Infective endocarditis refers to a bacterial or, rarely, a fungal virus from the cardiac valves. Virus of extracardiac endothelium is termed "endarteritis" and can cause disease that is clinically similar to endocarditis.
One of the most typical predisposing aspect for infective endocarditis is the presence of structurally abnormal cardiac valves. Consequently, sufferers with a history of rheumatic or congenital heart illness, mitral valve prolapse with an audible murmur, a prosthetic heart valve, or a history of prior endocarditis are at increased chance for infective endocarditis.
Infection involves the left side of the heart (mitral and aortic valves) almost exclusively, except in patients who are injection drug users or, less commonly, in sufferers with valve injury from a pulmonary artery (Swan-Ganz) catheter, in whom virus of the correct side of the heart (tricuspid or pulmonary valve) might occur.
The most typical infectious agents causing native valve infective endocarditis are gram-positive bacteria, including Streptococcus viridans, S aureus, and enterococci. The particular bacterial species causing endocarditis can often be anticipated on the basis of host elements.
Injection drug users generally introduce S aureus into the blood when nonsterile needles are utilized or the skin is not adequately cleaned before needle insertion. Sufferers with recent dental work are at chance for transient bacteremia with normal oral flora, particularly S viridans, with subsequent endocarditis.
Genitourinary tract infections with enterococci may lead to bacteremia and subsequent seeding of damaged heart valves. Patients with prosthetic heart valves are also at elevated risk for infective endocarditis resulting from skin flora such as S epidermidis or S aureus.
Prior to the availability of antibiotics, infective endocarditis was a progressively fatal illness. Even with antibiotics, the case fatality rate for endocarditis approaches 25%, and definitive cure often requires both prolonged antibiotic administration and urgent surgery to replace infected cardiac valves.
A number of hemodynamic factors predispose patients to endocarditis: (1) a high-velocity jet stream producing turbulent blood flow, (2) flow from a high-pressure to a low-pressure chamber, and (3) a comparatively narrow orifice separating the two chambers that creates a pressure gradient.
The lesions of infective endocarditis tend to form on the surface of the valve within the cardiac chamber with the lower pressure (eg, about the ventricular surface of an abnormal aortic valve and on the atrial surface of an abnormal mitral valve).
Endothelium damaged by turbulent blood flow results in exposure of extracellular matrix proteins, promoting the deposition of fibrin and platelets, which form sterile vegetations (nonbacterial thrombotic endocarditis or marantic endocarditis). Infective endocarditis occurs when microorganisms are deposited onto these sterile vegetations during the course of bacteremia.
Not all bacteria adhere equally well to these websites. For example, E coli, a frequent trigger of bacteremia, is rarely implicated as a trigger of endocarditis. Conversely, virulent organisms for example S aureus can invade intact endothelium, causing endocarditis within the absence of preexisting valvular abnormalities.
Once infected, these vegetations continue to enlarge through further deposition of platelets and fibrin, providing the bacteria a sanctuary from host defense mechanisms for example polymorphonuclear leukocytes and complement. Consequently, as soon as virus takes hold, the infected vegetation continues to grow in a largely unimpeded fashion.
Prolonged administration (4-6 weeks) of bactericidal antibiotics is needed to penetrate the vegetation and cure this illness. Bacteriostatic antimicrobial agents, which inhibit but do not kill the bacteria, are inadequate.
Surgical removal of the infected valve is sometimes required for cure, especially for infections with gram-negative bacilli or fungi, if there is mechanical dysfunction from the valve with resultant congestive center failure, or in prosthetic valve infections. A hallmark of infective endocarditis is persistent bacteremia, which stimulates both the humoral and cellular immune systems.
A variety of immunoglobulins are expressed, resulting in immune complex formation, elevated serum levels of rheumatoid aspect, and nonspecific hypergammaglobulinemia. Immune complex deposition along the renal glomerular basement membrane might result within the development of acute glomerulonephritis and renal failure.
Infective endocarditis is a multisystem disease with protean manifestations. For these causes, the signs can be nonspecific and the diagnosis might not be initially included in the differential diagnosis. Cutaneous findings suggestive of endocarditis consist of Osler's nodes, painful papules about the pads from the fingers and toes thought to be secondary to deposition of immune complexes;
and Janeway lesions, painless hemorrhagic lesions on the palms and soles caused by septic microemboli. Signs and signs of endocarditis may be acute, subacute, or chronic. The clinical manifestations reflect primarily (1) hemodynamic changes from valvular damage; (2) end-organ symptoms and indicators from septic emboli (right-sided emboli towards the lungs, left-sided emboli to the brain, spleen, kidney, and extremities); (3) end-organ symptoms and signs from immune complex deposition; and (4) persistent bacteremia with metastatic seeding of virus (abscesses or septic joints). Death is generally triggered by hemodynamic collapse or by septic emboli to the CNS, resulting in brain abscesses or mycotic aneurysms and intracerebral hemorrhage.
Chance elements for a fatal outcome consist of left-sided valvular virus, bacterial etiology other than S viridans, medical comorbidities, complications from endocarditis (congestive heart failure, valve ring abscess, or embolic disease), and, in one study, medical management without valvular surgery.