|Nonbacterial Thrombotic Endocarditis|
• Associated with disease states contributing
to hypercoaguability. This is a clinical association
without proof of hypercoaguability with an objective
measure, e.g. a measure of some coagulation factor.
• The only objective markers are demonstration of rare genetic deficiency of anti-thrombin III, protein S, or protein C.
•Unknown. The precise mechanisms causing the common
hypercoaguable states with thrombus formation in
various clinical settings, other than endothelial
injury and venous stasis, are unknown.
•Associated with following disease states:
•Metastatic carcinoma and other malignacies, with
prominence of mucus producing carcinomas.
•Debilitating chronic infections, e.g. T.B.
•Debilitating chronic disease states of any etiology,
e.g. coronary arteriosclerosis and myocardial scars
with heart failure.
•This is usually a terminal process in individuals
dying of the underlying disease, and is often an
unexpected autopsy finding.
•However the vegetations are extremely friable and
do cause embolic lesions, which may be clinically
apparent such as acute cerebral or myocardial infarcts.
|General Gross Description|
•One or a few rounded friable vegetations, usually
measuring no more than 6-7mm in diameter, are found
along the line of closure of the valves, where the
cusp edges contact during closure.
•Identical vegetations are also seen in systemic lupus erythematosus (SLE), but
vegetations on the undersurfaces of the valves
are charcteristic of SLE.
|General Micro Description|
•The histology consists of homogeneous sheets of
fibrin without any inflammatory response.
•Electron microscopic study shows that the bulk of
the lesion is mostly platelet constituted with
intermingled fibrin strands, in spite of the misleading
histologic appearence of fibrin deposition alone.
•Organization of the thrombus by an ingrowth of
fibroblasts is not seen, accounting for the friability
of the vegetations.
•The lesions associated with SLE are histologically
indistinguishable from this disease.
• Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 554-555.