Eosinophilic states that may occur in and underlie<unk>  (as well as the other stages of eosinophilic myocarditis) include primary and secondary eosinophilias or hypereosinophilias. Primary eosinophilias or hypereosinophilias (i.e. disorders in which the eosinophil appears to be intrinsically diseased) that lead to<unk>  are clonal hypereosinophilia, chronic eosinophilic leukemia and the hypereosinophilic syndrome. Secondary causes (i.e. disorders in which other diseases cause the eosinophil to become dysfunctional) include allergic and autoimmune diseases; infections due to certain parasitic worms, protozoa, and viruses; malignant and premalignant hematologic disorders commonly associated with eosinophilia or hypereosinophilia; and adverse reactions to various drugs. The disorder develops because of eosinophilic penetration into the cardiac tissues. This leads to a fibrotic thickening of portions of the heart (similar to that of endomyocardial fibrosis) and heart valves. In consequence, the heart becomes rigid and poorly contractile while the heart valves may become stenotic or insufficient, i.e. reduced in ability to open or close, respectively. The damaged heart may also develop mural thrombi, i.e. clots which lay against ventricle walls, tend to break off, and flow through and block arteries; this condition often precedes the fibrotic stage of eosinophilic myocarditis and is termed the thrombotic stage.
Loeffler endocarditis
Libman–Sacks endocarditis
Infective endocarditis
Nonbacterial thrombotic endocarditis
Subacute bacterial endocarditis
Nocardiosis
Tuberculous pericarditis
Eosinophilic myocarditis