Tetsuo Koike

Fibrinolytic therapy for acute embolic stroke: intravenous, intracarotid, and intra-arterial local approaches.

To clarify the efficacy and limitations of the intra-arterial local infusion of a high-dose fibrinolytic agent for acute embolic stroke, we analyzed the results of 44 patients and compared them with those of 51 patients treated with intracarotid (18 patients) or intravenous (33 patients) infusion therapy. Ten megaunits of recombinant tissue plasminogen activator or 24 x 10(4) IU of urokinase were administered through a microcatheter placed into or proximal to an embolus for 20 minutes. When arterial recanalization was not achieved, a second or third infusion was performed. The rates of complete and partial recanalization just after the local infusion were 52 and 32%, respectively. They were high in middle cerebral and basilar artery occlusion and low in internal carotid artery occlusion (69, 78, and 20%, respectively). In our use, there was no difference between tissue plasminogen activator and urokinase in restoring blood flow. The mean time interval from onset to recanalization in patients with middle cerebral artery occlusion showing marked improvement was 4.8 hours, and it was 5.8 hours with basilar artery occlusion. The size of infarction was reduced, and the outcome was good in patients with complete recanalization achieved. The incidence of hemorrhagic infarction within 24 hours was 22%, and only one patient clinically deteriorated. In the intracarotid infusion group (20 x 10(4) IU of urokinase for 30 min), only two patients showed partial recanalization without clinical improvement. The incidence of hemorrhagic infarction was 28%. The outcome in this group and the intravenous infusion group (18 x 10(4) IU of urokinase a day for 1 wk) was poor compared with that in the local infusion group showing complete recanalization. This preliminary study appears to suggest that intra-arterial local fibrinolytic therapy could be a new strategy for acute embolic stroke.

Angiographic follow-up study of cerebral arteriovenous malformations with reference to their enlargement and regression.

Twenty patients with cerebral arteriovenous malformations (AVMs) were followed up by angiography. Of the 20 AVMs, 16 were nontreated and the remaining 4 were residual. The follow-up periods between the two examinations were from 5 to 28 years, with a median interval of 15 years. At follow-up, the size of the AVM had increased in 4 patients (20%), decreased in 4 (20%), totally regressed in 4 (20%), and was unchanged in 8 (40%). In cases of enlarged AVMs, the patients were all young: from 0 to 11 years old at first angiography and from 6 to 30 at second angiography. The decrease or total regression of the AVM occurred in older patients (over 30 years old at second angiography), and the AVMs were relatively small and fed by single or a few feeders. The patients age and the size of AVM should be considered when operative indications are discussed.

Liver dysfunction in spontaneous intracerebral hemorrhage.

The purpose of this study was to investigate the relationship between mild degrees of liver dysfunction and spontaneous intracerebral hemorrhage (ICH) from the hemostatic standpoint. A detailed study of hemostatic systems was made in 462 patients with ICH. To compare ICH with the other cerebrovascular diseases, data from 120 patients with subarachnoid hemorrhage and 114 others with cerebral infarction were reviewed. At admission, the medical histories of the patients, including information about previous alcohol consumption, was taken, and blood samples were collected to perform the following studies: platelet count, fibrinogen level, prothrombin time, activated partial thromboplastin time, antithrombin III, plasminogen and alpha 2-antiplasmin activity, platelet aggregability, and liver function tests. The incidence of liver dysfunction and alcohol consumption in patients with ICH was significantly (P < 0.05) higher than in patients with subarachnoid hemorrhage and in those with cerebral infarction. Hematoma volume, mortality rate, and past alcohol consumption in patients with ICH significantly increased with worsening severity of liver dysfunction. Although almost all hemostatic parameters became worse with increasing severity of liver dysfunction, they changed within the normal limits. Platelet aggregability and alpha 2-antiplasmin activity in patients with liver dysfunction were remarkably deteriorated beyond normal limits. In conclusion, liver dysfunction associated with alcohol consumption appears to be an important factor in the deterioration of the clinical status of patients with ICH and may be one of the causative factors in the development of ICH. Although mildly impaired hemostatic systems may be partially responsible for these adverse effects of liver dysfunction on ICH, it seems probable that nonhemostatic mechanisms are attributed to the effects.

Hemostasis in spontaneous subarachnoid hemorrhage.

To comprehensively examine changes in the hemostatic systems early after spontaneous subarachnoid hemorrhage (SAH) and to assess the relationships between those changes and neurological findings, computed tomographic findings, and clinical outcomes, we reviewed 167 patients who were admitted within 24 hours of the onset of SAH. Blood was taken from all of the patients at admission for detailed examinations of the hemostatic systems. The following results were obtained: 1) the levels of the thrombin-antithrombin complex (elevation indicating the activation fo the blood coagulation system), plasmin-antiplasmin complex, and D-dimer (elevation indicating the activation of the fibrinolytic system) significantly increased with the neurological severity, amount of subarachnoid clot, and severity of clinical outcome; 2) the levels of the thrombin-antithrombin complexes and plasmin-antiplasmin complexes were significantly higher in patients with intracerebral or intraventricular hematomas than in patients without those hematomas; 3) in each of almost all the neurological and computed tomographic grades, the levels of the thrombin-antithrombin complexes were significantly higher in the patients with poor outcomes than in those with good outcomes; 4) the poor outcome rate significantly increased with neurological severity and the amount of subarachnoid clot. These data suggest that the activation of the blood coagulation system as well as of the fibrinolytic system occurred early in the course of SAH and that these systems were activated to a greater extent with the severity of neurological grades, computed tomographic findings, and clinical outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Long term results of ruptured aneurysms treated by coating

We report the long term results of the treatment of 23 intracranial ruptured aneurysms by coating. Twenty-three patients treated by coating were followed for a mean period of 11.2 years. The mean interval between the last hemorrhage and the operation was 22.4 days. Ten aneurysms underwent total coating, 9 with Biobond and 1 with Aron Alpha. Thirteen aneurysms underwent partial coating, 11 with Biobond and 2 with Aron Alpha. Six aneurysms were reinforced partially by other materials, but no aneurysm was wrapped totally with these materials. Rebleeding occurred in 6 patients, of whom 5 died. The mean interval between coating and rebleeding was 4 years. All patients suffering rebleeding had been treated with Biobond, and 3 patients had undergone total coating of aneurysms. The risk of recurrent hemorrhage after total coating with Biobond was 33%. One rebleeding patient underwent a second operation 10.5 years after total coating of the aneurysm. Biobond was found only at the tip of the aneurysmal sac. From these results, reinforcement of ruptured aneurysms with Biobond seems to be of little value, and a more reliable method must be developed for aneurysms that cannot be clipped.

Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysms, by magnetic resonance angiography.

OBJECTIVE The goal of this study was to assess the value of magnetic resonance angiography (MRA), compared with conventional angiography, in the diagnosis and follow-up monitoring of delayed cerebral vasospasm after subarachnoid hemorrhage resulting from rupture of intracranial aneurysms. METHODS For 32 patients undergoing examination by both MRA and conventional angiography during the period of risk for vasospasm, on the same day, the frequency and severity of and sequential changes in vasospasm were evaluated. The three-dimensional time-of-flight method was used. MRA was performed three times, i.e., before, during, and after the period of risk for vasospasm. Conventional angiography was performed twice, i.e., at admission and during the period of risk for vasospasm. Vasospasm was assessed at 22 regions of the cerebral arteries, including the bilateral anterior cerebral (A1, A2, and A3 segments), middle cerebral (M1, M2, and M3 segments), internal carotid (C1 and C2 segments), posterior cerebral (P1 and P2 segments), and posterior communicating arteries. RESULTS Seven patients were excluded because of poor MRA images. Twenty-two of 25 patients (125 arteries) showed vasospasm in conventional angiograms. Nineteen of the 22 patients also showed vasospasm in MRA images; however, 57 arteries (45.6%) were diagnosed as showing vasospasm by MRA, and 59 (47.2%) could not be evaluated because of artifacts. For the remaining three patients (nine arteries, 7.2%), vasospasm could not be detected by MRA. Sequential changes in vasospasm could be well evaluated by MRA. CONCLUSION MRA could be useful for management of cerebral vasospasm, although it cannot become a practical alternative to conventional angiography.

Serial Changes in Hemostasis after Intracranial Surgery

We performed hemostatic studies on eight patients undergoing clipping of unruptured cerebral aneurysms to assess the influence of intracranial surgery itself on hemostasis. Blood samples were collected from each patient 10 times: before and after the induction of anesthesia and 6, 12, and 24 hours and 2, 3, 5, and 7 days immediately after surgery. The changes and our interpretation of them include the following: 1) the elevation of thrombin antithrombin III complex levels (activation of blood coagulation) was transient and monophasic; 2) the elevation of plasmin alpha 2-antiplasmin complex and D-dimer levels (activation of fibrinolysis) was biphasic, despite the monophasic elevation of tissue plasminogen activator or plasminogen activator inhibitor-1 levels; 3) the elevation of beta-thromboglobulin and platelet-factor-4 levels (activation of platelet) was also biphasic; 4) fibrinogen level and alpha 2-antiplasmin activity increased in the acute phase of the postoperative course (acute phase reaction); 5) the changes in hematocrit appeared to parallel those in various other parameters, especially platelet count, antithrombin III, and plasminogen levels for 1 or 2 days after surgery; 6) fibronectin appeared to be consumed in the acute phase of postoperative course; and 7) general anesthesia did not significantly affect hemostasis. These serial changes seem to be related to the activation of hemostatic systems after intracranial surgery and the subsequent acute phase reaction.

Surgical experience with massive lobar haemorrhage caused by cerebral amyloid angiopathy

SummaryNineteen patients with massive lobar haemorrhage without angiographic lesions received direct or stereotactic surgery, and biopsy specimens were examined histologically. Ten patients (53%) were found to have vessels positive for Congo-red staining, and demonstrating amyloid angiopathy. In the patients with amyloid angiopathy, CT scan and surgical findings were investigated. Subarachnoid haemorrhage (9/10), irregularly shaped haematoma (9/10) and fluid-blood density level in the haematoma cavity (7/10) were frequently found on CT scan. The characteristic surgical findings in patients treated by direct surgery were subarachnoid haemorrhage adjacent to intracerebral haematoma (8/8) and the existence of a tangle of vessels in the haematoma cavity (4/8). Evacuation of haematomas was relatively easy, and difficulty of haemostasis was not encountered during surgery.

Dissecting aneurysm of the posterior cerebral artery treated with proximal ligation

A rare case of a dissecting aneurysm of the P3 segment of the right posterior cerebral artery is presented that seems to have occurred in association with mild head injury. The patient was treated surgically because of repeated intramural hemorrhage and enlargement of the aneurysm. Proximal ligation produced thrombosis of the aneurysm without resulting in infarction in the region of the posterior cerebral artery. The mechanisms of the dissection, diagnosis, and treatment are briefly discussed.

Blood Pressure Monitoring in Feeding Arteries of Cerebral Arteriovenous Malformations during Embolization: A Preventive Role in Hemodynamic Complications

To study the hemodynamics of arteriovenous malformations and to avoid hemodynamic complications during and after artificial embolization, we measured arterial blood pressures in 21 feeders in 14 patients through a microcatheter system. Before embolization, the pressures were significantly low in feeders with branches terminating in the malformation (terminal divided branches) and comparatively low in arteriovenous malformations with rapid blood flow through the malformation. The pressures in feeders with brain-nutrifying branches distal to the nidus (transient branches) were significantly high. Therefore, transient branches might be distinguishable from terminal divided branches with the use of feeder pressure monitoring. A hemorrhagic complication occurred in one patient. The feeder pressure in this patient was low before embolization and showed the maximum change among the patients after embolization. It seems that the lower the feeder pressure, the more likely complications are to occur, owing to remarkable hemodynamic alterations. Feeder pressure monitoring may be useful for preventing hemodynamic complications, especially when angiographic findings show feeding arteries giving off terminal divided or transient branches or rapid blood flow through the malformation.