Diagnostic and prognostic role of electrocardiogram in acute myocarditis: A comprehensive review

Figures

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  Figure 1. Electrocardiogram performed 11 days after symptom onset in a 19‐year‐old patient with perimyocarditis. It shows the following: PR segment depression in inferior and V2‐V6 leads, PR segment elevation in aVR, ST elevation in inferior and V1‐V3 leads, and T‐wave inversion in I, II, aVL, and V3‐V6 leads

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  Figure 2. Electrocardiogram performed at admission (a) and 3 days later (b) in a 30‐year‐old patient with perimyocarditis. Comparison between these two ECGs shows the following: disappearance of ST elevation with pericarditis pattern in inferior and lateral leads, disappearance of ST depression in aVR lead, and onset of T‐wave inversion in III e aVF leads

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  Figure 3. Possible ST‐elevation patterns in acute myocarditis: acute coronary syndrome‐like pattern (a), pericarditis pattern without terminal QRS notching or slurring (b), pericarditis pattern with terminal QRS notching (c), and pericarditis pattern with terminal QRS slurring (d)

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  Figure 4. Electrocardiogram performed 1 day after hospital admission in a 18‐year‐old patient with pure acute myocarditis. It shows a diffuse ST elevation with pericarditis pattern without terminal QRS notching or slurring and a reciprocal ST depression in aVR and V1 leads

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  Figure 5. A theory to explain T‐wave inversion in myocarditis. In a normal heart, action potential is longer in endocardial cells as compared with epicardial cells and therefore repolarization begins within the epicardial layer and ends within the endocardial layer, giving rise to a positive T wave (a). In transmural or epicardial myocarditis, myocardial damage causes a prolongation of the action potential within the epicardial layer; consequently, repolarization begins within the endocardial layer and ends within the epicardial layer, giving rise to a negative T wave (b). ENDO = endocardial layer, EPI = epicardial layer, D = depolarized cell, R = repolarized cell