Myocarditis is a general term referring to inflammation of the myocardium.
Clinical presentation is variable in severity, ranging from asymptomatic to cardiogenic shock, but it typically is associated with other viral symptoms, including fever and malaise. It typically occurs 7-10 days after the onset of the systemic illness.
Chest pain may occur, in a variety of typical and atypical presentations.
Commonly sought due to the clinical presentation, but demonstrates poor sensitivity. Findings include:
- sinus tachycardia
- non-specific, most common overall electrocardiographic manifestation
- concave, diffuse ST segment elevation
- interventricular conduction delays
- prolongation of the QRS complex duration (>0.12 seconds)
- poor prognostic factor 13
Myocarditis has a number of etiologies. Inflammation from viral etiologies is thought to be caused both by direct cellular damage by the infectious agent and also from involvement by the host's immune system.
- viral (most common etiology): e.g. Coxsackievirus, Echovirus, arbovirus
- bacterial, e.g. Corynebacterium diphtheriae, Streptococcus pyogenes, Staphylococcus aureus, Borrelia burgdorferi
- fungal, e.g. Candida spp.
- parasites, e.g. Trypanosoma cruzi
- antituberculous agents
- non-prescription/recreational drugs
- transplant rejection
- giant cell myocarditis
- systemic lupus erythematosus (SLE)
Although non-specific, cardiac CK and troponins (TnI, TnT, TnC) are elevated.
Myocarditis is classified into four categories based on the clinical and pathologic presentation: fulminant, acute, chronic active, and chronic persistent.
Not always useful but some case reports describe certain features that can be helpful such as delayed myocardial enhancement (i.e. similar to MRI) with iodinated contrast 10,11.
- regional or global wall motion abnormalities are common but nonspecific (biventricular wall motion abnormality, however, is the main predictor of death or transplantation)
- pericardial effusion is reported in ~45% (range 32-57%) of patients with myocarditis
T2 black blood
- T2 myocardial hyperintensity is compatible with edema
- T2 hyperintensity may be global and difficult to detect
early gadolinium enhancement
- regional vasodilatation and increased blood volume due to the inflammation in myocarditis causes early postcontrast enhancement
delayed gadolinium enhancement
- delayed myocardial enhancement in myocarditis is an indication of irreversible myocardial necrosis and fibrosis.
- distribution of enhancement is variable, but classically involves the subepicardial myocardium (mid-interventricular and focal transmural patterns are also possible)
Primarily useful to exclude alternative diagnoses which present in a similar manner, including ischemic heart disease, and evaluate for the presence or absence of a pericardial effusion (and potential tamponade physiology). Findings common in myocarditis include 12:
- global left ventricular systolic dysfunction
- diastolic dysfunction
- regional wall motion abnormalities
Lake Louise consensus criteria
Lake Louise consensus criteria is two out of the following three criteria to fulfill the diagnosis of myocarditis 5:
- T2 myocardium to skeletal muscle ratio >1.9
- delayed enhancement in subepicardial and or mid-myocardium in nonischemic distribution
- increased global myocardial early gadolinium enhancement ratio between myocardium and skeletal muscle in gadolinium-enhanced T1WI
Endomyocardial biopsy is considered the gold standard of diagnosis, although it is subject to sampling error and there is a risk of perforation or tamponade. Endomyocardial biopsy is graded according to the Dallas criteria, with gradations of myocarditis, borderline myocarditis, and no myocarditis.
A typical appearance of myocarditis on MRI in the correct clinical setting may obviate biopsy.
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