|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.
|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 Microscopic 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.
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|Nonbacterial Thrombotic Endocarditis
||Synopsis by: J. Hasson, M.D. (T38000M35150)