A clinico-pathologic study of carotid endarterectomy plaques.

Carotid endarterectomy specimens surgically removed in one piece were kept intact, processed pathologically, and serially sectioned at 8 microns. There were 34 cases with multiple hemispheric transient ischemic attacks (TIAs), 23 cases with multiple episodes of transient monocular blindness (TMBs), 33 asymptomatic cases, and 51 cases with prolonged or persisting neurologic deficits. The occurrence of TIAs and TMBs correlated best with severe carotid stenosis (1 mm. or less), less well with the presence of mural thrombus, and not at all with ulceration of plaque and intraplaque hemorrhage. The residual lumen in asymptomatic cases was wider. The persistence of neurologic deficits correlated best with carotid occlusion or near-occlusion (37 of 51). In only 3 cases was there evidence of embolism from ulceration with minor stenosis. There were many variations in the size, form, composition, site, and number of mural thrombi, ulcerations, and hemorrhages; to provide an accurate picture, serial sections are necessary. Large rounded cavities in plaques sometimes were empty, smooth-lined cul-de-sacs rather than eroding ulcerations (16 cases). Mural thrombi are probably not an important source of embolism. Ulceration and hemorrhage into plaque posed little or no threat in the present series. Using the pathologic and clinical data, inferences have been made concerning the relative frequency of embolism and hemodynamic failure in the mechanism of the varied events associated with carotid occlusion. Observations have been made on a few additional points--selective involvement of the lower extremity, prolonged TIAs, the onset of symptoms during sleep, unusual motor disorders, the occurrence of headache, retinal embolism and progression of stenosis.