strong\u003e) in the diagnosis of myocarditis. In plain terms, if troponin I is elevated, it strongly suggests heart muscle damage; but a normal level does not rule out myocarditis, because the test misses about two-thirds of cases.\u003c\/p\u003e\n\n\u003cp\u003eClinical and experimental data suggest that increased levels of cardiac troponin I are more common than increased levels of \u003cstrong\u003ecreatine kinase MB\u003c\/strong\u003e (another marker of heart muscle damage) in acute myocarditis.\u003c\/p\u003e\n\n\u003cp\u003eA few serologic and imaging biomarkers have been associated with poor clinical outcomes. For example:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eRelatively high serum levels of \u003cstrong\u003eFas ligand\u003c\/strong\u003e (a protein involved in cell death signaling) may predict an increased risk of death\u003c\/li\u003e\n  \u003cli\u003eRelatively high serum levels of \u003cstrong\u003einterleukin-10\u003c\/strong\u003e (an anti-inflammatory cytokine) may also predict an increased risk of death\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eHowever, these assays are not widely available in clinical practice.\u003c\/p\u003e\n\n\u003ch3\u003eElectrocardiography (ECG)\u003c\/h3\u003e\n\n\u003cp\u003eIn acute myocarditis, the electrocardiogram (a test that records the electrical activity of the heart) may show \u003cstrong\u003esinus tachycardia\u003c\/strong\u003e (a fast heart rate originating from the normal pacemaker) with nonspecific ST-segment and T-wave abnormalities. Occasionally, the ECG changes are suggestive of an acute myocardial infarction (heart attack) and may include:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eST-segment elevation\u003c\/li\u003e\n  \u003cli\u003eST-segment depression\u003c\/li\u003e\n  \u003cli\u003ePathologic Q waves\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003ePericarditis (inflammation of the sac around the heart) can also produce ECG changes that overlap with those of myocarditis, and the two conditions often occur together.\u003c\/p\u003e\n\n\u003ch2 id=\"scenarios\"\u003eClinical Scenarios: A Guide to Diagnosis and Prognosis\u003c\/h2\u003e\n\n\u003cp\u003eThe review article includes a valuable table outlining seven distinct clinical scenarios for the diagnosis of myocarditis. Each scenario combines the duration of illness, the pathological findings likely on biopsy, the expected prognosis, and the recommended treatment approach. Here is a plain-language explanation of each scenario:\u003c\/p\u003e\n\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHeart-attack-like syndrome with normal coronary arteries (illness lasting hours to days):\u003c\/strong\u003e Biopsy typically shows active lymphocytic myocarditis or, rarely, necrotizing eosinophilic myocarditis or giant-cell myocarditis. If lymphocytic myocarditis is present on biopsy, the prognosis is good. Treatment is supportive (managing symptoms and supporting heart function).\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHeart failure with normal-sized or dilated left ventricle and hemodynamic compromise (illness lasting less than 2 weeks):\u003c\/strong\u003e Biopsy usually shows active lymphocytic myocarditis or, less commonly, necrotizing eosinophilic myocarditis or giant-cell myocarditis. The prognosis is good in fulminant lymphocytic myocarditis, but acute care often requires inotropic medications (drugs that strengthen the heart's contractions) or mechanical circulatory support (devices that help the heart pump). Treatment is supportive, with possible use of corticosteroids or intravenous immune globulin (IVIG) in children.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHeart failure with dilated left ventricle plus new ventricular arrhythmias, high-degree heart block, or lack of response to usual care within 1 to 2 weeks (illness lasting weeks to months):\u003c\/strong\u003e Biopsy may reveal giant-cell myocarditis, eosinophilic myocarditis, or lymphocytic myocarditis. The prognosis is poor, with a high likelihood of death or need for cardiac transplantation if giant-cell myocarditis is found. Treatment is variable, guided by the histopathological (tissue) results.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHeart failure with dilated left ventricle without new ventricular arrhythmias or high-degree heart block (illness lasting weeks to months):\u003c\/strong\u003e Nonspecific changes are most likely on biopsy, with viral genomes present in \u003cstrong\u003e25 to 35%\u003c\/strong\u003e of patients and lymphocytic myocarditis (by Dallas criteria) in about \u003cstrong\u003e10%\u003c\/strong\u003e. The prognosis is good in the first several years, but there is a risk of late disease progression with heart failure and cardiomyopathy. Treatment is supportive; research into genomic predictors of risk is ongoing.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHeart failure with eosinophilia (elevated eosinophil count in the blood; illness of any duration):\u003c\/strong\u003e Biopsy shows eosinophilic or hypersensitivity myocarditis, or eosinophilic endomyocarditis. The prognosis is poor. Treatment is supportive, including identification and treatment of the underlying cause; corticosteroids may be used for hypersensitivity myocarditis.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHeart failure with dilated left ventricle plus new ventricular arrhythmias, high-degree heart block, or lack of response to usual care within 1 to 2 weeks (illness lasting more than several months):\u003c\/strong\u003e Biopsy may show cardiac sarcoidosis (idiopathic granulomatous myocarditis) or a specific infection (e.g., \u003cem\u003eTrypanosoma cruzi\u003c\/em\u003e or \u003cem\u003eBorrelia burgdorferi\u003c\/em\u003e); nonspecific changes are most likely. If sarcoidosis is confirmed on biopsy, there is an increased risk of needing a pacemaker or implantable cardioverter–defibrillator (ICD). Treatment is supportive, with corticosteroids for biopsy-proven cardiac sarcoidosis.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHeart failure with dilated left ventricle without new ventricular arrhythmias or high-degree heart block (illness lasting more than several months):\u003c\/strong\u003e Nonspecific changes are most likely, but sensitive immunostaining reveals increased numbers of inflammatory cells in up to \u003cstrong\u003e40%\u003c\/strong\u003e of patients, and viral genomes are present in \u003cstrong\u003e25 to 35%\u003c\/strong\u003e. The prognosis depends on functional class (how limited the patient is in daily activities), ejection fraction (the percentage of blood the heart pumps out with each beat), and the presence or absence of inflammation and viral genomes on biopsy. Treatment is supportive; antiviral treatment and immunosuppression are under investigation.\u003c\/li\u003e\n\u003c\/ol\u003e\n\n\u003ch2 id=\"implications\"\u003eWhat This Means for Patients\u003c\/h2\u003e\n\n\u003cp\u003eFor patients and families facing a possible myocarditis diagnosis, several key messages emerge from this review.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eFirst, the prognosis varies widely—but many patients do well.\u003c\/strong\u003e The most common scenario—a patient with mild, acute dilated cardiomyopathy and suspected myocarditis—carries a generally good short-term prognosis. Many patients recover with supportive care alone. However, the long-term picture matters: some patients, especially children, may not show the full burden of the disease for 6 to 12 years, when they may develop progressive heart failure or require transplantation.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eSecond, the cause matters enormously.\u003c\/strong\u003e Viral myocarditis is most common and often self-limiting, but giant-cell myocarditis carries a poor prognosis and demands aggressive, early treatment. Hypersensitivity myocarditis (from medications) may improve dramatically once the offending drug is stopped. Cardiac sarcoidosis requires specific treatment with corticosteroids and monitoring for rhythm problems that might need a pacemaker or ICD.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eThird, biopsy decisions are now more targeted.\u003c\/strong\u003e Rather than biopsying everyone, cardiologists increasingly use clinical clues to decide who should undergo endomyocardial biopsy. The goal is to identify the specific treatable disorders—like giant-cell myocarditis, eosinophilic myocarditis, or cardiac sarcoidosis—where knowing the diagnosis changes treatment. The presence of ventricular arrhythmias, heart block, or failure to respond to standard care within 1 to 2 weeks should prompt consideration of biopsy.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eFourth, the immune system is central to the disease—both as a defender and as a potential source of harm.\u003c\/strong\u003e Understanding that the disease involves T-cell responses (including Th1, Th2, and Th17 cells) and autoantibodies directed against heart proteins like cardiac myosin explains why researchers are testing both antiviral and immunosuppressive therapies. It also suggests that patients with severe cardiomyopathy and prominent autoimmune features might benefit from therapies that target T cells—though these remain investigational.\u003c\/p\u003e\n\n\u003ch2 id=\"limitations\"\u003eStudy Limitations\u003c\/h2\u003e\n\n\u003cp\u003eIt is important to understand what this review could and could not establish. The article is a narrative review, not a new clinical trial, so it synthesizes existing research rather than presenting new data.\u003c\/p\u003e\n\n\u003cp\u003eThe review notes several critical limitations in the field:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eThe true incidence of myocarditis is unknown\u003c\/strong\u003e, because endomyocardial biopsy is infrequently used and there is no widely accepted, sensitive histologic standard for diagnosis.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eThe Dallas pathological criteria are limited\u003c\/strong\u003e by variability in interpretation, lack of prognostic value, and low sensitivity due to sampling error.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eMost knowledge about pathogenesis comes from animal models and isolated cell systems\u003c\/strong\u003e, not from human tissue. Regulatory T-cell subgroups, for example, have not yet been studied in human myocarditis.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003ePrognostic data on rare forms of myocarditis\u003c\/strong\u003e (like fulminant lymphocytic and giant-cell myocarditis) are limited to relatively few patients.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eThe diagnostic value of cardiac MRI\u003c\/strong\u003e and the clinical utility of biopsy remain subjects of debate, without consensus.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eThe article was published in 2009\u003c\/strong\u003e, so it does not include advances from the past 15+ years, including updated consensus criteria for cardiac MRI (the Lake Louise criteria), newer antiviral and immunosuppressive trial results, or modern understanding of COVID-19–related myocarditis.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2 id=\"recommendations\"\u003eRecommendations for Patients\u003c\/h2\u003e\n\n\u003cp\u003eBased on the information in this review, here are practical recommendations for patients and their families:\u003c\/p\u003e\n\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSeek prompt medical evaluation for persistent symptoms.\u003c\/strong\u003e If you have unexplained shortness of breath, chest pain, palpitations, or fainting—especially after a recent viral illness with fever and muscle aches—see a doctor. While most cases are mild, some require rapid, aggressive treatment.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eMention recent medications.\u003c\/strong\u003e If you develop heart symptoms shortly after starting a new medication (including anticonvulsants, antibiotics, or antipsychotics) and have a rash or fever, inform your doctor. Drug-induced hypersensitivity myocarditis may improve when the offending medication is withdrawn.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eReport tick bites or travel to endemic areas.\u003c\/strong\u003e Lyme disease myocarditis and Chagas disease have specific treatments, and early diagnosis improves outcomes. Tell your doctor about any travel to rural Central or South America or exposure to ticks.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eUnderstand what your test results mean.\u003c\/strong\u003e A normal troponin level does \u003cem\u003enot\u003c\/em\u003e rule out myocarditis (the test has only 34% sensitivity). An ECG may look like a heart attack even when your coronary arteries are normal. These are known limitations that your cardiologist will keep in mind.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eAsk about endomyocardial biopsy if you have warning signs.\u003c\/strong\u003e If you have dilated cardiomyopathy with new ventricular arrhythmias, high-grade heart block, or no response to standard care within 1 to 2 weeks, discuss with your specialist whether a biopsy is appropriate to look for treatable conditions like giant-cell myocarditis or cardiac sarcoidosis.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eBe aware of long-term follow-up needs.\u003c\/strong\u003e Even if you recover from the acute episode, myocarditis can lead to dilated cardiomyopathy and heart failure years later—particularly in children, where the burden may not appear for 6 to 12 years. Ongoing follow-up with a cardiologist is important.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eWatch for medication side effects if you have HIV.\u003c\/strong\u003e Patients with HIV are at high risk for myocarditis (prevalence of 50% or more at autopsy), and both the virus and some antiviral medications can affect the heart. Discuss cardiac monitoring with your HIV specialist.\u003c\/li\u003e\n\u003c\/ol\u003e\n\n\u003c!-- ddn:faq:start --\u003e\n\u003ch2 id=\"ddn-faq\"\u003eFrequently Asked Questions\u003c\/h2\u003e\n\u003ch3\u003eWhat causes myocarditis?\u003c\/h3\u003e\n\u003cp\u003eViral infections are a major cause, including coxsackievirus B, adenovirus, parvovirus B19, and hepatitis C virus. Other infectious causes include Lyme disease, Chagas disease, and HIV. Drug-induced hypersensitivity reactions, autoimmune conditions, and rare disorders like giant-cell myocarditis and cardiac sarcoidosis can also cause myocarditis. The trigger determines treatment and prognosis.\u003c\/p\u003e\n\u003ch3\u003eWhat are the symptoms of myocarditis?\u003c\/h3\u003e\n\u003cp\u003eSymptoms are highly variable. Some people have no symptoms. Others experience fatigue, decreased exercise tolerance, palpitations, chest pain, fainting, or shortness of breath. Chest pain may come from associated pericarditis or coronary artery spasm. A viral prodrome with fever, muscle aches, and respiratory or gastrointestinal symptoms often occurs before heart symptoms.\u003c\/p\u003e\n\u003ch3\u003eHow is myocarditis diagnosed?\u003c\/h3\u003e\n\u003cp\u003eDoctors may use blood tests like troponin I, ECG, cardiac MRI, and endomyocardial biopsy. Troponin I has high specificity but low sensitivity, so a normal level does not rule out myocarditis. Biopsy uses the Dallas criteria or immunoperoxidase staining. Biopsy is recommended mainly when treatable conditions like giant-cell myocarditis or cardiac sarcoidosis are suspected.\u003c\/p\u003e\n\u003ch3\u003eWhat is the prognosis for myocarditis?\u003c\/h3\u003e\n\u003cp\u003ePrognosis varies widely. Many patients with mild acute dilated cardiomyopathy and suspected myocarditis recover with supportive care. Fulminant lymphocytic myocarditis often has a good prognosis if the patient survives the acute phase. However, acute lymphocytic myocarditis more often leads to death or transplantation. Giant-cell myocarditis has a poor prognosis. Long-term complications include dilated cardiomyopathy and heart failure.\u003c\/p\u003e\n\u003ch3\u003eWhat treatments are available for myocarditis?\u003c\/h3\u003e\n\u003cp\u003eTreatment is mostly supportive, managing symptoms and supporting heart function. This may include inotropic medications or mechanical circulatory support for severe cases. Corticosteroids are used for hypersensitivity myocarditis and biopsy-proven cardiac sarcoidosis. Intravenous immune globulin may be used in children. Stopping the offending drug is essential for drug-induced hypersensitivity myocarditis. Antiviral and immunosuppressive therapies are under investigation.\u003c\/p\u003e\n\u003ch3\u003eWhen is an endomyocardial biopsy needed?\u003c\/h3\u003e\n\u003cp\u003eBiopsy is not recommended for every patient. Doctors consider biopsy when there is a likelihood of finding specific treatable disorders. It should be considered if you have dilated cardiomyopathy with new ventricular arrhythmias, high-grade heart block, or no response to standard care within 1 to 2 weeks. Biopsy can diagnose giant-cell myocarditis, eosinophilic myocarditis, or cardiac sarcoidosis.\u003c\/p\u003e\n\u003ch3\u003eCan myocarditis cause long-term heart damage?\u003c\/h3\u003e\n\u003cp\u003eYes. The most common long-term consequence is dilated cardiomyopathy with chronic heart failure. Some patients, especially children, may not show the full burden of disease for 6 to 12 years, when they might develop progressive heart failure or need transplantation. Even after recovery from the acute episode, ongoing follow-up with a cardiologist is important.\u003c\/p\u003e\n\u003c!-- ddn:faq:end --\u003e\n\n\u003ch2 id=\"source\"\u003eSource Information\u003c\/h2\u003e\n\n\u003cp\u003e\u003cstrong\u003eOriginal Article Title:\u003c\/strong\u003e T h e n e w e ng l a n d j o u r na l o f m e dic i n e\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003ePublication:\u003c\/strong\u003e \u003cem\u003eThe New England Journal of Medicine\u003c\/em\u003e, 2009; Volume 360, pages 1526–1538. Published April 9, 2009.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eCopyright:\u003c\/strong\u003e © 2009 Massachusetts Medical Society. All rights reserved.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eNote:\u003c\/strong\u003e This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician or a qualified healthcare provider with questions about your medical condition.\u003c\/p\u003e","brand":"DiagnosticDetectives.Com","offers":[{"title":"Default Title","offer_id":47457934278812,"sku":null,"price":0.0,"currency_code":"JPY","in_stock":true}],"url":"https:\/\/diagnosticdetectives.jp\/products\/understanding-myocarditis-causes-symptoms-diagnosis-and-treatment","provider":"DiagnosticDetectives.Com","version":"1.0","type":"link"}