JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
NONBACTERIAL THROMBOTIC ENDOCARDITIS AS A CAUSE OF CEREBRAL AND MYOCARDIAL INFARCTION
KIZUKU KURAMOTOSATORU MATSUSHITAHIROSHI YAMANOUCHI
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1984 年 48 巻 9 号 p. 1000-1006

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Clinicopathologic correlations of nonbacterial thrombotic endocarditis (NBTE) were studied with special reference to their pathogenetic role in cerebral and myocardial infarction. In 2340 cases of consecutive autopsies of the aged, NBTE was observed in 217 cases or 9.3%. The age distribution of NBTE revealed a gradual increase with advancing age. The underlying diseases of NBTE were malignant neoplasm (51.6%), infection (28.3%) and other diseases (20.1%). The incidence of NBTE in each cancer was high in cancers of the colon (16.2%), pancreas (15.2%), gall bladder or bile duct (14.1%) and lung (13.0%). The vegetations of NBTE were found on the aortic valve in 46.1%, on the mitral valve in 40.6% and on the both valves in 8.3%. The incidence of myocardial infarction and scar was 51.2% in the NBTE group, while it was 38.6% in the non-NBTE control group (p < 0.02). This difference was marked in patients with a small infarction (10.6% vs. 5.3%) and a myocardial scar (30.4% vs. 19.0%). The grade of coronary stenosis was less in the NBTE group than in the control group (p < 0.001), suggesting that the origin of the myocardial ischemic lesion was embolism from NBTE. The incidence of large cerebral infarction was 14.7% in NBTE and 9.2% in the control group, and that of medium sized cerebral infarction was 35.0% and 23.6% respectively. In this latter group, cortical infarction comprised 57.9% in the NBTE group and 26.6% in the control group. In large cerebral infarction, cerebral atherosclerosis was less severe in NBTE than in the control group (p < 0.001), also suggesting an embolic mechanism. Disseminated intravascular coagulations was found in 41.9% of NBTE. The incidence of myocardial and cerebral infarctions showed no difference between the cases with DIC and those without DIC, suggesting that infarctions were derived not from in situ thrombosis but from embolism caused by NBTE.

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