TABLE 2.

Different molecular and immunopathogenic mechanisms involved in the disease process according to the disease phase: acute “hot” versus chronic “cold”.

Mechanisms of arrhythmia in the acute “hot” phase	Mechanisms of arrhythmia in the chronic “cold” phase
– Direct pathogen-mediated cytolysis	– Persistent active chronic inflammation
– Myocardial oedema, cytokines release, and cell death
– Gap junction dysfunction due to altered connexins expression (typical of Coxsackievirus B3)	– Post inflammatory myocardial scar formation
– Acute ischemia, microvascular disease and prolonged vasospasm (typical Parvovirus B19)
– Abnormal calcium handling	– Residual ventricular dysfunction
– Ion channel impairment (typical of myocardial channelopathies)
– Unmasking of structural genetic cardiomyopathy (e.g., AC)	– Electrical remodeling

AC, arrhythmogenic cardiomyopathy.