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Myocarditis (rare plural: myocarditides) 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:
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 several etiologies. Inflammation from viral etiologies is thought to be caused both by direct cellular damage by the infectious agent and also by 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
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 myocardial hyperintensity is compatible with edema
T2 hyperintensity may be global and difficult to detect
regional vasodilatation and increased blood volume due to the inflammation in myocarditis causes early postcontrast enhancement
late 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)
Lake Louise consensus criteria 2018
The original Lake Louise criteria 5 was updated in 2018. The following two main criteria (T1 and T2 criteria) now have to be fulfilled for the diagnosis of acute myocarditis 14:
T2-weighted: any of the following
standard T2 sequences: regional high signal
standard T2 sequences: global signal intensity ratio (myocardium/skeletal muscle) ≥2
T2 mapping: increased T2 relaxation times
T1-weighted: any of the following
late enhancement imaging: non-ischemic (subepicardial or mid-myocardial) late enhancement
native T1 mapping: increased T1 relaxation times or extracellular volume
signs of pericarditis: effusion or pericardial late enhancement
regional or global wall motion abnormalities
Primarily useful to exclude alternative diagnoses which present similarly, 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
regional wall motion abnormalities
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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