To establish guidelines for the surgical treatment of patients with infective endocarditis who have cerebrovascular complications, we conducted a detailed retrospective study of 181 of 244 patients with cerebral complications among 2523 surgical cases of infective endocarditis of the Japanese Association of Thoracic Surgery. The results showed that 9.7% of all patients with infective endocarditis had associated cerebral complications: 108 (44.3%) had active native valve endocarditis, 96 (39.3%) had healed native valve endocarditis, and 40 (16.4%) had prosthetic valve endocarditis. The hospital mortality of the patients with cerebral complications was 11.0% in the group as a whole: 13.9% in active native valve endocarditis, 3.1% in healed native valve endocarditis, and 37.5% in prosthetic valve endocarditis. Diseased valves included the following aortic valve in 55.5%, mitral valve 49.8%, tricuspid valve in 1.3%, and pulmonary valve in 1.3%. In 181 patients with cerebral complications, organisms were detected as follows: gram-positive cocci in 133 (73.5% [Streptococcus in 85, Staphylococcus in 32]), gram-negative in 18 (9.9%), fungus in 11 (6.1%), and unknown in 64.6%, cerebral bleeding in 31.5%, cerebral abscess in 2.8%, and meningitis in 1.1%. Hospital mortality rate and an exacerbation rate of cerebral complications, including related death, according to the interval from onset of cerebral infarction to cardiac surgery, were as follows: 66.3% and 45.5% within 24 hours, 31.3% and 43.8% between 2 and 7 days, 16.7% and 16.7% between 8 and 14 days, 10.0% and 10.0% between 15 and 21 days, 26.3% and 10.5% between 22 and 28 days, and 7.0% and 2.3% over 4 weeks later, respectively. A significant correlation existed between the interval and the exacerbation of cerebral complications (tied p = 0.008). Preoperative risk factors affecting exacerbation of cerebral complications were as follows: (1) severity of cerebral complications (p = 0.006), (2) intervals (p = 0.012), and (3) uncontrolled congestive heart failure as indications for cardiac surgery (p = 0.014). One patient underwent a cardiac operation within 24 hours of the onset of cerebral hemorrhage and died of cerebral damage. No exacerbations occurred in 10 patients who underwent their operation between 2 and 28 days. Nevertheless, exacerbations occurred in 19.0% of patients whose operation was done more than 4 weeks later. These data suggest that cardiac operations can be done safely 4 weeks after cerebral infarction, and if the delay is more than 2 weeks, the exacerbation rate will be around 10%. The risk of progression of cerebral damage is still significant 15 days and even 4 weeks after cerebral hemorrhage.

The goal of this study was to elucidate the association between the development of periventricular white matter lucency and autoregulation of cerebral blood flow in hypertensive patients through the arteriovenous oxygen saturation difference method. We studied 51 hypertensive patients who had previously suffered from minor strokes (lacunar infarction, 43; deep basal minor hemorrhage, 8). Patients were divided into three groups based on the findings of periventricular white matter lucency. We measured the absolute value of resting cerebral blood flow using the argon inhalation method, and stepwise reduction of blood pressure was obtained with patients on a tilting table. Intracerebral venous blood sampling was accomplished by direct cannulation into the jugular vein up to the jugular bulb. We calculated several cerebral circulatory parameters, such as cerebrovascular resistance and cerebral oxygen consumption, and also delineated individual C linicopathological studies suggest that arteriosclerosis resulting from the effects of chronic hypertension is related to the development of periventricular white matter lucency (PVL) or leukoaraiosis. 13 Clinical studies have indicated a connection between this radiological finding and neurological changes, Binswanger's disease in particular. -5Hypertension profoundly influences the autoregulation of cerebral blood flow (CBF) by shifting both lower and upper limits of autoregulatory range toward a higher blood pressure.6 " 8 This phenomenon has also been attributed to structural alterations in the small arteries related to hypertension.To our knowledge, a direct association between PVL and CBF autoregulation has not been investigated. We examined the relation between these two factors in patients with chronic hypertension to determine whether brain computed tomographic (CT) evidence of severe PVL was associated with impaired CBF autoregulation. MethodsWe studied 51 inpatients (34 men, 17 women; age range, 46 to 77 years; mean, 59.4±6.92 years) with chronic hypertension who had previously experienced some type of stroke (lacunar

We report 15 autopsy cases with cerebral atheromatous embolism (14 men and one woman, 57 to 76 years of age) and analyze their pathologic features. Cardiovascular surgery or catheterization triggered the atheromatous embolism in the brain in six cases (aortocoronary bypass, two; emergency aortocoronary bypass after percutaneous transluminal coronary angioplasty, one; graft implantation for thoracic aortic aneurysm, two; coronary angiography, one). The events that had triggered embolism were not clear in the remaining nine cases. Pathologic examination of the brains revealed that nine cases had single or multiple cortical hemorrhagic infarcts corresponding to the border zones between two main cerebral arterial territories. Many of the leptomeningeal arteries located in the subarachnoid spaces of cortical sulci and surfaces adjacent to the infarcts were occluded by atheromatous emboli composed mostly of cholesterol crystals. The internal diameters of the occluded arteries ranged from 50 to 300 microns. Arterial territorial infarcts were present in six cases, three of which had thromboemboli containing various amounts of cholesterol crystals occluding the major arteries or their large branches supplying the infarcted areas, which were pale in two cases and hemorrhagic in one. The other three cases had hemorrhagic infarcts in which atheromatous emboli were present only in the small leptomeningeal arteries and were composed mostly of cholesterol crystals. Atheromatous embolism in the brain frequently causes border-zone infarcts by occlusion of the terminal cortical branches, and sometimes causes arterial territorial infarcts if the emboli are associated with fibrin and sufficiently large to occlude the larger arteries.

Background and Purpose:We conducted the present study to elucidate the pathological mechanisms leading to intracranial hemorrhage complicating infective endocarditis.Methods: Neurological, neuroradiological, and histopathological analyses were performed in 16 patients (one surgical and 15 autopsy cases), 12 men and four women 26-68 years of age, who had demonstrated central nervous system complications during the course of infective endocarditis.Results: Intracranial hemorrhage was found in all cases; parenchymal hematomas were found in 12 cases, hemorrhagic infarcts in four cases, and primary subarachnoid hemorrhages in two cases. Chronological analysis of neurological examination and computed tomographic scan of the brain confirmed that antecedent cerebral ischemic events had occurred in five of 12 patients showing parenchymal hematomas at autopsy. Hemorrhagic infarct, indicated by petechial or diffuse hemorrhages within the infarct, was seen in another four patients, so that hemorrhagic transformation of the ischemic infarct was confirmed in nine patients. Although mycotic aneurysms were found in five patients, only three of these were ruptured; the other two were occluded with septic emboli. Pyogenic arteritis without aneurysm was found to be distributed in the small cortical arterial branches located in the spaces of cortical sulci, with rupture occurring in five patients.Conclusions: These results suggest that hemorrhagic transformation of the ischemic infarct due to septic emboli is the most frequent mechanism leading to intracerebral hemorrhage encountered in patients dying of infective endocarditis and that rupture of pyogenic arteritis may be responsible for such hemorrhage in many cases, with ruptures of mycotic aneurysms as an alternative mechanism. (Stroke 1992^3:843-850) KEY WORDS • cerebral hemorrhage • embolism • endocarditis, bacterial

Background and Purpose: Brain infarction localized in the anterior cerebral artery territory is rather uncommon, and its etiology has not yet been fully elucidated.Methods: Based on computed tomographic findings, 17 patients with solitary anterior cerebral artery territory infarction were selected from among 3,619 patients admitted consecutively to our institute. Patients without angiographic examinations were excluded. The angiographic findings and clinical category of stroke were analyzed in each patient.Results: Angiographic abnormalities were revealed in all patients. These consisted of occlusive changes (#i=10) or reversible segmental dilatation (n=3) of the anterior cerebral artery, Al hypoplasia («=5), and occlusive changes of the carotid artery (n=3). In one patient with anterior cerebral artery occlusion, the occluded artery was reopened and subsequently became reoccluded. The clinical category of stroke was classified as atherothrombotic in 10 patients, cardioembolic in three, and undetermined in the remaining four. In eight of the 10 patients with atherothrombotic infarction, the anterior cerebral artery was narrowed or occluded. In all patients with cardioembolic infarction, the Al segment contralateral to the infarction was hypoplastic.Conclusions: In our series, solitary anterior cerebral artery territory infarction was attributable most commonly to local atherothrombosis and occasionally to cardiogenic embolism. A hypoplastic Al segment may facilitate the occurrence of embolism in the anterior cerebral artery. Reversible dilatatory and occlusive changes of this artery may be another important cause of infarction. (Stroke 1993;24:549-553) KEY WORDS • angiography • cerebral arteries • cerebral infarction