Conduction tissue inflammation is a major determinant of electrical instability in human myocarditis

Background: Arrhythmic presentation of myocarditis has been attributed to pro-arrhythmic CT involvement, but its implication is still unproved. Methods: We retrospectively enrolled consecutive patients with acute myocarditis who underwent EMB. Patients were categorized according to clinical manifestation in arrhythmic presentation [premature ventricular beats >1000/24 hours, supraventricular tachyarrhythmias, non-sustained/sustained ventricular tachycardia, survivors of ventricular fibrillation] with pre-served cardiac contractility – [Left Ventricular Ejection Fraction (LVEF) ≥ 50%] (Group A) and car-diomyopathic phenotype (with symptoms and signs of heart failure, LVEF ≤ 45%) including in-farct-like phenotype (Group B). All patients had a biopsy-proven myocarditis; sections of CT were identified by morphologic (Ashoff and Monkeberg criteria) findings and positive immunohisto-chemistry for HCN4. CT inflammation was sustained by presence of CD45Ro+ T lymphocytes with necrosis of adjacent small and loosely arranged myocytes. Polimerase Chain Reaction for cardio-tropic viruses, extent of myocardial fibrosis, vasculitis and CT inflammation were evaluated in the two groups. Results: Among 217 myocarditis patients, 107 had an arrhythmic presentation. CT was observed in 33 (30.8%) patients of Group A and 31 (28.2%) of Group B. In patients with biopsy-evidence of CT, no significant difference was reported in mean age. Inflamed CT was documented in 2 (6.5%) cases of Group B and in 33 (100%) of Group A (p<0.001). No statistically difference was observed between Group A and B regarding presence of viral genomes, vasculitis and myocardial fibrosis. Conclusion: CT inflammation is a major determinant of electrical instability in human myocardi-tis with arrhythmic presentation.