Endocarditis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The turbulent blood flow around the heart valves is a risk factor for the development of endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged endothelium of these areas becomes a site for attachment of infectious agents in infectious endocarditis. Dental procedures, colorectal cancer, urinary tract infections and intravenous drug use are the most common routes of introducing the infectious agent into the bloodstream. The three most common pathogens are strepotococcus viridans, staphylococcus and enterococcus. In non-bacterial thrombotic endocarditis (NBTE), the damaged part of a heart valve becomes covered with a blood clot which organizes.

Pathophysiology

Pathogenesis

The pathogenesis of infective endocarditis includes:

Pathogenic Factors	Mechanism
Valvular Damage	Altered and turbulent flow Catheters, electrodes, and other intracardic devices Solid particles from repeated intravenous injections Chronic inflammation
Bacteremia	Dental procedures Intravenous drug use Complicated urinary tract infections Colorectal cancer
Poor Immune Response	Lack of blood supply to the valves Therapeutic drugs have difficulty reaching infected valves

Since the valves of the heart do not receive any dedicated blood supply, defensive immune mechanisms (such as white blood cells) cannot directly reach the valves via the bloodstream. If an organism (such as bacteria) attaches to a valve surface and forms a vegetation, the host immune response is blunted. The lack of blood supply to the valves also has implications on treatment, since drugs also have difficulty reaching the infected valve. Normally, blood flows smoothly past these valves. If they have been damaged the risk of bacterial attachment is increased. Damage to the valves and endocardium can be caused by altered or turbulent flow, catheters, electrodes, other intracardic devices, and chronic inflammation.

Causes of Bacteremia

Dental Procedures

The bacteremia is often caused by dental procedures, such as a cleaning or extraction of a tooth. It is important that a dentist or a dental hygienist therefore be told of any heart problems before beginning the procedure. Prophylactic antibiotics are administered to patients with certain heart conditions as a precaution.

Entrance of Bacteria Into the Bloodstream

Another cause of infective endocarditis is a scenario in which an excess number of bacteria enter the bloodstream. Colorectal cancer, serious urinary tract infections, and IV drug use can all introduce large numbers of such bacteria. When a large burden of bacteria are introduced, a normal heart valve may be infected. A more virulent organism (such as Staphylococcus aureus, but see below for others) is often responsible for infecting a normal valve.

Intravenous Drug Use

Infections of the tricuspid valve and less frequently the pulmonic valve tend to occur in intravenous drug users given the high pathogen burden from their introduction in the vein. The diseased valve is most commonly affected when there is a pre-existing disease. In rheumatic heart disease this is the aortic valve and the mitral valves, on the left side of the heart.

Pathology

Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

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  Heart; Breast intraductal papilloma metastasis. Thrombotic Nonbacterial Endocarditis (Infected): Gross mitral valve natural color vegetations well illustrated these were secondarily infected with staphylococcus case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases. Aortic valve also involved
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  Thrombotic Nonbacterial Endocarditis Infected: Micro low mag H&E fibrin vegetation with masses of staphylococci and inflammatory cells in valve secondarily infected case 8 year survival breast papillary intraductal adenocarcinoma with extensive metastases gross is aortic valve lesions.