Yoshihiro Kuriyama

Surgical management of infective endocarditis associated with cerebral complications : multi-center retrospective study in Japan

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.

Periventricular white matter lucency and cerebral blood flow autoregulation in hypertensive patients.

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 autoregulation curves. Cerebrovascular resistance was significantly greater in patients with severe periventricular white matter lucency than in patients without it (P < .05). Impaired autoregulation was also significantly more prevalent in patients with more severe periventricular lesions (P < .05). Multiple regression analysis revealed that the impaired autoregulation was significant and an independent determinant of the severity of such periventricular lesions (R = .34, P < .05). In conclusion, our findings indicated that hypertensive patients with severe periventricular white matter lucency were more likely to have impaired autoregulation of cerebral blood flow and suggest that stricter blood pressure control is required in such patients to prevent deterioration of the cerebral microcirculation.

Histopathological analysis of the mechanisms of intracranial hemorrhage complicating infective endocarditis.

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.

Hemorrhagic and ischemic cerebrovascular complications of active infective endocarditis of native valve.

Cerebrovascular events complicate the management of infective endocarditis. The purpose of this study is to analyze clinical features of cerebrovascular complications in infective endocarditis and to establish the appropriate time schedule of chemotherapy and cardiosurgical intervention. We studied the clinical data of 123 patients with active infective endocarditis of native valves retrospectively. Thirty-three patients (18 males and 15 females, age 17-57 years) had cerebrovascular complications such as cerebral ischemia (n = 22) or intracranial hemorrhage (n = 11). The majority of complications (21 ischemic and 13 hemorrhagic episodes) occurred prior to or within 1 month after chemotherapy. Fatal neurological deterioration developed after cardiac surgery in 2 patients. Both of them needed emergency cardiac surgery, because of worsening hemodynamic state, which was performed within 5 days after cerebral embolic events. The remaining patients undertaking cardiac surgery did all survive; in whom there were chemotherapeutic intervals of 11 days after ischemic events or of 23 days after hemorrhagic events. These medical records suggest that early cardiosurgical intervention, if necessary, needs at least 2-3 weeks of preceding chemotherapy. In cases undergoing more than 1 month of chemotherapy, cerebrovascular complications may be well managed by medical treatment alone.

Brain damage after open heart surgery in patients with acute cardioembolic stroke.

We evaluated 14 patients with acute cardiogenic embolism who underwent open heart surgery soon after the onset to determine the cerebral and cardiac factors that influence neurologic outcome. The mean interval from onset of cerebral embolism to surgery was 5.3 (range 1-16) days. Five of the 14 patients had vegetations from infective endocarditis (including prosthetic valve endocarditis) as embolic sources, eight had intracardiac thrombi, and one had atrial myxoma. The diagnosed site of infarction before surgery was based on computed tomographic and/or angiographic findings. Of the 14 patients, four had infarcts due to major artery occlusion, seven due to cortical branch occlusion, and two due to perforating artery occlusion; one patient presented with a transient ischemic attack without computed tomographic abnormalities. Ten patients (71%) showed no clinical aggravation after open heart surgery; however, two patients died of massive cerebral hemorrhage, one died of deterioration of brain edema, and another became comatose from midbrain hemorrhage immediately after surgery. The four patients with clinical aggravation comprised three with septic embolism and one with aseptic occlusion of a major artery. From these results, infective endocarditis and a large infarct appear to be possible aggravating factors when patients with recent cerebral embolism undergo open heart surgery.

To-and-Fro Movement and External Escape of Carotid Arterial Blood in Brain Death Cases. A Doppler Ultrasonic Study

In brain death cases who showed nonfilling phenomena in the internal carotid angiograms, the blood flow velocity patterns of the common carotid arteries were characterized by involvement of a single systolic peak and a marked reverse flow component which had never been observed in healthy subjects. The individuality of each blood flow velocity pattern in the common, internal and external carotid arteries was made clear by placing the transducer in contact with the respective artery in a certain case. The Doppler signal from the internal carotid artery involving a signal from a reverse flow was slightly detectable, even if the blood pressure was elevated by norepinephrine infusion and the external carotid artery was temporarily compressed. The blood flow velocity pattern of the external carotid artery was similar to the pattern of the common carotid artery. The peculiar flow pattern indicates that a brain death case has a to-and-fro movement in the internal carotid blood flow and an external carotid escape of common carotid arterial blood.

Angiographic evaluation of brain infarction limited to the anterior cerebral artery territory.

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 (n = 10) or reversible segmental dilatation (n = 3) of the anterior cerebral artery, A1 hypoplasia (n = 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 A1 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 A1 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)

Effect of chronic middle cerebral artery stenosis on the local cerebral hemodynamics.

In 36 patients with angiographically proven middle cerebral artery (MCA) stenosis, local cerebral hemodynamics were studied employing angiography, 133Xe inhalation regional cerebral blood flow (rCBF) measurements and CT scans. They had transient ischemic attacks in 8 and completed stroke in 28. The patients with less than 50% stenosis (n = 16) had no hemodynamic abnormality in angiographical and rCBF examinations. The infarction in this group was small and located in the basal ganglia area. The patients with 50 to 74% stenosis (n = 9) often revealed a delayed filling of MCA branches in the angiography, however, they showed no significant rCBF reduction. The infarction in this group was also small and located in the basal ganglia area. The patients with 75 to 99% stenosis (n = 11) exhibited a significant flow depression both in angiographical and rCBF examinations. Three of them had large cerebral infarction in the watershed zone or the cerebral cortex. The results of the present study suggest that the hemodynamic effect of MCA stenosis begins to manifest at 50% in grade and becomes apparent at 75%. The danger of hemodynamic crisis as well as the risk of large cerebral infarction may increase when MCA stenosis exceeds 75% in grade.

Identification of recent lacunar lesions in cases of multiple small infarctions by magnetic resonance imaging.

In nine patients with recent lacunar stroke who revealed multiple small lesions in x-ray computed tomography (CT) and magnetic resonance imaging (MRI), CT and MRI enhancement studies were performed on the same day employing iodinated contrast medium and gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA), respectively. In CT, the injection of contrast medium enhanced recent lesions in only four of the nine patients; furthermore, the effect was weak. In MRI, the injection of Gd-DTPA enhanced recent lesions in all patients except for one who was examined 4 weeks after ictus, and the effect was excellent. Recent infarcts could be identified only by Gd-DTPA-enhanced MRI in four of the nine patients. In patients with multiple small infarctions, identification of recent small infarcted lesions by CT or MRI is sometimes difficult; however, the use of Gd-DTPA in MRI makes it possible to distinguish recent infarcts from other lesions definitively.

Cerebral infarction associated with protein C deficiency.

Background and Purpose A deficiency of plasma protein C, both the hereditary and acquired types, is one cause of thromboembolic disease. Several antineoplastic agents have been reported to decrease the production of protein C in the liver by impairing either the absorption or metabolism of vitamin K, leading to acquired protein C deficiency. Case Description We treated a young woman with protein C deficiency, who had developed a cerebral infarction of the right parietal cortex of sudden onset On admission, the antigenic level of plasma protein C was 38%. Serial cerebral angiography revealed occlusion of the right middle cerebral artery, which subsequently recanalized completely. This patient had taken fluorouracil derivatives orally for as long as 3 years following a left mastectomy for stage II breast cancer. Tests revealed that the patients mother had only one-half the normal activity of plasma protein C despite a normal antigenic level. Conclusions We speculate that the etiology of the cerebral infarction in this patient might involve an embolic mechanism associated with protein C deficiency induced by an interaction between inherited and acquired factors.