Myocarditis
Updates to Article Attributes
Myocarditis (rare plural: myocarditides) is a general term referring to inflammation of the myocardium.
Clinical presentation
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.
Lab values are typically non-specific, with increased ESR and leucocytosis. Creatine kinase, CK-MB, and troponins may be elevated. A viral titre may be positive.
ECG
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
right bundle branch block common in acute Chagas myocarditis
-
prolongation of the QRS complex duration (>0.12 seconds)
poor prognostic factor 13
Pathology
Myocarditis has several aetiologies. Inflammation from viral aetiologies is thought to be caused both by direct cellular damage by the infectious agent and also by involvement by the host's immune system.
Aetiology
Infectious aetiologies
viral (most common aetiology): 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
Non-infectious aetiologies
-
drugs
antibiotics
antituberculous agents
anticonvulsants
anti-inflammatories
diuretics
non-prescription/recreational drugs
Covid-19 vaccines15
radiation
transplant rejection
-
systemic disease
Markers
Although non-specific, cardiac creatine kinase (CK) and troponins I, T and C (TnI, TnT and TnC) are elevated.
Classification
Myocarditis is classified into four categories based on the clinical and pathologic presentation: fulminant, acute, chronic active, and chronic persistent.
Radiographic features
CT
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.
MRI
-
cine SSFP
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 oedema
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 have beenwas 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-ischaemic (subepicardial or mid-myocardial) late enhancement
native T1 mapping: increased T1 relaxation times or extracellular volume
-
supportive criteria:
signs of pericarditis: effusion or pericardial late enhancement
regional or global wall motion abnormalities
Echocardiography
Primarily useful to exclude alternative diagnoses which present similarly, including ischaemic 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
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.
-<p><strong>Myocarditis</strong> (rare plural: myocarditides) is a general term referring to inflammation of the myocardium. </p><h4>Clinical presentation</h4><p>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.</p><p>Chest pain may occur, in a variety of typical and atypical presentations.</p><p>Lab values are typically non-specific, with <a href="/articles/erythrocyte-sedimentation-rate">increased ESR</a> and leucocytosis. <a href="/articles/creatine-kinase">Creatine kinase</a>, CK-MB, and <a href="/articles/troponin">troponins</a> may be elevated. A viral titre may be positive.</p><h5>ECG</h5><p>Commonly sought due to the clinical presentation, but demonstrates poor sensitivity. Findings include:</p><ul>-<li>-<p>sinus tachycardia</p>-<ul><li><p>non-specific, most common overall electrocardiographic manifestation</p></li></ul>-</li>-<li><p>concave, diffuse ST-segment elevation</p></li>-<li>-<p>interventricular conduction delays</p>-<ul><li><p><a href="/articles/right-bundle-branch-block">right bundle branch block</a> common in acute <a href="/articles/chagas-disease">Chagas</a> myocarditis</p></li></ul>-</li>-<li>-<p>prolongation of the QRS complex duration (>0.12 seconds)</p>-<ul><li><p>poor prognostic factor <sup>13</sup></p></li></ul>-</li>-</ul><h4>Pathology</h4><p>Myocarditis has several aetiologies. Inflammation from viral aetiologies is thought to be caused both by direct cellular damage by the infectious agent and also by involvement by the host's immune system.</p><h5>Aetiology</h5><h6>Infectious aetiologies</h6><ul>-<li><p>viral (most common aetiology): e.g. Coxsackievirus, Echovirus, arbovirus</p></li>-<li><p>bacterial, e.g. <em>Corynebacterium diphtheriae</em>, <em>Streptococcus pyogenes</em>, <em>Staphylococcus aureus</em>, <em>Borrelia burgdorferi</em></p></li>-<li><p>fungal, e.g. Candida spp.</p></li>-<li><p>parasites, e.g. <a href="/articles/chagas-disease">Trypanosoma cruzi</a></p></li>-</ul><h6>Non-infectious aetiologies</h6><ul>-<li>-<p>drugs</p>-<ul>-<li><p>antibiotics</p></li>-<li><p>antituberculous agents</p></li>-<li><p>anticonvulsants</p></li>-<li><p>anti-inflammatories</p></li>-<li><p>diuretics</p></li>-<li><p>non-prescription/recreational drugs</p></li>-<li><p>Covid-19 vaccines<sup>15</sup></p></li>-</ul>-</li>-<li><p>radiation</p></li>-<li><p>transplant rejection</p></li>-<li><p><a href="/articles/giant-cell-myocarditis">giant cell myocarditis</a></p></li>-<li>-<p>systemic disease</p>-<ul>-<li><p><a href="/articles/systemic-lupus-erythematosus">systemic lupus erythematosus (SLE)</a></p></li>-<li><p><a href="/articles/scleroderma">scleroderma</a></p></li>-</ul>-</li>-</ul><h5>Markers</h5><p>Although non-specific, cardiac <a href="/articles/creatine-kinase">creatine kinase (CK)</a> and <a href="/articles/troponin">troponins I, T and C (TnI, TnT and TnC)</a> are elevated.</p><h5>Classification</h5><p>Myocarditis is classified into four categories based on the clinical and pathologic presentation: fulminant, acute, chronic active, and chronic persistent.</p><h4>Radiographic features</h4><h5>CT</h5><p>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 <sup>10,11</sup>.</p><h5>MRI</h5><ul>-<li>-<p><strong>cine SSFP</strong></p>-<ul>-<li><p>regional or global wall motion abnormalities are common but nonspecific (biventricular wall motion abnormality, however, is the main predictor of death or transplantation)</p></li>-<li><p><a href="/articles/pericardial-effusion">pericardial effusion</a> is reported in ~45% (range 32-57%) of patients with myocarditis</p></li>-</ul>-</li>-<li>-<p><a href="/articles/t2-black-blood"><strong>T2 black blood</strong></a></p>-<ul>-<li><p>T2 myocardial hyperintensity is compatible with oedema</p></li>-<li><p>T2 hyperintensity may be global and difficult to detect</p></li>-</ul>-</li>-<li>-<p><a href="/articles/early-gadolinium-enhancement"><strong>early gadolinium enhancement</strong></a></p>-<ul><li><p>regional vasodilatation and increased blood volume due to the inflammation in myocarditis causes early postcontrast enhancement</p></li></ul>-</li>-<li>-<p><a href="/articles/late-gadolinium-enhancement-2"><strong>late gadolinium enhancement</strong></a></p>-<ul>-<li><p><a href="/articles/late-gadolinium-enhancement-2">late enhancement</a> in myocarditis is an indication of irreversible myocardial necrosis and fibrosis.</p></li>-<li><p>distribution of enhancement is variable but classically involves the subepicardial myocardium (mid-interventricular and focal transmural patterns are also possible)</p></li>-</ul>-</li>-</ul><h6>Lake Louise consensus criteria 2018</h6><p>The original Lake Louise criteria <sup>5</sup> have been updated in 2018. The following two main criteria (T1 and T2 criteria) now have to be fulfilled for the diagnosis of acute myocarditis <sup>14</sup>:</p><ul>-<li>-<p>T2-weighted: any of the following</p>-<ul>-<li><p>standard T2 sequences: regional high signal</p></li>-<li><p>standard T2 sequences: global signal intensity ratio (myocardium/skeletal muscle) ≥2</p></li>-<li><p>T2 mapping: increased T2 relaxation times</p></li>-</ul>-</li>-<li>-<p>T1-weighted: any of the following</p>-<ul>-<li><p>late enhancement imaging: non-ischaemic (subepicardial or mid-myocardial) late enhancement</p></li>-<li><p>native T1 mapping: increased T1 relaxation times or extracellular volume</p></li>-</ul>-</li>-<li>-<p>supportive criteria:</p>-<ul>-<li><p>signs of <a href="/articles/pericarditis">pericarditis</a>: effusion or pericardial late enhancement</p></li>-<li><p>regional or global wall motion abnormalities</p></li>-</ul>-</li>-</ul><h5>Echocardiography</h5><p>Primarily useful to exclude alternative diagnoses which present similarly, including ischaemic heart disease, and evaluate for the presence or absence of a <a href="/articles/pericardial-effusion">pericardial effusion</a> (and potential <a href="/articles/cardiac-tamponade">tamponade</a> physiology). Findings common in myocarditis include <sup>12</sup>:</p><ul>-<li><p>global left ventricular <a href="/articles/left-ventricular-ejection-fraction-echocardiography">systolic dysfunction</a></p></li>-<li><p><a href="/articles/diastolic-dysfunction-point-of-care-ultrasound">diastolic dysfunction</a></p></li>-<li><p>regional <a href="/articles/wall-motion-score-index-echocardiography">wall motion abnormalities</a></p></li>- +<p><strong>Myocarditis</strong> (rare plural: myocarditides) is a general term referring to inflammation of the myocardium. </p><h4>Clinical presentation</h4><p>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.</p><p>Chest pain may occur, in a variety of typical and atypical presentations.</p><p>Lab values are typically non-specific, with <a href="/articles/erythrocyte-sedimentation-rate">increased ESR</a> and leucocytosis. <a href="/articles/creatine-kinase">Creatine kinase</a>, CK-MB, and <a href="/articles/troponin">troponins</a> may be elevated. A viral titre may be positive.</p><h5>ECG</h5><p>Commonly sought due to the clinical presentation, but demonstrates poor sensitivity. Findings include:</p><ul>
- +<li>
- +<p>sinus tachycardia</p>
- +<ul><li><p>non-specific, most common overall electrocardiographic manifestation</p></li></ul>
- +</li>
- +<li><p>concave, diffuse ST-segment elevation</p></li>
- +<li>
- +<p>interventricular conduction delays</p>
- +<ul><li><p><a href="/articles/right-bundle-branch-block">right bundle branch block</a> common in acute <a href="/articles/chagas-disease">Chagas</a> myocarditis</p></li></ul>
- +</li>
- +<li>
- +<p>prolongation of the QRS complex duration (>0.12 seconds)</p>
- +<ul><li><p>poor prognostic factor <sup>13</sup></p></li></ul>
- +</li>
- +</ul><h4>Pathology</h4><p>Myocarditis has several aetiologies. Inflammation from viral aetiologies is thought to be caused both by direct cellular damage by the infectious agent and also by involvement by the host's immune system.</p><h5>Aetiology</h5><h6>Infectious aetiologies</h6><ul>
- +<li><p>viral (most common aetiology): e.g. Coxsackievirus, Echovirus, arbovirus</p></li>
- +<li><p>bacterial, e.g. <em>Corynebacterium diphtheriae</em>, <em>Streptococcus pyogenes</em>, <em>Staphylococcus aureus</em>, <em>Borrelia burgdorferi</em></p></li>
- +<li><p>fungal, e.g. Candida spp.</p></li>
- +<li><p>parasites, e.g. <a href="/articles/chagas-disease">Trypanosoma cruzi</a></p></li>
- +</ul><h6>Non-infectious aetiologies</h6><ul>
- +<li>
- +<p>drugs</p>
- +<ul>
- +<li><p>antibiotics</p></li>
- +<li><p>antituberculous agents</p></li>
- +<li><p>anticonvulsants</p></li>
- +<li><p>anti-inflammatories</p></li>
- +<li><p>diuretics</p></li>
- +<li><p>non-prescription/recreational drugs</p></li>
- +<li><p>Covid-19 vaccines<sup>15</sup></p></li>
- +</ul>
- +</li>
- +<li><p>radiation</p></li>
- +<li><p>transplant rejection</p></li>
- +<li><p><a href="/articles/giant-cell-myocarditis">giant cell myocarditis</a></p></li>
- +<li>
- +<p>systemic disease</p>
- +<ul>
- +<li><p><a href="/articles/systemic-lupus-erythematosus">systemic lupus erythematosus (SLE)</a></p></li>
- +<li><p><a href="/articles/scleroderma">scleroderma</a></p></li>
- +</ul>
- +</li>
- +</ul><h5>Markers</h5><p>Although non-specific, cardiac <a href="/articles/creatine-kinase">creatine kinase (CK)</a> and <a href="/articles/troponin">troponins I, T and C (TnI, TnT and TnC)</a> are elevated.</p><h5>Classification</h5><p>Myocarditis is classified into four categories based on the clinical and pathologic presentation: fulminant, acute, chronic active, and chronic persistent.</p><h4>Radiographic features</h4><h5>CT</h5><p>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 <sup>10,11</sup>.</p><h5>MRI</h5><ul>
- +<li>
- +<p><strong>cine SSFP</strong></p>
- +<ul>
- +<li><p>regional or global wall motion abnormalities are common but nonspecific (biventricular wall motion abnormality, however, is the main predictor of death or transplantation)</p></li>
- +<li><p><a href="/articles/pericardial-effusion">pericardial effusion</a> is reported in ~45% (range 32-57%) of patients with myocarditis</p></li>
- +</ul>
- +</li>
- +<li>
- +<p><a href="/articles/t2-black-blood"><strong>T2 black blood</strong></a></p>
- +<ul>
- +<li><p>T2 myocardial hyperintensity is compatible with oedema</p></li>
- +<li><p>T2 hyperintensity may be global and difficult to detect</p></li>
- +</ul>
- +</li>
- +<li>
- +<p><a href="/articles/early-gadolinium-enhancement"><strong>early gadolinium enhancement</strong></a></p>
- +<ul><li><p>regional vasodilatation and increased blood volume due to the inflammation in myocarditis causes early postcontrast enhancement</p></li></ul>
- +</li>
- +<li>
- +<p><a href="/articles/late-gadolinium-enhancement-2"><strong>late gadolinium enhancement</strong></a></p>
- +<ul>
- +<li><p><a href="/articles/late-gadolinium-enhancement-2">late enhancement</a> in myocarditis is an indication of irreversible myocardial necrosis and fibrosis.</p></li>
- +<li><p>distribution of enhancement is variable but classically involves the subepicardial myocardium (mid-interventricular and focal transmural patterns are also possible)</p></li>
- +</ul>
- +</li>
- +</ul><h6>Lake Louise consensus criteria 2018</h6><p>The original Lake Louise criteria <sup>5</sup> was updated in 2018. The following two main criteria (T1 and T2 criteria) now have to be fulfilled for the diagnosis of acute myocarditis <sup>14</sup>:</p><ul>
- +<li>
- +<p>T2-weighted: any of the following</p>
- +<ul>
- +<li><p>standard T2 sequences: regional high signal</p></li>
- +<li><p>standard T2 sequences: global signal intensity ratio (myocardium/skeletal muscle) ≥2</p></li>
- +<li><p>T2 mapping: increased T2 relaxation times</p></li>
- +</ul>
- +</li>
- +<li>
- +<p>T1-weighted: any of the following</p>
- +<ul>
- +<li><p>late enhancement imaging: non-ischaemic (subepicardial or mid-myocardial) late enhancement</p></li>
- +<li><p>native T1 mapping: increased T1 relaxation times or extracellular volume</p></li>
- +</ul>
- +</li>
- +<li>
- +<p>supportive criteria:</p>
- +<ul>
- +<li><p>signs of <a href="/articles/pericarditis">pericarditis</a>: effusion or pericardial late enhancement</p></li>
- +<li><p>regional or global wall motion abnormalities</p></li>
- +</ul>
- +</li>
- +</ul><h5>Echocardiography</h5><p>Primarily useful to exclude alternative diagnoses which present similarly, including ischaemic heart disease, and evaluate for the presence or absence of a <a href="/articles/pericardial-effusion">pericardial effusion</a> (and potential <a href="/articles/cardiac-tamponade">tamponade</a> physiology). Findings common in myocarditis include <sup>12</sup>:</p><ul>
- +<li><p>global left ventricular <a href="/articles/left-ventricular-ejection-fraction-echocardiography">systolic dysfunction</a></p></li>
- +<li><p><a href="/articles/diastolic-dysfunction-point-of-care-ultrasound">diastolic dysfunction</a></p></li>
- +<li><p>regional <a href="/articles/wall-motion-score-index-echocardiography">wall motion abnormalities</a></p></li>