Non‑infective endocarditis
Non‑infective endocarditis describes sterile pathology of the endocardium and valves that mimics infective endocarditis on clinical or imaging grounds.
The two entities most relevant to emergency practice are Loeffler’s endocarditis (eosinophilic endomyocardial disease, usually part of hypereosinophilic syndrome) and Non‑Bacterial Thrombotic Endocarditis (NBTE, “marantic” endocarditis).
Both carry a high risk of systemic embolisation and may cause valvular dysfunction or restrictive cardiomyopathy. Emergency care focuses on stabilisation, recognising embolic complications, preventing further thromboembolism, identifying the underlying systemic cause and arranging urgent specialist input.
Key national guidance to inform decisions: NICE on hypereosinophilic syndrome and therapies (TA846), NICE guidance on venous thromboembolic disease and VTE prevention (NG158, NG89) for anticoagulation and investigation of hypercoagulability, and NICE infective endocarditis guidance (CG64) to distinguish infective from sterile causes.
Pathophysiology and how the two differ
- Common mechanism: sterile thrombotic or inflammatory lesions (platelet‑fibrin thrombus or eosinophil‑mediated injury) rather than microorganisms, with lesions often friable and prone to embolisation.
- Loeffler’s endocarditis (eosinophilic endomyocardial disease)
- Caused by sustained peripheral and tissue eosinophilia; eosinophil degranulation causes myocardial necrosis followed by mural thrombosis and eventual endomyocardial fibrosis producing restrictive physiology.
- Classical course: acute necrotic (myocarditis) → thrombotic (mural thrombi/vegetations) → fibrotic (endomyocardial fibrosis).
- Associations: hypereosinophilic syndrome (HES), parasitic disease, drug reactions and haematological disorders.