In the present case, the direct antagonist actions of a potential hyperadrenergic state that may have led to the myocarditis state with a beta-adrenergic blocker (metoprolol) may have justified the prompt recovery, although further actions of the angiotensin-converting enzyme inhibitor (ACEi) (lisinopril) and mineralocorticoid antagonist (spironolactone) may have exerted synergistic protective effects on ACE expression and balance between its receptors. Here, ACE is linked to myocarditis.