The Role of Inflammasomes as Potential Therapeutic Target to Prevent Chronic Active Myocarditis: Translating Basic Science into Clinical Practice: A Case Report and Review of the Literature

Despite substantial progress in medical care, acute myocarditis remains a life-threatening disorder with a sudden onset, often unexpectedly complicating a simple and common upper respiratory tract infection. Myocarditis is most triggered by viral infections (over 80% of cases), with an estimated incidence of 10–106 per 100,000 annually. The clinical course may worsen in cases of mixed etiology, where a primary viral infection is complicated by secondary bacterial pathogens, leading to prolonged inflammation and an increased risk of progression to chronic active myocarditis or dilated cardiomyopathy. We included a case report as illustration of the clinical problem resulting from the progression of acute myocarditis into a chronic active disease. A central element of host defense is the inflammasome—an intracellular complex that activates pyroptosis and cytokine release (IL-1β, IL-18). While these processes help combat pathogens, their persistent activation may sustain inflammation and trigger heart failure and cardiac fibrosis, eventually leading to dilated cardiomyopathy. In this review, we summarize the current understanding of inflammasome pathways and their dual clinical role in myocarditis: essential for controlling acute infection but potentially harmful when over activated, contributing to chronic myocardial injury. Additionally, we discuss both novel and established therapeutic strategies targeting inflammatory pathways and anti-fibrotic mechanisms, including IL-1 receptor blockers (anakinra, canakinumab), NOD-like receptor protein 3 (NLRP3) inhibitors (colchicine, MCC950, dapansutrile, INF200), NF-κB inhibitors, angiotensin receptor-neprilysin inhibitors (ARNI). and microRNAs. Our aim is to highlight the clinical importance of early identification of patients at risk of progression from acute to chronic inflammation, role of inflammasomes and to present emerging therapies that may improve outcomes by balancing effective pathogen elimination with limitation of chronic cardiac damage.