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Epidemiology
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Inflammatory disorder of the heart
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Incidence : 0.02-1.5% of general population
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Cause : Infection(Viral MC), Toxin, Autoimmune
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Sudden cardiac death under 40 years 12% cause of death
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20~50s , Men(Estrogen decrease myocardial inflammation)
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Complications : Dysrhythmia, HF(0.5~4%), Fulminant myocarditis
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Pathophysiology and Microbiology
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First phase : a few days (Virus entering)
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Virus entering the myocytes through endothelial receptors
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This receptor is highly expressed in the brain and heart
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Second phase : a few weeks to several months (Immune reactions, Cardiac damage)
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Involves autoimmune reactions
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Virus specific T lymphocytes are activated
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Cardiac damage and impairment of the contractile function
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The third phase : chronic phase (Myocardial remodeling)
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Subtypes ( Lymphocytic(MC), Giant cell, Eosinophilic )
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Lymphocytic myocarditis – Virus infection MC
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Giant cell myocarditis - T-cell-induced inflammation secondary to autoimmune disease
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Eosinophilic myocarditis - Drug or allergic hypersensitivity reactions
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Infectious and noninfectious etiologies
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bacteria, viruses, parasites, autoimmune disorders, cardiotoxins, and hypersensitivity reactions
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Coxsackie B is one of the most common viral causes
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Drugs
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Anthracycline toxicity is the most common
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Cocaine has also been increasingly implicated, but there are many other medications that can cause cardiotoxicity and can lead to myocarditis
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History and Physical examination
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Variety History & Physical Examination challenging diagnosis
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Ranging mild symptoms with normal hemodynamics to cardiogenic shock and death
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Pediatric patients
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Viral prodrome (fever, malaise, myalgias, cough, vomiting, diarrhea)
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Tachypnea(MC), Tachycardia(58%), Chest pain(45%), Lethargy(39%), New murmur (32%), Fever(30%), Respiratory distress(28–68%), Hepatomegaly(27–36%), GI symptoms(27%), Hypotension(23%)
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Supraventricular or ventricular dysrhythmias
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Fulminant myocarditis - hemodynamic unstable, reduced cardiac output, poor perfusion
Adult patients
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Viral prodrome (Early stages) : Fever, malaise, and myalgias, Diffuse muscle tenderness, fatigue, chest pain, palpitations, dyspnea, edema
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Dyspnea(72%,MC), chest pain(32%)
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2 weeks to 3 months after viral prodrome : New or worsening heart failure symptoms
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RVHF(peripheral edema, hepatomegaly, and elevated jugular venous pressure)
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LVHF(pulmonary congestion, dyspnea)
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MR, TR worsening symptoms and a new murmur
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Life-threatening dysrhythmias or cardiogenic shock : fulminant myocarditis and worse outcomes
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Laboratory testing
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ECG, complete blood count, renal and liver function, electrolytes, ESR, CRP, troponin, BNP
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ECG
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Normal or nonspecific ST changes, APC, VPC, A.fib, Ventricular dysrhythmia, BBB, AVB
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High positive predictive value, the negative predictive value and sensitivity are low
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Normal ECG cannot exclude the diagnosis
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Pericarditis with diffuse concave ST elevations and PR depressions
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High-grade AVB can occur in Lyme disease or rheumatologic causes of myocarditis
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More severe case : ST abnormalities diffusely or Specific anatomic regions
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Fulminant form and poor prognosis : Wide QRS, QTc prolongation, abnormal QRS axis
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CBC : eosinophilia if eosinophilic myocarditis
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ESR or CRP elevation (99% of adult patients)
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Troponin elevated in both pediatric and adult patients with symptoms for < 1 month
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Troponin is more commonly elevated in those with acute myocarditis
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The American Heart Association and European Society of Cardiology recommend obtaining troponin to evaluate for myocarditis But should not be used as a prognostic factor
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Brain natriuretic peptide level may be elevated due to myocyte distension and reduced cardiac function
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Over 50% of patients with myocarditis will have an elevated BNP
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4. Imaging
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Over 50% CXR is abnormal (cardiomegaly, pulmonary edema, and pleural effusions)
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Normal chest radiograph cannot be used to exclude the diagnosis
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Echocardiography is one of the most important test
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Diffuse systolic dysfunction is the most common finding
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Regional wall motion abnormalities, Atrial or Ventricular chamber dilatation
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Early stages of disease can be associated with a normal or mildly reduced ejection fraction
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One-quarter of patients decreased LVEF
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8.5% of patients had right ventricular dysfunction
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Pericardial effusion(26%)
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mitral regurgitation, tricuspid regurgitation, or intracardiac thrombi
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Cardiac magnetic resonance imaging (CMRI), cardiac catheterization, and endomyocardial biopsy
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CMRI provides functional and morphological assessment of cardiac tissues
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edema (T2-weighted imaging), hyperemia (T1-weighted imaging), and fibrosis (late gadolinium enhancement)
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Overall sensitivity and specificity for CMRI ranges from 68–89% and 74–96%
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CMRI sensitivity and specificity are highest in those with acute rather than chronic myocarditis
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Cardiac catheterization – DDX coronary syndrome
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Definitive diagnosis includes endomyocardial biopsy
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biopsy is rarely helpful and has little impact on clinical management
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The 2010 Heart Failure Society Guideline recommends biopsy
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Heart failure of unknown origin within 2 weeks and hemodynamic instability
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Heart failure of 2 weeks to 3 months in duration with a dilated left ventricle, ventricular dysrhythmias, and highgrade atrioventricular block or symptoms that are unresponsive to therapy within 1–2 weeks
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Management – Hemodynamic support
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Hemodynamic and volume status include inotropic support, afterload reduction, diuresis, and ventilatory support
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Important to assess volume status and avoid excessive intravenous fluids
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Norepinephrine - vascular tone, cardiac contractility
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Epinephrine
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predominantly inotropic effects at low doses (0.01–0.05 μg/kg/min i.v.)
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increasing not only afterload but also the risk of tachycardias and dysrhythmias
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increase in 90-day mortality as well as worsening renal and cardiac markers
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Recent meta-analysis demonstrated increase in short-term mortality with epinephrine use in cardiogenic shock
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Norepinephrine combined with inotropic agent is preferred over epinephrine monotherapy
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Normal blood pressure + depressed EF -> inotropic support (Milrinone, Dobutamine)
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Milrinone
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afterload reduction agent, dilating pulmonary vasculature and improving hemodynamics in acute decompensated heart failure
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long half-life and is more dysrhythmogenic than dobutamine
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Dobutamine
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lower risk of side effects and shorter half-life
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Angiotensin-converting enzyme inhibitors & beta-blockers prevent ventricular remodeling and relieve vasospasm after myocarditis
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Volume overload patient - diuretics (e.g., furosemide)
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Noninvasive positive pressure ventilation reducing left ventricular afterload and left ventricular wall tension
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Early management for pulmonary edema with respiratory distress
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Intubation decrease the oxygen consumption of the myocardium and respiratory muscles
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Intubation in patients with myocardial dysfunction can be challenging
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Etomidate or ketamine is recommended to reduce the risk of further hemodynamic compromise during induction
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Clinicians should consider having vasopressors immediately available in case the blood pressure acutely lowers
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Additional agents remain controversial
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Nonsteroidal anti-inflammatory drugs (NSAIDs) should avoided (worsen mortality)
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Adult patients, corticosteroids / intravenous immunoglobulin (IVIG) No Benefit
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prednisone with azathioprine or cyclosporine did not decrease survival or improve LVEF as compared with placebo
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IVIG in pediatric patients also demonstrated no benefit
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Adult patients with Parvovirus B19 and a high viral load, high-dose IVIG at 2 g/kg was found to improve their New York Heart Association functional class and LVEF
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IVIG has benefit, specifically in pediatric acute decompensated myocarditis, improving LV function and decreasing the number of fulminant dysrhythmias
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IVIG has short- and long-term benefit in some studies, others have equivocal findings
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Giant cell or eosinophilic myocarditis
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Corticosteroids are the foundation of treatment to correct the underlying condition
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Immunosuppressants (e.g., cyclosporine, sirolimus, muromonab) increased transplant-free survival
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In vitro data suggested a potential benefit, there are no data to suggest that antiviral agents (e.g., ribavirin) improve outcomes in vivo
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Mechanical circulatory support (e.g., intra-aortic balloon pump, extracorporeal membrane oxygenation, ventricular assist device) should be considered in patients with refractory hypotension despite vasopressors and inotropic support
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Pediatric patients of ECMO
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use of ECMO in 20% of patients, with 80% surviving to discharge, and 60% full myocardial recovery
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61% survival-to-discharge rate using multicenter data from 1995–2006
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Adult patients requiring ECMO
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46–85% of patients survived to discharge
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Ventricular assist devices (VADs) allow for single-ventricle support
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27% mortality and a 67% successful transplant rate
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Myocarditis is a potentially fatal condition
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inflammation of the heart musculature causes cardiac dysfunction
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Symptoms may vary from mild to severe and are often preceded by a viral prodrome
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Laboratory assessment and an ECG can assist with the diagnosis, echocardiography is the ideal test in the ED setting
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Treatment is primarily focused on respiratory and hemodynamic support
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Initial hemodynamic management often includes vasopressors and inotropes, though more severe cases may require an IABP, ECMO, or an VAD
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NSAIDs should be avoided while IVIG is controversial.
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It is important for emergency clinicians to be aware of the diagnosis and management of acute myocarditis.
