• All kinds of infection or wound at skin and mucosa with bacteria often cause it, such as operation, using instruments.
• If bacteria in circulating system locate nonbacterial excrescence, IE can happen.
kinds
According to course of diseases acute or subacute
According to etiology 1. Natsthetic valve endocarditis 3. Endocarditis in intravenous drug abusers
endocarditis in intravenous drug abusers
Commonly seen in young male originating from skin infections, the main
causative organism is Staph. Aureus previously normal valve is involved beyond 50% of the patient show tricuspid
• Subacute IE: viridans group of streptococci is the most common
prosthetic valve endocarditis
• early stage of prosthetic valve endocarditis (often staphylococcus): Less than 60 days after cardiac operation
platelet micro thrombus and fibrin accumulate nodular nonbacterial excrescence, which is important factor to bacteria locate valve surface.
3. Transient bacteremia
Ⅱ. Acute the mechanism is not clear yet, mainly
involve normal valve membrane.
the causative bacteria comes from active infection focus at skin, muscle, bone or lung, the amount of bacteria in blood is big, the bacteria ability is strong. Aortic valve is often involved.
such as ventricular septal defect, mitral regurgitation and aortic regurgitation, many of which are haemodynamically insignificant.
2. Nonbacterial thrombus endocarditis
• Later stage of prosthetic valve endocarditis (often viridans group of streptococci ): 60 days or more after cardiac operation, except that excrescence or vegetations is formed, artificial valve is damaged, the aortic valve is involved most commonly.
Native valve endocarditis
Etiology: native valve endocarditis of streptococcus and Staphylococcus aureus is 65% and 25% respectively.
• Acute IE: mainly caused by staphylococcus aureus
Infective Endocarditis (IE)
generalization
• infective endocarditis is formed by microbic excrescence on inner layer of the heart, the endocardium.
• The most common structures involved are the heart valves, defective septum, chordae tendineae and heart wall intimae.
damage.
Mechanism of NVE
I. Subacute form account for at least 2/3 of the cases, the following factors are concerned:
1. Hemodynamics
Many acquired and congenital cardiac lesions are vulnerable to endocarditis, particularly areas of endocardial damage caused by a high-pressure jet of blood
4. bacteria infect nonbacterial excrescence
• the frequency of bacteremia and bacteria amount in circulating blood
• bacteria ability to adhere to platelet micro thrombus and fibrin