Literature review: Pathophysiology of endocarditis: Mechanism of infection and immune response

Infective endocarditis (IE) is a severe and potentially fatal condition characterized by infection of the endocardial surface, particularly affecting cardiac valves. The disease arises from a multifactorial process involving endothelial injury, bacteremia, and host immune responses. Endothelial disruption promotes platelet-fibrin deposition, forming a sterile thrombus that facilitates microbial adhesion and colonization. Subsequent vegetation formation provides a protective microenvironment for pathogens, enabling persistence and resistance to host defenses and antimicrobial therapy. The immune response involves both innate and adaptive mechanisms, including activation of macrophages, neutrophils, and cytokine signaling pathways. However, dysregulated immune responses may contribute to tissue destruction and systemic complications such as embolization and immune complex deposition. Various factors, including host genetics, comorbidities, microbiota, and medical interventions, influence disease progression. A comprehensive understanding of the pathophysiology of endocarditis is essential to improve diagnostic strategies and therapeutic outcomes.