Infective endocarditis (IE) is the term used to designate an infection on any of the anatomic components of the heart and their endothelial surfaces.  These include, mural endocardium, valves and their apparatuses,   prosthetic or implanted  components, including: valves, homografts, pacemakers, intracardiac cardioverter-defibrillators and their leads, ventricular assist devices, surgical shunts and septal defect occluders, endovascular devices or clips).

The pathogenesis of IE is believed to be initiated by endothelial injury.  This can be due to aberrant jet streams and turbulent flow in the setting of diseased cardiac valves and septal defects or direct trauma from intravascular devices. A platelet/fibrin clot is formed over the exposed underlying extracellular matrix as the reparative process ensues. If transient bacteremia occurs before a protective layer of endothelium forms, colonization of the fibrin may develop and progress to an infected vegetation. Colonization of the clot is mediated by bacterial surface molecules that interact with host extracellular matrix molecules.  Adherent bacteria attract monocytes and induce them to produce tissue factors and pro-inflammatory cytokines that activate platelets and the coagulation cascade.  This, in turn, encourages growth of fibrin-platelet clot into a vegetation.  The lack of blood vessels in valves and vegetations protects the organisms from cellular and soluble host defenses which favors rapid bacterial proliferation.  IE can also occur in surfaces with intact endothelium, caused by virulent pathogens (e.g. Staphylococcus aureus) or intracellular organisms (e.g. Coxiella burnetii) that invade and survive inside endothelial cells. Invasion triggers inflammation and production of tissue factors by endothelial cells creating a vicious cycle that promotes the formation of a vegetation.

Traditionally, IE has been classified into acute, subacute and chronic according to its course and presentation that are largely determined by the virulence of the pathogen and the underlying valve pathology. Diagnosis is difficult due to variable clinical presentation; therefore clinical criteria have been proposed to guide the diagnosis of IE, of which the modified Duke criteria is currently the most widely used.  Based on these criteria, clinical diagnosis of IE is defined as definite or possible.

A classification that takes into account whether the infection was acquired in the community or related to health care has gained some popularity because of its potential practicality.  A practical approach used in the classification of IE is based on site and predisposition as follows: left-sided native valve endocarditis (NVE), prosthetic valve endocarditis (PVE), right-sided endocarditis (RSE), healthcare-associated endocarditis (HCAE ) and endocarditis of intravascular devices (EIVD).