Heart 1998;79:1-2 ( January )
Editorial
Immune responses in endocarditis
| The first 150 words of the full text of this article appear below. |
In 1885 William Osler delivered the Gulstonian lectures describing the broad clinical manifestations of bacterial endocarditis.1 The past 30 years have seen concerted attempts to explain the pathogenetic mechanisms behind the syndrome: heart failure out of proportion to the valve insufficiency; the presence of renal lesions in the majority of cases; arthritis, vasculitis, and splenomegaly as well as the classic cutaneous signs. What is clear is that an encounter between a circulating bacterium and an abnormal valve, with subsequent embolisation, can explain neither the initial establishment of the vegetation nor the myriad of extracardiac sequelae. Moreover, in most cases the microorganisms implicated are of low virulence, but when sequestered in a vegetation they are capable of inducing uncharacteristically severe disease.
The understanding of endocarditis as an immune complex mediated
syndrome and the identification of factors necessary for the genesis of
the vegetation have clarified some of these contradictions. Recent
appreciation of the
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