Radiologic observations in cerebral embolization from left heart myxomas.

Abstract

Cerebral embolization of tumor tissue is a well known complication in patients with left heart myxomas (11). Surprisingly, cerebral angiography has rarely been employed in evaluation, and, even in the few cases in which it has been performed (2, 3, 6, 15), little discussion of the findings and only one set of reproductions (6) are presented in the literature. The purpose of this paper is to present a short review of this subject and report 2 cases in which angiocardiographic and pathologic demonstration of left heart myxomas were coupled with cerebral angiograms showing cerebral vascular abnormalities. Review Metastatic lesions constitute 90 to 95 per cent of all cardiac tumors, but of the primary tumors approximately 50 per cent are myxomas (13, 14). About 75 per cent arise in the left atrium. The majority of the others originate in the right atrium (14), with only 4 reported in the left ventricle (7, 12, 17, 18). Few typical clinical features exist (4, 5, 8, 9). The lesion may be entirely silent clinically, or it may simulate mitral valve disease with obstruction of the mitral orifice. The friable lesions can produce embolization to many different areas (11), resembling the pictures associated with a mural thrombus or subacute bacterial endocarditis. In Aldrich and Greenwood's series onethird of left atrial myxomas were associated with systemic embolization, half of which were cerebral (1). There is a frequent association of cerebral embolization with renal, splenic, and coronary emboli. A particularly suggestive situation, not given much emphasis previously but well illustrated in the literature and in the two cases to be presented herein, is the presence of systemic embolic phenomena in young patients (9). In this respect the cerebral angiographic findings, as suggested by the two cases below, may prove extremely helpful. Case Reports Case I: A 29-year-old male was first admitted to Vanderbilt Hospital May 29, 1963, with complaints of pain and tenderness in a leg muscle for four or five months. At about the time of the beginning of the tenderness minute hemorrhagic spots appeared in the nail beds of his fingers. One week prior to admission, while the patient was doing heavy lifting, a marked whitening developed in the left second through fifth fingers and also in his right fifth finger. This lasted approximately thirty minutes and was associated with coldness of the involved fingers followed by marked hyperemia and a jabbing pain. Also of recent origin were numerous small red spots in the palms of both hands. The patient's past history was essentially normal. Positive physical findings included small splinter hemorrhages in the nail beds of both hands, absence of the right dorsalis pedis pulse, and tenderness of the fingers and both calves. Cardiac examinationwas normal except for a questionable increase in the amplitude of the second pulmonic sound.