
| Myocarditis is a condition where the heart muscle is inflamed and damaged without coronary artery blockage, resulting in a decrease in cardiac function. |

| Patient with recent infection presents with fever, viral prodromes, chest pain, joint pain, myalgias, fatigue, dyspnea palpitations, or heart failure. Establish characteristics of chest pain, presence of sick contacts, cardiac toxic medications/drugs, cardiac history, family history of cardiac disease. |

| Fever, signs of diminished cardiac output, tachycardia, weak pulses, cool extremities, muffled heart sounds, presence of S3, JVD, and edema. Ongoing myocardial inflammation may result in dilated cardiomyopathy, restrictive CMP, or acute LV failure without LV dilatation. |

| Diffuse T wave inversions and ST segment elevations. Severe changes could have bundle branch, high-degree AV blocks, and Q waves. |

| CXR: Cardiomegaly, pulmonary effusion. Echocardiogram evaluates LVEF, chamber size (presence of left ventricular dilation), wall motion abnormalities, increased LV EDV, presence of effusions. Cardiac MRI reveals inflammation, delayed contrast enhancement, following gadolinium infusion and increased T2 signals. |

| MYO-U = Uncomplicated Myocarditis. MYO-C = Myocarditis with cardiac dysfunction. MYO-S = Myocarditis with severe dysfunction and morbidity. ST = Supportive Therapy (for uncomplicated conditions: symptomatic therapy, best rest, pain control, NSAIDs). MT = Medical Therapy (if cardiac dysfunction is present, use ACEI, inotropes (milrinone), digoxin, diuretics, IVIG, steroids, carvedilol). UNRES-MT = Patient UNRESponsive to Medical Therapy. EMBX = EndoMyocardial Biopsy. AVT = AntiViral Therapy (antiviral therapy with ribavirin/interferon alpha immunosuppressive therapy with corticosteroids, cyclosporine, azathioprine). UNRES-AVT = Patient UNRESponsive to AntiViral Therapy. |

| MYO-U = ST MYO-C = MT MOC-C + UNRES-MT = EMBX MYO-S = AVT MYO-S + UNRES-AVT = EMBX |

| – Myocarditis can cause mild disease with self-resolution, chest pain, heart failure, arrhythmias, and sudden cardiac death. – Common causes are virus (coxsackie, parvoirus, EBV, CMV, adenovirus), bacteria (Borrelia, Brucella, Rickettsia, Haemophilus), protozoa (trypanosome), fungal (Aspergillus) hypersensitivity to drugs, autoimmune reactions, and toxins. – Routine use of immunosuppressive therapy is not recommended in myocarditis. – Endomyocardial biopsy is recommended in patients with acute deterioration of cardiac function of unknown etiology who are unresponsive to medical therapy. Transcriptomic biomarkers from a single endomyocardial biopsy can improve the clinical detection of patients with inflammatory diseases of the heart. This approach advances the clinical management and treatment of cardiac disorders with highly variable outcome. |

| – 20% of sudden cardiac deaths are from myocarditis. – Complete recovery of ventricular function is seen is as much as 50% of patients. – Most causes/etiologies are not found; definite diagnosis requires heart muscle biopsy. – Place patient on telemetry/electrocardiographic monitoring. Check CBC, blood cultures, cardiac enzymes (CKMB, troponin I), LDH, serial ECG, Echo, ESR/CRP, IgM serology of viruses and cultures, LFTs, anti-alpha myosin autoantibodies, anti-cardiac IgG. |

| Mahrholdt H, et al. Presentation, Patterns of Myocardial Damage, and Clinical Course of Viral Myocarditis. Circulation. 2006;114:1581. Gerzen P, et al. Acute Myocarditis. A Follow-up Study. Br Heart J. 1972;34:575. Heidecker B, et al. Transcriptomic Biomarkers for the Accurate Diagnosis of Myocarditis. Circulation. 2011;123:1174–1184. |