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Infective endocarditis
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==Pathogenesis== [[File:Endocarditis.png|thumb|Drawing of endocarditis]] Damaged valves and [[endocardium]] contribute to the development of infective endocarditis.<ref name="NEJM Review, Hoen" /> Specifically, the damaged part of a [[heart valve]] forms a local [[blood clot]], a condition known as [[Nonbacterial thrombotic endocarditis|non-bacterial thrombotic endocarditis (NBTE)]]. The platelet and fibrin deposits that form as part of the blood clotting process allow bacteria to take hold and form [[Vegetation (pathology)|vegetations]]. As previously mentioned, the body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply. This combination of damaged valves, bacterial growth, and lack of a strong immune response results in infective endocarditis.{{citation needed|date=February 2021}} Damage to the valves and endocardium can be caused by:<ref name="NEJM Review, Hoen" /> * Altered, turbulent blood flow. The areas that fibrose, clot, or roughen as a result of this altered flow are known as jet lesions. Altered blood flow is more likely in high pressure areas, so [[ventricular septal defect]]s or [[patent ductus arteriosus]] can create more susceptibility than [[atrial septal defect]]s. * Catheters, electrodes, and other intracardiac prosthetic devices. * Solid particles from repeated intravenous injections. * Chronic inflammation. Examples include [[auto-immune]] mechanisms and degenerative valvular lesions. The [[#Risk factors|risk factors]] for infective endocarditis provide a more extensive list of conditions that can damage the heart.
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