Abstracts of Literature
Cognitive Deficits in the Acute Stage After Subarachnoid Hemorrhage—Hütter BO (Dept of Neurosurgery, Univ of Technology [RWTH] Aachen, 52057 Aachen, Pauwelsstr 30, Germany), Kreitchmann-Andermahr I, Gilsbach JM—Neurosurgery. 1998;43:1054–1065.
OBJECTIVE: In spite of fundamentally improved medical management of subarachnoid hemorrhage (SAH), many patients remain mentally impaired. However, the causes of these disturbances are unclear. The present study was performed to elucidate the significance of the hemorrhage itself and related events in the neuropsychological performance of patients in the acute stage after SAH.
METHODS: A series of 51 patients were examined, by means of a battery of cognitive tests, 1 to 13 days (mean, 5.9 d) after SAH. Thirty-three patients had experienced ruptured aneurysms, and 18 had sustained SAH of unknown origin. Furthermore, 25 patients who had undergone surgical treatment (a mean of 5.0 d earlier) of prolapsed lumbar discs served as a control group.
RESULTS: The cognitive deficits of the patients after aneurysmal SAH proved to be comparable to those after spontaneous SAH of unknown origin, with the single exception of a significantly worse (P=0.003) concentration capacity in the surgically treated group. The severity of SAH in computed tomographic scans correlated (up to r=0.57, P<0.001) with poor performance on tests of memory, concentration, divided attention, and perseveration. Frontal intracerebral hemorrhage led to significantly more errors in an aphasia screening test (P<0.001) and a test of perseveration (P<0.001). If acute hydrocephalus was present, the patients exhibited worse long-term memory (P<0.001), showed slower reaction times (P=0.01), and made more errors in the perseveration test (P=0.004). Patients with intraventricular blood performed at significantly lower levels in the concentration (P=0.001), divided attention (P=0.01), long-term memory (P<0.001), and perseveration (P=0.003) tests.
CONCLUSION: The results emphasize that the severity of SAH (Fisher score) is the most important factor related to cognitive dysfunction, but frontal hematoma, intraventricular hemorrhage, and acute hydrocephalus were also associated with cognitive deficits, compared with patients with SAH without these findings.
Key Words: subarachnoid hemorrhage, cognition
Prothrombotic Disorders in Infants and Children With Cerebral Thromoembolism—deVeber G (Div of Neurology, Hospital for Sick Children, 555 Univ Ave, Toronto, Ontario, Canada M5G 1X8), Monagle P, Chan A, MacGregor D, Curtis R, Lee S, Vegh P, Adams M, Marzinotto V, Leaker M, Massicotte P, Lillicrap D, Andrew M—Arch Neurol. 1998;55:1539–1543.
Background: To our knowledge, the contribution of prothrombotic conditions to cerebral thromboembolism has never been prospectively studied in a large series of pediatric patients.
Methods: The Hospital for Sick Children, Toronto, Ontario, established a program in January 1992 to diagnose and treat children (term newborn to 18 years old) with arterial ischemic stroke or sinovenous thrombosis. The routine evaluation for prothrombotic conditions included plasminogen, antithrombin, protein C, free protein S, activated protein C resistance, IgG and IgM anticardiolipin antibody, and lupus anticoagulant. We analyzed samples taken within 2 years of the event. We report results on patients seen from January 1, 1992, to January 1, 1997.
Results: Ninety-two patients (47 males and 45 females) entered the program during the study interval. Patients ranged from newborn to 18 years in age. Arterial ischemic stroke occurred in 78% of patients while sinovenous thrombosis occurred in 22%. All were tested for prothrombotic disorders. One or more abnormal results were present in 35 (38%) of the 92 patients. The majority (21/35) had multiple abnormal test results. The abnormal test results were anticardiolipin antibody (33%), plasminogen (9.5%), activated protein C resistance (9%), protein C (7%), antithrombin (12.5%), lupus anticoagulant (8%), and free protein S (11.5%). Male sex predicted the presence of prothrombotic abnormalities (relative risk, 1.7; 95% confidence interval, 1.2–2.5), but stroke type (relative risk, 0.8; 95% confidence interval, 0.7–1.1), age group, and presence of other risk factors did not predict abnormal testing.
Conclusions: A significant proportion (38%) of children with cerebral thromboembolism had evidence of prothrombotic conditions. In particular, there was a predominance of children with anticardiolipin antibody (33%). These data support a recommendation that children with cerebral thromboembolism be evaluated for prothrombotic disorders.
Key Words: child, thrombosis
Clinical Predictors of Early Embolic Recurrence in Presumed Cardioembolic Stroke—Arboix A (Servicio de Neurologia Hospital del Sagrat Cor. Viladomat 288 E-08029 Barcelona, Spain), Garcia-Eroles L, Oliveres M, Massons JB, Targa C—Cerebrovasc Dis. 1998;8:345–353. Copyright © 1998 S. Karger AG, Basel.
Background: We determined clinical predictive factors of in-hospital embolic recurrence in presumed cardioembolic stroke patients by means of multivariate analysis based on clinical and neuroimaging prognostic variables assessed within 48 h of stroke onset. Methods: Data of 347 consecutive patients with presumed cardioembolic stroke included in a prospective stroke registry were collected. Demographic characteristics, clinical events. and outcome in the recurrent and nonrecurrent embolization group were compared. The independent predictive value of each variable on the development of early embolic recurrence was analyzed in two multiple liner regression models—one based on eight demographic, anamnestic, and clinical variables and another based on 10 clinical, neuroimaging, and outcome variables. Results: In-hospital recurrent embolization was diagnosed in 25 (6.9%) patients. The latency period was 12.1 days. The overall in-hospital mortality was 70.8% in the recurrent embolization group and 24.4% in the nonrecurrent embolization group (p<0.001). Alcohol abuse, the combination of hypertension, valvular heart disease, and atrial fibrillation, nausea and vomiting, and previous cerebral infarction were predictors of recurrent embolization in the model based on clinical variables. In addition to these four variables, cardiac events were selected in the model based on clinical, neuroimaging, and outcome variables. Conclusions: A small number of clinical features that can be easily obtained on the patient’s initial assessment may help clinicians to identify a subgroup of patients with cardioembolic stroke at the highest risk of developing early recurrent brain or systemic embolization.
Key Words: cardioembolic stroke, risk factors
Recovery of Swallowing After Dysphagic Stroke Relates to Functional Reorganization in the Intact Motor Cortex—Hamdy S, Aziz Q, Rothwell JC, Power M, Singh KD, Nicholson DA, Tallis RC, Thompson DG (Section of Gastroenterology, Hope Hospital, Eccles Old Road, Manchester M6 8HD, England)—Gastroenterology. 1998;115:1104–1112. Copyright © 1998 by the American Gastroenterological Association.
Background & Aims: The aim of this study was to determine the mechanism for recovery of swallowing after dysphagic stroke. Methods: Twenty-eight patients who had a unilateral hemispheric stroke were studied 1 week and 1 and 3 months after the stroke by videofluoroscopy. Pharyngeal and thenar electromyographic responses to magnetic stimulation of multiple sites over both hemispheres were recorded, and motor representations were correlated with swallowing recovery. Results: Dysphagia was initially present in 71% of patients and in 46% and 41% of the patients at 1 and 3 months, respectively. Cortical representation of the pharynx was smaller in the affected hemisphere (5±1 sites) than the unaffected hemisphere (13±1 sites; P≤0.001). Nondysphagic and persistently dysphagic patients showed little change in pharyngeal representation in either hemisphere at 1 and 3 months compared with presentation, but dysphagic patients who recovered had an increased pharyngeal representation in the unaffected hemisphere at 1 and 3 months (15±2 and 17±3 vs. 9±2 sites; P≤0.02) without change in the affected hemisphere. In contrast, thenar representation increased in the affected hemisphere but not the unaffected hemisphere at 1 and 3 months (P≤0.01). Conclusions: Return of swallowing after dysphagic stroke is associated with increased pharyngeal representation in the unaffected hemisphere, suggesting a role for intact hemisphere reorganization in recovery.
Key Words: stroke outcome, dysphagia
Wallerian Degeneration of the Pyramidal Tract Does Not Affect Stroke Rehabilitation Outcome—Miyai I (Dept of Neurology, Toneyama National Hospital, 5-1-1 Toneyama, Toyonaka City, Osaka 560-8552, Japan), Suzuki T, Kii K, Kang J, Kubota K—Neurology. 1998;51:1613–1616. Copyright © 1998 by the American Academy of Neurology.
Objective: To test whether Wallerian degeneration (WD) of the pyramidal tract as signaled by MRI affects rehabilitation outcome in patients with subcortical infarction (internal capsule or corona radiata). Background: Recent radiologic evidence suggests that WD occurs no earlier than 3 months after a subcortical infarction. Methods: A total of 77 consecutive patients with pure motor hemiparesis due to an initial subcortical infarction were assessed on admission and discharge with the Functional Independence Measure (FIM) for disability and Stroke Impairment Assessment Set (SIAS, full=25) for impairment. WD was defined by a high-intensity area detected along the pyramidal tract below the level of lesion on T2-weighted MR image (WD+). Results: Age, sex, side of stroke, Mini-Mental State Examination score, and volume of lesion were comparable for each group. Length of stay (LOS) was significantly longer (p<0.05) in WD+ (130 days) than in WD− (105 days). There was no difference in the change of FIM (WD+, 99 to 111; WD−, 95 to 107) or SIAS measures (WD+, 12 to 16; WD−, 13 to 16) made on admission and discharge, nor was there any effect of the timing of the rehabilitation experience (≤90 days or >90 days after stroke). Conclusions: After stroke, apparent WD of the pyramidal tract may slow functional recovery but does not limit final rehabilitation outcome of pure motor hemiparesis. Study of the mechanisms of compensation for this delayed pyramidal tract degeneration will enhance the scientific basis for rehabilitation.
Key Words: stroke outcome, rehabilitation
Stroke and Intracranial Venous Thrombosis During Pregnancy and Puerperium—Lanska DJ (VA Medical Center, 500 East Veterans St, Tomah, WI 54660), Kryscio RJ—Neurology. 1998;51:1622–1628. Copyright © 1998 by the American Academy of Neurology.
Objective: To determine nationally representative estimates of the incidence of stroke and intracranial venous thrombosis during pregnancy and the puerperium, and to identify potential risk factors for these conditions. Methods:National Hospital Discharge Survey data were analyzed for the period 1979 to 1991. Nationally representative estimates of risk were calculated by age, race, presence of pregnancy-related hypertension, census region, hospital ownership, and number of hospital beds. Multivariate models were developed using logistic regression. Results: There were an estimated 8,918 cases of stroke and 5,723 cases of intracranial venous thrombosis during pregnancy and the puerperium in the United States among 50,264,631 deliveries, giving risks of 17.7 cases of stroke and 11.4 cases of intracranial venous thrombosis per 100,000 deliveries. In the multivariate models, stroke was associated strongly with pregnancy-related hypertension, larger hospital size, and proprietary hospital ownership, and inversely associated with living in the South. Intracranial venous thrombosis was associated with maternal age. Conclusions: Stroke and intracranial venous thrombosis are relatively common complications of pregnancy and the puerperium. Collectively, rates for these conditions are about 50% greater for the entire period of pregnancy and the puerperium than for the immediate peripartum period.
Key Words: thrombosis, pregnancy
Leukocyte Count and Aggregation During the Evolution of Cerebral Ischemic Injury—Silvestrini M (Clinica Neurologica. Universitá di Roma “Tor Vergata” Ospedale S. Eugenio P. le dell “Umanesimo,” 10 I-00144 Roma, Italy), Pietroiusti A, Troisi E, Franceschelli L, Piccolo P, Magrini A, Bernardi G, Galante A—Cerebrovasc Dis. 1998;8:305–309. Copyright © 1998 S. Karger AG, Basel.
We evaluated leukocyte aggregation by means of the leukergy test and count in 26 patients with atherothrombotic stroke and in 10 patients with transient ischemic attacks. The evaluation was performed within 24 h from the onset of symptoms and then repeated on day 2, 4, 6 and 8. Data were compared with those of 10 healthy controls. Stroke patients were followed until day 30 when a clinical examination and brain computed tomography were performed to evaluate the extent and outcome of cerebral damage. Both leukocyte aggregation and count were significantly increased in stroke patients with respect to controls. While leukocyte count was not able to differentiate the severity of neurological impairment in stroke patients, leukocyte aggregation was significantly higher in major than in minor stroke patients on days 2 and 4 (p<0.05). Moreover, while values of leukocyte count recorded at entry remained substantially stable in the following determinations in all groups, leukocyte aggregation showed a significant increase (p<0.05) on day 4 with respect to all the other determinations in major stroke patients. These findings show that the extent and temporal profile of changes in leukocyte count and aggregation are different in patients with cerebrovascular disease and suggest an involvement of altered leukocyte rheology in the development of cerebral ischemic injury.
Key Words: cerebral infarction, leukocytes
Hu23F2G, an Antibody Recognizing the Leukocyte CD11/CD18 Integrin, Reduces Injury in a Rabbit Model of Transient Focal Cerebral Ischemia—Yenari MA (Dept of Neurosurgery and Neurology, Stanford Stroke Center, Stanford Univ Medical Center, Palo Alto, CA 94304), Kunis D, Sun GH, Onley D, Watson L, Turner S, Whitaker S, Steinberg GK—Exp Neurol. 1998;153:223–233. Copyright © 1998 by Academic Press.
Neutrophils are known to mediate injury in acute ischemic stroke especially during reperfusion. Migration of neutrophils into regions of ischemic injury involves binding to the endothelial cell’s intercellular adhesion molecule (ICAM-1) through the leukocyte integrin, CD11/CD18. We studied the potential for neuroprotection with a humanized antibody that binds to and blocks the functions of the CD11/CD18 integrin in a rabbit model of transient focal ischemia. Fifteen New Zealand White rabbits underwent transorbital occlusion of the left middle cerebral, anterior cerebral, and internal carotid arteries using aneurysm clips for 2 h, followed by 6 h of reperfusion. Treatment with a maximally saturating dose (4 mg/kg) of a humanized CD11/CD18 monoclonal antibody (Hu23F2G, ICOS Corp., Bothell, WA) (n=8) or placebo (n=7) was administered 20 min after occlusion and given as a single intravenous bolus. Hemispheric ischemic neuronal damage (IND) as seen on hematoxylin- and eosin-stained sections was significantly reduced in Hu23F2G-treated animals by 57% (Hu23F2G: 15±6.9%; placebo: 35±5%; mean±SEM, P<0.05, t-test). Immunohistochemical staining with neutrophil elastase confirmed the presence of neutrophils within regions of IND in control brains. Treatment with Hu23F2G resulted in marked reduction of neutrophil infiltration. (No. of neutrophils/IND area: Hu23F2G 36.1±36.7 cm−2, placebo 460.6±101.8 cm−2, P=0.001.) Antagonism of neutrophil migration at the level of the CD11/CD18 integrin reduces ischemic injury in experimental stroke.
Key Words: cerebral ischemia, focal, integrin
Hyperhomocysteinemia Increases Intimal Hyperplasia in a Rat Carotid Endarterectomy Model—Southern FN, Cruz N, Fink LM, Cooney CA, Barone GW, Eidt JF, Moursi MM (Div of Vascular Surgery, VA Medical Center, Vascular Lab [112PV/LR], 4300 W 7th St, Little Rock, AR 72205)—J Vasc Surg. 1998;28:909–918. Copyright © by the Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter.
Purpose: This preliminary study investigated the ability to elevate the serum homocysteine (H[e]) levels and investigated the increases in postoperative neointimal hyperplasia (IH) in an environment with hyperhomocysteinemia and the resultant restenosis in a rat carotid endarterectomy (CEA) model.
Method: The 9 rats for the control group were fed rat chow, and the 8 rats for the H(e) group were fed H(e)-supplemented rat chow for 2 weeks before and after CEA. The animals underwent anesthesia, and a left common CEA was performed. After 14 days, the serum H(e) levels were measured and the left carotid artery was harvested and elastin stained. Morphometric measurements were used to calculate the area of stenosis of the lumen. The mean and the standard deviation of the mean were determined. The 2 groups were compared with the Mann-Whitney test and a linear regression model. Three additional rats per group were studied, with carotid artery sectioning with double immunohistochemical staining for 5-bromodeoxyuridine (BrdU) and α-smooth muscle (α-SM) actin.
Result: The serum H(e) level in the H(e) group was 36.32 μmol/L±15.28, and in the control group the level was 5.53 μmol/L±2.06 (P=.0007). IH presented as percent lumen stenosis was 21.89%±4.82% in the H(e) group and 4.82%±1.64% in the control group (P=.0007). The linear regression model of the serum H(e) levels and the percent stenosis showed a linear relationship (r2=.72). The α-SM actin staining revealed that nearly all of the cells in the IH area were of smooth muscle or myofibroblast origin and that 10.1%±2.6% of the cells were stained for BrdU in the control group versus 23%±7.1% in the H(e) group. Also, 9.3%±2.6% of the cells in the IH area were stained for BrdU and for α-SM actin versus 19.1%±5.6% stained for both BrdU and α-SM actin in the H(e) group.
Conclusion: This is the first study to examine IH after CEA and hyperhomocysteinemia in rats. The study shows that the elevation of serum H(e) levels can be obtained by feeding rats modified diets with added H(e). The consistent elevation of serum H(e) levels was associated with more than 4 times the amount of IH after a CEA in a rat model.
Key Words: carotid endartectomy, hyperhomocysteinemia
Identifying Hypoxic Tissue After Acute Ischemic Stroke Using PET and 18F-Fluoromisonidazole—Read SJ (Dept of Neurology, Austin & Repatriation Medical Centre, Studley Road, Heidelberg, VIC, 3084 Australia), Hirano T, Abbot DF, Sachinidis JI, Tochon-Danguy HJ, Chan JG, Pharm B, Egan GF, Scott AM, Bladin CF, McKay WJ, Donnan GA—Neurology. 1998;51:1617–1621. Copyright © 1998 by the American Academy of Neurology.
Objective: To show that PET with 18F-fluoromisonidazole (18F-FMISO) can detect peri-infarct hypoxic tissue in patients after ischemic stroke. Background: PET with 15O-labeled oxygen and water is the only established method for identifying the ischemic penumbra in humans. We used PET with 18F-FMISO in patients after ischemic stroke to identify hypoxic but viable peri-infarct tissue likely to represent the ischemic penumbra, and to determine how long hypoxic tissues persist after stroke. Methods: Patients with acute hemispheric ischemic stroke were studied using PET with 18F-FMISO either within 48 hours or 6 to 11 days after stroke onset. The final infarct was defined by CT performed 6 to 11 days after stroke. Tracer uptake was assessed objectively by calculating the mean activity in the contralateral (normal) hemisphere, then identifying pixels with activity greater than 3 SDs above the mean in both hemispheres. Positive studies were those with high-activity pixels ipsilateral to the infarct. Results: Fifteen patients were studied; 13 within 48 hours of stroke, 8 at 6 to 11 days, and 6 during both time periods. Hypoxic tissue was detected in 9 of the 13 patients studied within 48 hours of stroke, generally distributed in the peripheries of the infarct and adjacent peri-infarct tissues. None of the 8 patients studied 6 to 11 days after stroke exhibited increased 18F-FMISO activity. All 6 patients studied both early and late exhibited areas of increased activity during the early but not the late study. Conclusions: PET with 18F-FMISO can detect peri-infarct hypoxic tissue after acute ischemic stroke. The distribution of hypoxic tissue suggests that it may represent the ischemic penumbra. Hypoxic tissues do not persist to the subacute phase of stroke (6 to 11 days).
Key Words: tomography, emission computed, stroke, acute
Migraine With Aura and Right-to-Left Shunt on Transcranial Doppler: A Case-Control Study—Del Sette M (Dept of Neurosciences and Neurorehabilitation, Univ of Genova, Via De Toni 5 I-16132 Genova, Italy), Angeli S, Leandri M, Ferriero G, Bruzzone GL, Finocchi C, Gandolfo C—Cerebrovasc Dis. 1998;8:327–330. Copyright © 1998 S. Karger AG, Basel.
Right-to-left shunt (RLS), usually due to patent foramen ovale, is a well-established risk factor for ischemic stroke in young patients, while the role of migraine as an independent factor is still debated. We evaluated 44 patients suffering from migraine with aura, and compared them with 73 patients younger than 50 with focal cerebral ischemia, and 50 controls, asymptomatic for cerebrovascular disease, and without a history of migraine. All the subjects underwent bilateral transcranial Doppler with injection of contrast medium in an antecubital vein. The test was performed during normal ventilation and during Valsalva maneuver, recording both the middle cerebral arteries and the basilar artery. Criteria for diagnosing RLS was the presence of at least 3 microbubbles within 15 s from injection. Eighteen out of 44 migraine patients (41%) showed RLS, as opposed to 8 of 50 controls (16%) (p<0.005). Twenty-six out of 73 patients with cerebral ischemia had RLS (35%). We conclude that the prevalence of RLS in patients with migraine with aura is significantly higher than in normal controls, and is similar to the prevalence of RLS in young patients with stroke. These findings could be helpful in understanding the relationship between migraine and stroke.
Key Words: foramen ovale, patent, ultrasonography, Doppler, transcranial
Warfarin Use Following Ischemic Stroke Among Medicare Patients With Atrial Fibrillation—Brass LM (Dept of Neurology, LCI-700, Yale Univ School of Medicine, 15 York St, PO Box 208018, New Haven, CT 06520-8018), Krumholz HM, Scinto JD, Mathur D, Radford—Arch Intern Med. 1998;158:2093–2100.
Background: Elderly patients with ischemic stroke and atrial fibrillation are at especially increased risk for recurrent stroke. Warfarin sodium is highly effective in reducing this risk.
Objective: To determine the use of warfarin among a population sample of elderly patients with atrial fibrillation hospitalized for ischemic stroke.
Methods: The Connecticut Peer Review Organization conducted a chart review of Medicare patients, aged 65 years or older, hospitalized in 1994 with a diagnosis of atrial fibrillation. Patients with a principal diagnosis of acute myocardial infarction or another indication for anticoagulation were excluded.
Results: Among 635 patients (402 women: 585 white: 218≥85 years old: 147 with a new diagnosis of atrial fibrillation), 334 had stroke as a principal diagnosis. Among those discharged alive after a stroke, only 147 (53%) of 278 were prescribed warfarin at discharge. Furthermore, among 130 (47%) of 278 patients not prescribed warfarin at discharge, 81 (62%) of 130 were also not prescribed aspirin. Increased potential benefit (additional vascular risk factors) was not associated with a higher rate of warfarin use. Low risk for anticoagulation (lack of risk factors for bleeding) was associated with a slightly higher rate of warfarin use. Among those with an increased risk of stroke and a low risk for bleeding (ideal candidates), 124 (62%) of 278 were discharged on a regimen of warfarin.
Conclusion: Anticoagulation of elderly stroke patients with atrial fibrillation, even among ideal candidates, is underused. The increased use of warfarin among these patients represents an excellent opportunity for reducing the risk of recurrent stroke in this high-risk population.
Key Words: warfarin, atrial fibrillation
Anticoagulation Is Unnecessary After Biological Aortic Valve Replacement—Moinuddeen K, Quin J, Shaw R, Dewar M, Tellides G, Kopf G, Elefteriades J (Yale Univ School of Medicine, Section of Cardiothoracic Surgery, 121 FMB, 333 Cedar St, New Haven, CT 06520)—Circulation. 1998;98(suppl II):II-95–11-99. Copyright © 1998 American Heart Association, Inc.
Background: Opinion differs as to whether anticoagulation is beneficial in preventing ischemic stroke in the early postoperative period after biological aortic valve replacement (AVR). The purpose of this study was to determine whether early anticoagulation with heparin and warfarin confers any significant advantage for patients undergoing such replacement.
Methods and Results: Patients undergoing biological AVR between 1987 and 1996 were divided retrospectively into 2 groups based on their postoperative anticoagulation. Group A (109 patients) received heparin followed by warfarin for 3 months (prothrombin time, 20 to 25 seconds). Group B (76 patients) received no postoperative anticoagulation. Patients were followed for cerebral ischemic events, bleeding, repeat operation, hospital stay, and survival. There were 5 (4.6%), 3 (2.8%), and 12 (11%) postoperative cerebral ischemic events for group A at time points of <24 hours, 24 hours to 3 months, and >3 months, respectively; for group B patients, 3 (3.9%), 2 (2.6%), and 9 (11.8%) events were seen during the same respective time periods. There were no statistically significant differences for ischemic events during any of these time periods for the 2 groups. Bleeding complications occurred in 10 (9.2%) group A and 7 (9.2%) group B patients. Mean hospital stay was 12 days for both groups. Repeat operative AVR was required in 6 (5.5%) group A and 7 (9.2%) group B patients. A comparison of Kaplan-Meier survival rates between groups A and B (mean follow-up, 47±26 and 59±30 months, for groups A and B, respectively) was not statistically significant (P=0.60). Survival rates were 93%, 84%, and 62% at 1, 5, and 7 years for group A and 87%, 74%, and 67% for group B, respectively.
Conclusions: Early anticoagulation after AVR confers no advantage in the prevention of early cerebral ischemic events after biological AVR. No disadvantage in terms of bleeding or prolonged hospital stay was incurred by early anticoagulation. Long-term valve function and survival were not adversely affected by withholding early anticoagulation. We conclude that early anticoagulation after biological AVR is unnecessary.
Key Words: aortic valve, anticoagulants
Randomised Double-Blind Placebo-Controlled Trial of Thrombolytic Therapy With Intravenous Alteplase In Acute Ischaemic Stroke (ECASS II)—Hacke W (Dept of Neurology, Univ of Heidelberg Medical School, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany), Kaste M, Fieschi C, Kummer RV, Davalos A, Mejer D, Larrue V, Bluhmki E, Davis S, Donnan G, Schneider D, Diez-Tejedor E, Trouillas P—Lancet. 1998;352:1245–1251.
Background Thrombolysis for acute ischaemic stroke has been investigated in several clinical trials, with variable results. We have assessed the safety and efficacy of intravenous thrombolysis with alteplase (0.9 mg/kg bodyweight) within 6 h of stroke onset.
Methods This non-angiographic, randomised, double-blind, trial enrolled 800 patients in Europe, Australia, and New Zealand. Computed tomography was used to exclude patients with signs of major infarction. Alteplase (n=409) and placebo (n=391) were randomly assigned with stratification for time since symptom onset (0–3 h or 3–6 h). The primary endpoint was the modified Rankin scale (mRS) at 90 days, dichotomised for favourable (score 0–1) and unfavourable (score 2–6) outcome. Analyses were by intention to treat.
Findings 165 (40.3%) alteplase-group patients and 143 (36.6%) placebo-group patients had favourable mRS outcomes (absolute difference 3.7%, p=0.277). In a post-hoc analysis of mRS scores dichotomised for death or dependency, 222 (54.3%) alteplase-group and 180 (46.0%) placebo-group patients had favourable outcomes (score 0–2; absolute difference 8.3%, p=0.024). Treatment differences were similar whether patients were treated within 3 h or 3–6 h. 85 (10.6%) patients died, with no difference between treatment groups at day 90±14 days (43 alteplase, 42 placebo). Symptomatic intracranial haemorrhage occurred in 36 (8.8%) alteplase-group patients and 13 (3.4%) placebo-group patients.
Key Words: thrombolytic therapy, stroke, acute
Rapid-Staged Strategy for Concomitant Critical Carotid and Left Main Coronary Disease With Left Ventricular Dysfunction: IABP Use—Allie DE (Cardiovascular Institute of the South, PO Box 61160, Lafayette, LA 70596-1160), Lirtzman M, Malik AP, Kowalski JM, Barker EA, Walker CM—Ann Thorac Surg. 1998;66:1230–1235. Copyright © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc.
Background. Few reports address the high-risk patient population with concomitant critical carotid and left main coronary disease with left ventricular dysfunction. To decrease the risks involved with the simultaneous and traditional staged surgical approaches, we developed a rapid staging strategy using an intraaortic balloon pump.
Methods. Between 1992 and 1996, 20 patients presented with a high-risk “triad” defined by greater than 70% stenosis of the left main coronary artery, ejection fraction less than 0.30, and greater than 90% stenosis of the internal carotid artery. An intraaortic balloon pump was placed immediately before carotid endarterectomy under angiographic guidance. Less than 24 hours later (mean, 18 hours) coronary artery bypass grafting was performed, and the intraaortic balloon pump was removed the day of coronary artery bypass grafting in all cases (total IABP duration, <36 hours).
Results. Eighteen patients (18/20) were extubated on the day of coronary artery bypass grafting (mean, 12 hours). Sixteen patients (16/20) were transferred from the intensive care unit within 48 hours, with total hospital stay ranging from 6 to 12 days (mean, 8 days). There were no 30-day postoperative deaths, myocardial infarctions, or neurologic, vascular, bleeding, or other major complications. At a mean 29.4-month follow-up, there were two noncardiac deaths and no neurologic events. Six-month, 1-year, and 2-year follow-up ultrasounds showed all operative carotid arteries remained patent.
Conclusions. A rapid staged procedure with angiographically guided placement of the intraaortic balloon pump was safe and effective in this very high risk patient population. It may be an option to decrease the risks involved with simultaneous operations and increase the efficiency and safety of “traditional” staged carotid and coronary artery bypass grafting procedures.
Key Words: bypass surgery, carotid endartectomy
Brain Damage After Aortic Arch Repair Using Selective Cerebral Perfusion—Ohmi M (Dept of Thoracic and Cardiovascular Surgery, Tohoku Univ School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai 980-8574, Japan), Tabayashi K, Hata M, Yokoyama H, Sadahiro M, Saito H—Ann Thorac Surg. 1998;66:1250–1253. Copyright © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc.
Background. Selective cerebral perfusion is one of the most popular methods for cerebral protection during aortic arch repair. However, causes of postoperative brain damage are not fully understood. We analyzed brain damage after aortic arch repair using selective cerebral perfusion for true aortic arch aneurysm in regard to preoperative cerebral infarction and intracranial and extracranial occlusive arterial disease.
Methods. Over a 9-year period, 60 patients with true aortic arch aneurysm underwent aortic arch repair using selective cerebral perfusion. Postoperative brain damage was evaluated in regard to preoperative cerebral infarction detected by computed tomography, magnetic resonance imaging, or both in 50 patients and intracranial and extracranial occlusive arterial disease detected by digital subtraction angiography, magnetic resonance angiography, or both in 35 patients.
Results. Seven (12%) of the 60 patients died within 30 days of operation. Postoperative brain damage occurred in 6 (10.5%) (3, coma, and 3, hemiplegia) of 57 patients; 3 patients who died without awakening were excluded. Preoperatively, old cerebral infarction was detected in 9 patients (18%), and silent cerebral infarction (lacunar infarction and leukoaraiosis) was diagnosed in 26 patients (52%). Postoperative brain damage occurred in 3 (33%) of the 9 patients with preoperative cerebral infarction and in 3 (23%) of 13 patients with negative preoperative brain findings; this excludes 2 patients who died without awakening. No patient with silent cerebral infarction had postoperative brain damage. Occlusive arterial disease was detected in 7 patients (20%). The incidence of brain damage in these patients was 71% (5/7), which was significantly greater than that of 4% (1/28) in patients without occlusive arterial disease (p<0.001).
Conclusions. Silent cerebral infarction may not be a risk factor for postoperative brain damage. Preoperative evaluation of intracranial and extracranial occlusive arterial disease provides important information as to whether a patient might sustain brain damage after aortic arch repair using selective cerebral perfusion.
Key Words: aortic arch, perfusion
Significance of Carotid Restenosis Following Endarterectomy—Ganesan R (c/o Dr R. Cote, Dept of Neurology and Neurosurgery, Montreal General Hospital, L7-408 Montreal, Que, H3G1A4 Canada), Cote R, Mackey A—Cerebrovasc Dis. 1998;8:338–344. Copyright © 1998 S. Karger AG, Basel.
Background and Purpose: The clinical significance of restenosis after carotid endarterectomy as detected by duplex ultrasound has not been clearly established. To address this problem, we retrospectively evaluated the experience at two university-affiliated hospitals. Methods: All charts of patients with carotid endarterectomies between June 1987 and April 1995 were reviewed. Inclusion required neurological assessment and postoperative duplex ultrasound. Exclusion was based on a known source of cardioembolic disease, or recent (<6 months) myocardial infarction. Primary clinical endpoints were ipsilateral transient ischemic attack (TIA) or ischemic stroke. Contributing vascular risk factors were also identified. The effect of restenosis on event-free survival was analyzed using life tables and Gehan-Wilcoxon rank sum test. Logistic regression was used to identify independent risk factors for restenosis and vascular events. Results: One hundred and eighty-seven patients were identified who underwent a total of 207 endarterectomies. Mean follow-up was 30.4±20.9 months during which a total of 64 vascular events, including 42 TIAs, 18 strokes, and 4 vascular deaths occurred. Of these 21 TIAs and 8 strokes were ipsilateral to the side of endarterectomy. Event rates were compared for patients with ipsilateral high- (≥50%) and low-grade (<50%) restenosis. These two groups were comparable in terms of baseline risk factors. There was no significant difference in vascular event rates (for either ipsilateral events or events in any vascular territory) between the group with high- and low-grade restenosis. Nor was any such difference in event rates shown for patients who showed ipsilateral progression of carotid disease on serial ultrasound. However, patients operated for symptomatic carotid disease had a significantly higher risk of neurological events (p=0.035). Logistic regression failed to disclose any other risk factors that were independently predictive of either restenosis or vascular events during follow-up. Conclusion: This study does not show a difference in vascular event rates for higher grades of carotid restenosis after carotid endarterectomy. Routine surveillance with carotid ultrasound does not appear to identify patients at higher risk for postoperative cerebrovascular events.
Key Words: carotid stenosis, carotid endartectomy
Items of Interest
Prevalence, Incidence, Prognosis, and Predisposing Conditions For Atrial Fibrillation: Population-Based Estimates—Kannel WB, Wolf PA, Benjamin EJ, Levy D (reprints not available)—Am J Cardiol. 1998;82:2N–9N. Copyright © by Excerpta Medica, Inc.
MR Arteriography of Intracranial Circulation—Barboriak DP (Dept of Radiology, Box 3808, Duke Univ Medical Center, Durham, NC 27710), Provenzale JM—AJR Am J Roentgenol. 1998;171:1469–1478. Copyright © American Roentgen Ray Society.
The Phenotypic Spectrum of CADASIL: Clinical Findings in 102 Cases—Dichgans M (Dept of Neurology, Klinikum Großhadern, Ludwig-Maximilians-Universität, Munich, Marchioninistr 15, D-81377 Munich, Germany), Mayer M, Uttner I, Brüning R, Müller-Höcker J, Rungger G, Ebke M, Klockgether T, Gasser T—Ann Neurol. 1998;44:731–739. Copyright © by the American Neurological Association.
Impaired Clearance of Emboli (Washout) Is an Important Link Between Hypoperfusion, Embolism, and Ischemic Stroke—Caplan LR (Neurology Dept, Beth Israel Deaconess Medical Ctr, 330 Brookline Ave, Boston, MA 02115), Hennerici M—Arch Neurol. 1998:55:1475–1482.
New Concepts For Drug Therapy After Stroke: Can We Enhance Recovery?—Wahlgren NG (Dept of Neurology, Karolinska Hospital, S-17176 Stockholm, Sweden), Martinsson L—Cerebrovasc Dis. 1998;8:33–38. Copyright © S. Karger AG, Basel.
Matrix Metalloproteinases in Cerebrovascular Disease—Mun-Bryce S (Dept of Neurology, Univ of New Mexico, Albuquerque, NM 87131), Rosenberg GA—J Cereb Blood Flow Metab. 1998;18:1163–1172. Copyright © The International Society of Cerebral Blood Flow and Metabolism.
Medial Temporal Lobe Atrophy in Stroke Patients: Relation to Pre-Existing Dementia—Hénon H, Pasquier F (Dept of Neurology, Memory Unit, Hôpital Roger Salengro, F-59037 Lille, France), Durieu I, Pruvo JP, Leys D—J Neurol Neurosurg Psychiatry. 1998;65:641–647.
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Clinical Effects of Anterior Cerebral Artery Infarction—Nagaratnam N (Blacktown-Mount Druitt Health, Blacktown, NSW 2148, Australia), Davies D, Chen E—J Stroke Cerebrovasc Dis. 1998;7:391–397. Copyright © 1998 by National Stroke Association.
Stroke—Lancet. 1998;352(suppl III):1–30.
Unruptured Intracranial Aneurysms—Risk of Rupture and Risks of Surgical Intervention—The International Study of Unruptured Intracranial Aneurysms Investigators—(David O. Wiebers, ISUIA Coordinating Center, Mayo Clinic, 200 First St SW, Rochester, MN 55905)—N Engl J Med. 1998;339:1725–1733. Copyright © 1998, Massachusetts Medical Society.
Mechanism of Neuronal Damage in Brain Hypoxia/Ischemia: Focus on the Role of Mitochondrial Calcium Accumulation—Budd SL (CNS Research Institute, Brigham and Women’s Hospital and Program in Neuroscience, Harvard Medical School, Boston, MA 02115)—Pharmacol Ther. 1998;80:203–229. Copyright © 1998 Elsevier Science Inc.
The abstracts in this section have been typeset for consistency with journal format but otherwise appear as in the original articles.
- Copyright © 1999 by American Heart Association