Abstracts of Literature
Systemic Administration of the Potassium Channel Activator Cromakalim Attenuates Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage—Kwan A-L, Lin C-L, Yanamoto H, Howng S-L, Kassell NF, Lee KS (Box 420 HSC, Department of Neurological Surgery, University of Virginia, Charlottesville, VA 22908)—Neurosurgery. 1998;42:347–351.
OBJECTIVE: Cerebral vasospasm is a primary complication after aneurysmal subarachnoid hemorrhage (SAH). Recent evidence indicates that the activation of potassium (K+) channels may be of benefit in relieving spastic constriction. The present study examined the effects of systemic administration of a K+ channel activator, cromakalim, on cerebral vasospasm after experimental SAH.
METHODS: Experimental SAH was performed in rabbits by injecting autologous blood into the cisterna magna. Intravenous injections of cromakalim or vehicle were administered twice daily with the first injection administered 1 hour after induction of SAH. Animals were killed by perfusion-fixation 48 hours after SAH. Basilar arteries were removed and sectioned, and the luminal cross-sectional areas were measured.
RESULTS: Experimental SAH induced cerebral vasospasm in untreated and vehicle-treated animals. Cromakalim attenuated cerebral vasospasm in a dose-dependent manner. This effect achieved statistical significance at doses of 0.1 and 0.3 mg/kg.
CONCLUSION: These results support the concept that targeting vascular K+ channels can be of benefit in preventing the development of cerebral vasospasm. The findings also indicate that cromakalim represents a potential therapeutic agent for the treatment of cerebrovascular pathophysiology after SAH.
Key Words: vasospasm, subarachnoid hemorrhage
Neuroprotective Effect of an Antioxidant, Ebselen, in Patients With Delayed Neurological Deficits After Aneurysmal Subarachnoid Hemorrhage—Saito I (Dept of Neurosurgery, School of Medicine, Kyorin Univ, 6-20-2, Shinkawa Mitaka-shi, Tokyo 181, Japan) Asano T, Sano K, Takakura K, Abe H, Yoshimoto T, Kikuchi H, Ohta T, Ishibashi S—Neurosurgery. 1998;42:269–278.
OBJECTIVE: The effect of ebselen, a seleno-organic compound with antioxidant activity through a glutathione peroxidase-like action, on the outcome of subarachnoid hemorrhage was evaluated in a multicenter placebo-controlled double-blind clinical trial.
METHODS: Patients who suffered aneurysmal subarachnoid hemorrhages of Hunt and Kosnik Grades II through IV at admission and were able to start drug treatment within 96 hours of the ictus were enrolled. Early surgery was performed whenever possible. Oral administration of ebselen granules suspended in water (150 mg, twice a day) or placebo was started immediately after admission and continued for 2 weeks. The major end points were the Glasgow Outcome Scale at 2 weeks, 1 month, and 3 months after the start of treatment. The incidence of delayed ischemic neurological deficits clinically diagnosed as resulting from vasospasm and the incidence and extent of low-density areas on postoperative computed tomographic scans were also studied as secondary outcome measures.
RESULTS: Intent-to-treat analysis of the 286 patients enrolled in the trial (145 patients administered ebselen and 141 administered placebo) revealed that the incidence of clinically diagnosed delayed ischemic neurological deficits was unaltered. There were 52 (receiving ebselen) and 58 (receiving placebo) patients with delayed deficits; however, a significantly better outcome was observed after ebselen treatment than after placebo (P=0.005, χ2 test). There was a corresponding decrease in the incidence and extent of low-density areas (P=0.032, Wilcoxon rank sum test).
CONCLUSION: Ebselen reduced brain damage in patients with delayed neurological deficits after subarachnoid hemorrhage and may be a promising neuroprotective agent.
Key Words: subarachnoid hemorrhage, neuroprotection
Total Quality Improvement Method for Reduction of Delays Between Emergency Department Admission and Treatment of Acute Ischemic Stroke—Tilley BC (Division of Biostatistics and Research Epidemiology, Henry Ford Health Sciences Center, 1 Ford Place, Suite 3E, Detroit, MI 48202), Lyden PD, Brott TG, Lu M, Levine SR, Welch KMA—Arch Neurol. 1997;54:1466–1474.
Objective: To develop an approach for reducing time between emergency department (ED) admission and treatment in patients with acute ischemic stroke to meet the challenge of providing tissue plasminogen activator treatment within 180 minutes.
Design: An observational study.
Setting: Forty trial-affiliated hospitals, including 30 community hospitals.
Participants: A total of 17 324 consecutive patients admitted to trial-affiliated hospital EDs within 24 hours of possible stroke, from January 1991 through October 1994.
Intervention: Appraisal of the process of triage, evaluation, diagnosis, and treatment by means of total quality improvement techniques in each hospital. Staff participating in the process identified sources of variation and modifications by flow charting the process.
Main Outcome Measure: Time between ED admission and treatment with study medication.
Results: Total quality improvement methods identified hospital-specific process improvements. Many improvements were administrative, requiring no additional resources. More than 50% of screened patients arrived too late to be treated. Only 1268 patients were admitted between 0 and 125 minutes from stroke onset with no other trial exclusion criteria; 48% were treated. Of 243 patients admitted between 126 and 170 minutes from stroke onset with no exclusion criteria, 4% were treated. Mean time from ED admission to treatment was similar in teaching and community hospitals.
Conclusions: Total quality improvement methods identified ED-specific sources of process variability and reduced time between ED admission and treatment. Therefore, these methods should be considered in developing and monitoring emergent stroke treatment protocols.
Key Words: emergency service, hospital, stroke, acute
Exaggerated Blood Pressure Responses During Mental Stress Are Associated With Enhanced Carotid Atherosclerosis in Middle-aged Finnish Men: Findings From the Kuopio Ischemic Heart Disease Study—Kamarck TW (Dept of Psychology and Psychiatry, Univ of Pittsburgh, Suite 520, Bellefield Professional Building, 130 N Bellefield Ave, Pittsburgh, PA 15260), Everson SA, Kaplan GA, Manuck SB, Jennings JR, Salonen R, Salonen JT—Circulation. 1997;96:3842–3848. ©1997 American Heart Association, Inc.
Background Exaggerated cardiovascular reactivity to mental stress is hypothesized to increase atherosclerotic risk. We examined this hypothesis using cross-sectional data from the Kuopio Ischemic Heart Disease study, a population-based epidemiological sample.
Methods and Results 901 Eastern Finnish men from four age cohorts (age, 42 to 60 years) were administered a standardized testing battery to assess cardiovascular reactivity to mental stress. Ultrasound measures of intima-medial thickness (IMT) and plaque height from the common carotid arteries were used as noninvasive markers of atherosclerosis. Diastolic blood pressure (DBP) responses to mental stress were significantly associated with mean IMT (b=.021, P=.006), maximum IMT (b=.026, P=.013), and mean plaque height (b=.017, P=.041). Significant associations were also shown between stress-related systolic blood pressure (SBP) reactivity and mean IMT (b=.0151, P=.042). When examined separately by age, associations with IMT were significant only in the youngest half of the sample (age, 46 and 52 years, n=433; for mean IMT, DBP b=.033, P=.0002, SBP b=.0266, P=.003; for maximum IMT, DBP b=.039, P=.002, SBP b=.032, P=.011). Results remained significant in the younger subjects after adjustment for smoking, lipid profiles, fasting glucose, and resting blood pressure (b=.024, P=.011); results also remained significant in a subgroup of unmedicated younger subjects without symptomatic cardiovascular disease (n=135; for SBP reactivity, b=.031, P=.036; for DBP, b=.037, P=.007).
Conclusions The tendency to show exaggerated pressor responses to mental stress is a significant independent correlate of atherosclerosis in this population sample of Finnish men. The effect does not appear to be accounted for by the confounding influence of other risk factors or preexisting clinical disease.
Key Words: stress, psychological, carotid artery diseases
Low Circulating Folate and Vitamin B6 Concentrations: Risk Factors for Stroke, Peripheral Vascular Disease, and Coronary Artery Disease—Robinson K (Desk F15, Dept of Cardiology, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195), Arheart K, Refsum H, Brattström L, Boers G, Ueland P, Rubba P, Palma-Reis R, Meleady R, Daly L, Witteman J, Graham I—Circulation. 1998;97:437–44. ©1998 American Heart Association, Inc.
Background—A high plasma homocysteine concentration is a risk factor for atherosclerosis, and circulating concentrations of homocysteine are related to levels of folate and vitamin B6. This study was performed to explore the interrelationships between homocysteine, B vitamins, and vascular diseases and to evaluate the role of these vitamins as risk factors for atherosclerosis.
Methods—In a multicenter case-control study in Europe, 750 patients with documented vascular disease and 800 control subjects frequency-matched for age and sex were compared. Plasma levels of total homocysteine (before and after methionine loading) were determined, as were those of red cell folate, vitamin B12, and vitamin B6.
Results—In a conditional logistic regression model, homocysteine concentrations greater than the 80th percentile for control subjects either fasting (12.1 μmol/L) or after a methionine load (38.0 μmol/L) were associated with an elevated risk of vascular disease independent of all traditional risk factors. In addition, concentrations of red cell folate below the lowest 10th percentile (<513 nmol/L) and concentrations of vitamin B6 below the lowest 20th percentile (<23.3 nmol/L) for control subjects were also associated with increased risk. This risk was independent of conventional risk factors and for folate was explained in part by increased homocysteine levels. In contrast, the relationship between vitamin B6 and atherosclerosis was independent of homocysteine levels both before and after methionine loading.
Conclusions—Lower levels of folate and vitamin B6 confer an increased risk of atherosclerosis. Clinical trials are now required to evaluate the effect of treatment with these vitamins in the primary and secondary prevention of vascular diseases.
Key Words: folic acid, risk factors
Diagnosis of Intracranial Vasculitis: A Multi-disciplinary Approach—Chu CT, Gray L, Goldstein LB, Hulette CM (Dept of Pathology, Neuropathology Section, Box 2900, Duke Univ Medical Center, Durham, NC 27710)—J Neuropathol Exp Neurol. 1998;57:30–38. ©1998 by the American Association of Neuropathologists.
Intracranial vasculitis, or primary angiitis of the central nervous system (PACNS), is an uncommon, often fatal disorder that frequently responds to aggressive immunosuppressive therapy. Magnetic resonance imaging (MRI), cerebral angiography, and brain biopsy are diagnostic modalities that vary in invasiveness and diagnostic accuracy. The purpose of this study was to determine whether certain clinical or radiologic features were predictive of a diagnostic biopsy. Thirty consecutive patients undergoing brain biopsy to “rule out vasculitis” were studied. Nine patients demonstrated granulomatous or lymphocytic vasculitis, 1 had lymphocytic vasculitis and encephalitis secondary to arbovirus infection, 5 had thickened vessels consistent with hypertensive changes, 5 had amyloid angiopathy and/or changes of Alzheimer disease, 5 demonstrated no pathologic abnormalities, and 1 each had acute infarct, vascular malformation, aneurysm, acellular fibrinoid necrosis, and demyelination. The spectrum of MRI and angiographic changes associated with PACNS were nonspecific, overlapping extensively with changes of chronic hypertension and amyloid deposition. The predictive values of brain biopsy (90–100%) were significantly higher than those of angiography (37–50%) or MRI (43–72%). In this study, morbidity associated with aggressive immunosuppression was significantly greater than that associated with cerebral angiography or brain biopsy. Thus, wedge biopsy of cortical and leptomeningeal tissues is central to the multi-disciplinary approach to a patient with clinical suspicion of PACNS.
Key Words: vasculitis, angiography
Helicobacter pylori Infection: A Risk Factor for Ischemic Cerebrovascular Disease and Carotid Atheroma—Markus HS (Dept of Neurology, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK), Mendall MA—J Neurol Neurosurg Psychiatry. 1998;64:104–107.
Objectives—Chronic Helicobacter pylori infection has been associated with ischaemic heart disease although the mechanism by which it mediates this effect remains unclear. The objective was to determine whether it is also a risk factor for ischaemic cerebrovascular disease.
Methods—A total of 238 patients and 119 controls were studied. Patients were characterised into stroke subtypes based on pathogenic mechanisms and carotid atheroma load was estimated using duplex ultrasound. H pylori seropositivity was determined on serum samples.
Results—H pylori seropositivity was more common in cases (58.8% v 44.5%, p=0.01). The odds ratio for cerebrovascular disease associated with seropositivity was 1.78 (95% confidence interval (95% CI) 1.14–2.77), and this remained significant after controlling for other risk factors including socioeconomic status (1.63 (95% CI 1.02–2.60). H pylori seropositivity was associated with large vessel disease (odds ratio 2.58 (95% CI 1.44–4.63), p=0.001) and lacunar stroke (odds ratio 2.21 (95% CI 1.12–4.38), p=0.02) but not stroke due to cardioembolism or unknown aetiology (odds ratio 1.16 (95% CI 0.66–2.02), p=0.5). Mean (SD) carotid stenosis was greater in patients seropositive for H pylori (37.3 (29.7) v 27.9 (26.2)%, p=0.01). There was no difference in the prevalence of seropositivity between patients with stroke and transient ischaemic attack (59.6% v 58.6%, p=0.9).
Conclusion—Chronic H pylori infection is an independent risk factor for ischaemic cerebrovascular disease and may act, at least in part, by increasing atherosclerosis.
Key Words: infection, risk factors
Large Infarcts in the Middle Cerebral Artery Territory: Etiology and Outcome Patterns—Heinsius T, Bogousslavsky J (Dept of Neurology, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland), Melle GV—Neurology. 1998;50:341–350. ©1998 by the American Academy of Neurology.
Large supratentorial infarctions play an important role in early mortality and severe disability from stroke. However, data concerning these types of infarction are scarce. Using data from the Lausanne Stroke Registry, we studied patients with a CT-proven infarction of the middle cerebral artery (MCA) territory that covered at least two of three MCA subterritories (deep, superficial anterior [superior] and posterior [inferior] territory). We compared these patients with patients presenting more limited infarction in the MCA territory. Our study group of large MCA (laMCA) infarction contained 208 patients, corresponding to 7.6% of all ischemic infarctions in the Lausanne Stroke Registry. Seventy-two patients had complete infarction in the whole MCA territory (coMCA). Internal carotid artery (ICA) occlusion (41%) and ICA dissection (12%) were more common than in limited superficial MCA (lsMCA) infarct and anterior circulation infarct (p<0.001). Among the patients without ICA occlusion, atrial fibrillation (33%; p<0.002) and cardiogenic embolism in general (54%; p<0.001) were more frequent in laMCA than in lsMCA infarct. Severe neurologic deficit (hemiplegia and hemisensory loss in the face, arm and leg, hemianopia, global aphasia, reduced consciousness) was more common than in other types of infarct. A combination of these symptoms had a positive predictive value for laMCA infarction of 0.73 (sensitivity for left side laMCA infarcts, 0.56). Mortality (17%) and severe disability (50%) were higher with laMCA than for other infarcts (p<0.001). Sixteen of the 35 deaths could be attributed to brain edema. Reduced consciousness, hemianopia, and coMCA infarction were independent predictors of death or severe disability; for death only, coma was an independent predictor. Patients who died because of brain edema were younger than patients whose death was due to other causes (mean age, 57 versus 73 years; p<0.001); they also died sooner (mean time of death after stroke, 5 versus 37 days; p<0.001). Furthermore, patients who developed coma on the day of admission were more likely to die because of brain death (p<0.001). Large middle cerebral artery infarction is associated with cardiogenic embolism, ICA occlusion, and ICA dissection. It is a major predictor of death and severe disability, although a lower frequency of malignant brain infarction was found than previously reported.
Key Words: middle cerebral artery, stroke outcome
Impact of Atrial Fibrillation on Mortality, Stroke and Medical Costs—Wolf PA (Boston Univ School of Medicine, 715 Albany St, B608, Boston, MA 02118-2526), Mitchell JB, Baker CS, Kannel WB, D’Agostino RB—Arch Intern Med. 1998;158:229–234.
Background: The impact of atrial fibrillation (AF) on mortality, stroke, and medical costs is unknown.
Methods: We conducted a prospective cohort study of hospitalized Medicare patients with AF and 1 other cardiovascular diagnosis (CVD) compared with a matched group without AF (n=26 753), randomly selected in 6 age-sex strata from 1989 MedPAR files of more than 1 million patients diagnosed as having AF. Stroke rates were also determined in another cohort free of CVD (n=14 267). Total medical costs after hospitalization were available from a 1991 cohort. Cumulative mortality, stroke rates, and costs following index admission were adjusted by multivariate and proportional hazard regression analyses.
Results: Mortality rates were high in individuals with CVD, ranging from 19.0% to 52.1% in 1 year. Adjusted relative mortality risk was approximately 20% higher in patients with AF in all age-sex strata during each of the 3 years studied (P<.05). Incidence of stroke was high in individuals with CVD, 6.2% to 15.4% in 1 year, with and without AF, and was at least 5-fold higher than in individuals without CVD. In those with CVD, stroke rates were approximately 25% higher in women with AF (P<.05) but only 10% higher in men. Adjusted total Medicare spending in 1 year was 8.6- to 22.6-fold greater in men, and 9.8- to 11.2-fold greater in women with AF (P<.05). Second- and third-year costs were increased as well.
Conclusion: Prevention of AF and treatment of patients with AF and associated CVD may yield benefits in reduced mortality and stroke as well as reducing health care costs.
Key Words: atrial fibrillation, stroke outcome
Hyperhomocysteinemia Is Associated With an Increased Risk of Cardiovascular Disease, Especially in Non–Insulin-Dependent Diabetes Mellitus: A Population-Based Study—Hoogeveen EK (Institute for Research in Extramural Medicine, Vrije Universiteit, Van der Boechorststraat 7, NL-1081 BT Amsterdam, Netherlands), Kostense PJ, Beks PJ, Mackaay AJC, Jakobs C, Bouter LM, Heine RJ, Stehouwer CDA—Arterioscler Thromb Vasc Biol. 1998;18:133–138. ©1998 American Heart Association, Inc.
A high serum total homocysteine (tHcy) level is an independent risk factor for cardiovascular disease. Because it is not known whether the strength of the association between hyperhomocysteinemia and cardiovascular disease is similar for peripheral arterial, coronary artery, and cerebrovascular disease, we compared the three separate risk estimates in an age-, sex-, and glucose tolerance–stratified random sample (n=631) from a 50- to 75-year-old general white population. Furthermore, we investigated the combined effect of hyperhomocysteinemia and diabetes mellitus with regard to cardiovascular disease. The prevalence of fasting hyperhomocysteinemia (>14.0 μmol/L) was 25.8%. After adjustment for age, sex, hypertension, hypercholesterolemia, diabetes, and smoking, the odds ratios (ORs; 95% confidence intervals) per 5-μmol/L increment in tHcy were 1.44 (1.10 to 1.87) for peripheral arterial, 1.25 (1.03 to 1.51) for coronary artery, 1.24 (0.97 to 1.58) for cerebrovascular, and 1.39 (1.15 to 1.68) for any cardiovascular disease. After stratification by glucose tolerance category and adjustment for the classic risk factors and serum creatinine, the ORs per 5-μmol/L increment in tHcy for any cardiovascular disease were 1.38 (1.03 to 1.85) in normal glucose tolerance, 1.55 (1.01 to 2.38) in impaired glucose tolerance, and 2.33 (1.11 to 4.90) in non–insulin-dependent diabetes mellitus (P=.07 for interaction). We conclude that the magnitude of the association between hyperhomocysteinemia and cardiovascular disease is similar for peripheral arterial, coronary artery, and cerebrovascular disease in a 50- to 75-year-old general population. High serum tHcy may be a stronger (1.6-fold) risk factor for cardiovascular disease in subjects with non–insulin-dependent diabetes mellitus than in nondiabetic subjects.
Key Words: homocyst(e)ine, risk factors
Thrombomodulin Expression in Bovine Brain Capillaries: Anticoagulant Function of the Blood-Brain Barrier, Regional Differences, and Regulatory Mechanisms—Wang L, Tran ND, Kittaka M, Fisher MJ, Schreiber SS, Zlokovic BV (2025 Zonal Ave, RMR 506, Los Angeles, CA 90033)—Arterioscler Thromb Vasc Biol. 1997;17:3139–3146.©1997 American Heart Association, Inc.
Thrombomodulin (TM), a key cofactor of the TM-protein C pathway, is of major biologic significance for the antithrombotic properties of endothelial cells. Yet, there is uncertainty whether TM is expressed in brain and what mechanisms govern brain endothelial anticoagulant activity. In this study, bovine brain capillaries were used as an in vitro model of the blood-brain barrier to determine factors involved in the regulation of TM expression in cerebral vasculature. Quantitative competitive-polymerase chain reaction assay revealed significant regional differences in the amount of brain capillary TM mRNA, ie, cortical > cerebellar > pontine, consistent with the reverse transcription-polymerase chain reaction findings in which the abundance of TM mRNA was analyzed relative to β-actin mRNA. Regional differences in TM mRNA brain capillary level correlated well with differences in protein C activation. The TM mRNA and activity were not detectable in brain parenchyma. Pathogenic mediators of ischemic stroke, interleukin 1β (10 U/mL), and tumor necrosis factor α (10 U/mL), produced a time-dependent decrease in brain capillary TM mRNA (t1/2 of 2.1 and 3.9 hours, respectively) and reduced endothelial TM activity. Incubation of brain capillaries with retinoic acid (10 μmol/L) and dibutyryl cAMP (3 mmol/L) resulted in a 4-fold increase in TM mRNA at 4 and 8 hours, respectively, followed by an increase in protein C activation. We conclude that TM at the blood-brain barrier is likely to be an important physiologic anticoagulant in brain microcirculation. Its downregulation by cytokines may contribute to ischemic brain damage and potentially could be counteracted by retinoic acid and cAMP.
Key Words: anticoagulants, thrombomodulin
Increased Formation of Reactive Oxygen Species After Permanent and Reversible Middle Cerebral Artery Occlusion in the Rat—Peters O, Back T (Dept of Neurology, Ludwig-Maximilians-Univ Munich, Marchioninistr, 15, D-81377, Munich, Germany), Lindauer U, Busch C, Megow D, Dreier J, Dirnagl U—J Cereb Blood Flow Metab. 1998;18:196–205. ©1998 by Lippincott-Raven Publishers, Philadelphia.
In barbiturate-anesthetized rats, we induced 3 hours of permanent middle cerebral artery occlusion (MCAO) by an intraluminal thread (n=6), or 1 hour MCAO followed by 2 hours of reperfusion (n=6). Through a closed cranial window over the parietal cortex, the production of reactive oxygen species (ROS) was measured in the infarct border using online in vivo chemiluminescence (CL) while monitoring the appearance of peri-infarct depolarizations (PID). The border-zone localization of the ROS and direct current (DC) potential measurements was confirmed in additional experiments using laser-Doppler scanning, mapping regional CBF changes through the cranial window after permanent (n=5) or reversible (n=5) MCAO. CL measurements revealed a short period (10 to 30 minutes) of reduced ROS formation after vessel occlusion, followed by a significant increase (to 162±51%; baseline=100%; P<.05) from 100 minutes of permanent MCAO onward. Reperfusion after a 1-hour period of MCAO led to a burst-like pattern of ROS production (peak: 489±330%; P<.05). When the experiments were terminated 3 hours after induction of MCAO, CL was still significantly increased above baseline after permanent and reversible MCAO (to 190±67% and 211±64%, respectively; P<.05). Simultaneous DC potential recordings detected 6.4±2.7 PID in the first, 4.7±2.3 in the second, and 2.8±2.0 in the third hour after permanent MCAO. In animals with reversible MCAO, PID were abolished from 15-minutes recirculation onward. There was no temporal relationship between ROS production and peri-infarct DC potential shifts. In conclusion, using a high temporal resolution ROS detection technique (CL), we found that permanent MCAO (after an initial decrease) was accompanied by a steady increase of ROS production during the 3-hour observation period, while reperfusion after 1 hour of MCAO produced a burst in ROS formation. Both patterns of ROS production were not related to the occurrence of PID.
Key Words: oxygen radical, middle cerebral artery occlusion
Effects of Ifenprodil, a Polyamine Site NMDA Receptor Antagonist, on Reperfusion Injury After Transient Focal Cerebral Ischemia—Doğan A, Rao AM, Başkaya MK, Rao VLR, Rastl J, Donaldson D, Dempsey RJ (Dept of Neurological Surgery, Univ of Wisconsin, H4/338 Clinical Science Center, 600 Highland Ave, Madison, WI 53792)—J Neurosurg. 1997;87:921–926.
Polyamines and N-methyl-d-aspartate (NMDA) receptors are both thought to play an important role in secondary neuronal injury after cerebral ischemia. Ifenprodil, known as a noncompetitive inhibitor of polyamine sites at the NMDA receptor, was studied after transient focal cerebral ischemia occurred. Spontaneously hypertensive male rats, each weighing between 250 and 350 g, underwent 3 hours of tandem middle cerebral artery (MCA) and common carotid artery occlusion followed by reperfusion for a period of 3 hours or 21 hours. Intravenous ifenprodil (10 μg/kg/minute) or saline infusion was started immediately after the onset of MCA occlusion and continued throughout the ischemic period. Physiological parameters including blood pressure, blood gas levels, blood glucose, hemoglobin, and rectal and temporal muscle temperatures were monitored. Six rats from each group were evaluated at 6 hours postocclusion for brain water content, an indicator of brain edema, and Evans blue dye extravasation for blood-brain barrier breakdown. Infarct volume was also measured in six rats from each group at 6 and 24 hours postocclusion. Ifenprodil treatment significantly reduced brain edema (82.5±0.4% vs. 83.5±0.4%, p<0.05) and infarct volume (132±14 mm3 vs. 168±25 mm3, p<0.05) compared with saline treatment, with no alterations in temporal muscle (brain) or rectal (body) temperature (35.9±0.4°C vs. 36.2±0.2°C; 37.7±0.4°C vs. 37.6±0.6°C; not significant). These results demonstrate that ifenprodil has neuroprotective properties after ischemia/reperfusion injury in the absence of hypothermia. This indicates that antagonists selective for the polyamine site of the NMDA receptors may be a viable treatment option and helps to explain some of the pathophysiological mechanisms involved in secondary injury after transient focal cerebral ischemia has occurred.
Key Words: glutamate antagonist, reperfusion injury
Tolerization Against Loss of Neuronal Function After Ischemic-Reperfusion Injury—Munyao N, Kaste M, Lindsberg PJ (Dept of Clinical Neurosciences, Univ of Helsinki, Haartmaninkatu 4, FIN-00290 Helsinki, Finland)—Neuroreport. 1998;9:321–325. ©Rapid Science Publishers.
To investigate whether sublethal ischemia preserves neuronal function otherwise lost after stroke, anesthesized rabbits were subjected to clamping of abdominal aorta to cause lumbar spinal cord ischemia. An occlusion period of 12.5 min was followed 12 or 48 h later by a second occlusion for 30 min. When scored 24 h later for hindlimb function on a 0–6 scale, the rabbits that underwent tolerizing ischemia 12 h before infarction had better motor function (n=7; 4.29±0.21, p<0.0001) than sham-operated controls (n=7; 1.00±0.27), but those infarcted at 48 h had mixed outcomes (n=5; 2.20±0.21, ns). In correlation, the proportion of neurons with histological evidence of damage was lower in the tolerized rabbits (0.15±0.04) than in sham-operated controls (0.74±0.09, p<0.001). We conclude that ischemic tolerance also improves neurological function of infarcted spinal cord and could be studied for clinical application.
Key Words: reperfusion injury, neuroprotection
Diffusion-Weighted MRI in Transient Global Amnesia: Elevated Signal Intensity in the Left Mesial Temporal Lobe in 7 of 10 Patients—Strupp M (Dept of Neurology, Klinikum Grosshadern, Univ of Munich, Marchioninistraße 15, 81366 Munich, Germany), Brüning R, Wu RH, Deimling M, Reiser M, Brandt T—Ann Neurol. 1998;43:164–170. ©1998 by the American Neurological Association.
Prompted by the findings of previous studies with positron emission tomography and single photon emission computed tomography, which demonstrated hypoperfusion or hyperperfusion in the left temporal lobe in isolated patients with transient global amnesia (TGA), we compared the sensitivity of diffusion-weighted (DW) magnetic resonance imaging (MRI) with that of conventional T1- and T2-weighted MRI in patients with TGA. Ten patients with the typical syndrome of a pure TGA were included in the study. For all patients, a coronal DW sequence, a steady-state free precession (SSFP) sequence, and conventional T1- and T2-weighted turbo spin-echo sequences were obtained. Seven of the 10 patients had elevated signal intensity in the left hippocampal region on DW MRI; moreover, 3 of these 7 patients exhibited bilateral signal abnormality in this sequence. All conventional T1- and T2-weighted images as well as all follow-up studies were normal. The signal elevation in DW MRI correlates with a decrease in the interstitial space and with cellular edema in the temporal lobe during TGA. The underlying pathomechanism causing this cellular edema cannot be clearly outlined using DW MRI. Our data are, however, compatible with spreading depression. This is the first study to show that DW MRI is a sensitive MRI method for evaluating TGA, especially in the early stage of the disease.
Key Words: magnetic resonance imaging, amnesia
Cocaine-Induced Cerebral Vasoconstriction Detected in Humans With Magnetic Resonance Angiography—Kaufman MJ (Brain Imaging Center, McLean Hospital, 115 Mill St, Belmont, MA 02178), Levin JM, Ross MH, Lange N, Rose SL, Kukes TJ, Mendelson JH, Lukas SE, Cohen BM, Renshaw PF—JAMA. 1998;279:376–380.
Context.—Clinical observations and case reports suggest that there are important cerebrovascular complications of cocaine use, but no studies have documented a direct link.
Objective.—To determine whether low-dose cocaine administration induces cerebral vasoconstriction in healthy cocaine users.
Design.—Randomized controlled trial.
Subjects.—Twenty-four healthy and neurologically normal men (mean age, 29 years) reporting median cocaine use of 8 lifetime exposures (range, 3 to >40).
Intervention.—Double-blind intravenous administration of cocaine (0.4 or 0.2 mg/kg) or placebo, with cerebral magnetic resonance angiography performed at baseline and 20 minutes following infusion.
Main Outcome Measure.—Cocaine-induced angiographic change indicative of vasoconstriction, as independently and concordantly rated by 2 reviewers blind to treatment condition.
Results.—Cocaine-induced cerebral vasoconstriction in a dose-related fashion (P=.03), with angiograms indicative of vasoconstriction found in 5 of 8 and 3 of 9 subjects receiving 0.4- and 0.2-mg/kg cocaine, respectively, compared with 1 of 7 subjects administered placebo. Outcome stratification by frequency of self-reported lifetime cocaine use (3–10 times, 11–40 times, or >40 times) revealed a statistically stronger dose-related effect (P<.001), suggesting that greater lifetime cocaine use was associated with a greater likelihood of vasoconstriction.
Conclusions.—Cocaine administration induced dose-related cerebral vasoconstriction on magnetic resonance angiograms. These changes occurred at low cocaine doses and in the absence of other risk factors, including polydrug abuse, hypertension, or cerebrovascular disease. Outcome stratification by prior cocaine use statistically strengthened the relationship between cocaine administration and vasoconstriction, suggesting that cocaine may have a cumulative residual effect in promoting cerebrovascular dysfunction.
Key Words: angiography, magnetic resonance, cocaine
Regional Differences in Cerebral Blood Flow and Glucose Utilization in Diabetic Man: The Effect of Insulin—Cranston I (Dept of Medicine, 4th Floor North Wing, St Thomas’ Hospital, Lambeth Palace Rd, London, England, UK SE1 7EH), Marsden P, Matyka K, Evans M, Lomas J, Sonksen P, Maisey M, Amiel SA—J Cereb Blood Flow Metab. 1998;18:130–140. ©by Lippincott-Raven Publishers, Philadelphia.
To determine the effect of insulin on regional cerebral blood flow (rCBF) and glucose metabolism (CMRglu), we performed quantitative dynamic PET scanning of labeled water (H215O) and deoxyglucose (18FDG) using two protocols in 10 diabetic men. In protocol A, to test reproducibility of the technique, insulin was infused at 1.5 mU · kg−1 · min−1 twice (n=5). In protocol B, low (0.3 mU · kg−1 · min−1) and high (3 mU · kg−1 · min−1) dose insulin was given on separate occasions (n=5). Euglycemia (5 mmol/L) was maintained by glucose infusion. In protocol A, CMRglu was 6% higher during the first infusion, and catecholamines were also increased, indicating stress. Blood flow was not different. Changing free insulin levels from 20.5±4.8 to 191±44.5 mU/L (P<0.001, low versus high dose, protocol B) did not alter total or regional CMRglu (whole brain 36.6±4.0 versus 32.8±6.2 μmol · 100 g−1 · min−1, P=0.32) or CBF (41.7±5.1 and 45.6±9.7 mL · 100 g−1 · min−1, P=0.4) or rCBF. In cerebellum, CMRglu was lower than in cortex and the ratio between rate constants for glucose uptake and phosphorylation (K1 and k3) was reversed. There are regional differences in cerebral metabolic capacity that may explain why cerebral cortex is more sensitive to hypoglycemia than cerebellum. Brain glucose metabolism is not sensitive to insulin concentration within the physiologic range. This suggests that intracerebral insulin receptors have a different role from those in the periphery.
Key Words: cerebral blood flow, diabetes mellitus
Correlation of Neuropsychological, Morphological and Functional (Regional Cerebral Blood Flow and Glucose Utilization) Findings in Cerebral Microangiopathy—Sabri O (Dept of Nuclear Medicine, Aachen Univ of Technology, Pauwelsstrasse 30, D-52057 Aachen, Germany), Hellwig D, Schreckenberger M, Cremerius U, Schneider R, Kaiser HJ, Doherty C, Mull M, Ringelstein EB, Buell U—J Nucl Med. 1998;39:147–154.
Cerebral microangiopathy, indicated in MRI by lacunar infarctions (LIs) and deep white matter lesions (DWMLs), is said to be accompanied by vascular dementia, which is reportedly caused by LI and DWML. Methods: To confirm this assumption, 57 patients with cerebral microangiopathy were assessed for changes in regional cerebral blood flow (rCBF) and glucose utilization (rMRGlu) in both white matter and cortex, and these findings were correlated to the results of extensive neuropsychological testing (cognitive, mnestic and attentiveness tests), as well as to MRI findings. A special head holder ensured reproducibility of positioning during measurement of rCBF (99mTc-HMPAO SPECT) and rMRGlu (18F-FDG PET) and MRI. White matter and cortex were quantified with regions of interest defined on MRI and superimposed to corresponding PET/SPECT slices. The rMRGlu was calculated according to Sokoloff, and rCBF was determined from normalization to the cerebellum. LI and DWML were graded by number and extent. Brain atrophy was classified as no to slight inner and/or outer atrophy (Group A) or moderate-to-severe inner and outer atrophy (Group B). Results: Even in severe DWMLs and in multiple LIs, rCBFs and rMRGlu values were not reduced. Analysis of variance identified atrophy and neuropsychological deficits as the main determinants for reduced rCBF and rMRGlu values (p<0.05). However, 60% of patients (19 of 31) with neuropsychological deficits in attentiveness tests and 61% of patients (23 of 38) with mnestic deficits belonged to Group A and revealed decreased rCBF and rMRGlu values. Neuropsychological deficits correlated well with decreased rCBF and rMRGlu, whereas MRI patterns, such as LI and DWML, did not. Conclusion: We conclude that LI and DWML are epiphenomena that morphologically characterize cerebral microangiopathy. Dementia or neuropsychological deficits, however, are exclusively reflected by functional criteria (rCBF and rMRGlu), as long as cerebral atrophy does not occur.
Key Words: cerebral blood flow, cerebral ischemia
MR Angiography of the Supra-aortic Arteries Using a Dedicated Head and Neck Coil: Image Quality and Assessment of Stenoses—Fellner C (Institute of Medical Physics, Friedrich-Alexander Univ Erlangen-Nürnberg, Krankenhausstraße 12, D-91054 Erlangen, Germany), Strotzer M, Fraunhofer S, Held P, Spies V, Seitz J, Fellner F—Neuroradiology. 1997;39:763–771. ©Springer-Verlag.
Our purpose was to evaluate a dedicated head and neck coil for demonstration of supra-aortic arteries with optimised magnetic resonance angiography techniques. We performed 47 examinations with a 1.5-T system. We used coronal 3D fast imaging with steady precession (FISP), axial 3D tilted optimised nonsaturating excitation (TONE) and 2D fast low-angle shot (FLASH) for the carotid bifurcation, axial 3D TONE with or without magnetisation transfer (MT) for intracranial arteries, and axial 3D FISP or TONE for the aortic arch. Evaluation included visual assessment of image quality and grading of stenoses near the carotid bifurcation; digital subtraction angiography was used as the reference method. Axial 3D TONE gave superior image quality at the carotid bifurcation, MT-TONE intracranially, and 3D FISP for the aortic arch vessels. Nevertheless, sensitivity and specificity for detection of significant stenoses were similar with coronal 3D FISP (96.3%, 94.0%), axial 3D TONE (92.6%, 92.5%) and axial 2D FLASH (96.3%, 86.6%). Image quality at the aortic arch needs further improvement.
Key Words: angiography, magnetic resonance, aortic arch
Experience With Transcranial Doppler Monitoring Reduces the Incidence of Particulate Embolization During Carotid Endarterectomy—Smith JL (Smith JL, Dept of Surgery, Clinical Sciences Bldg, Univ of Leicester, PO Box 65 Leicester LE2 7LX, UK), Evans DH, Gaunt ME, London NJM, Bell PRF, Naylor AR—Br J Surg. 1998;85:56–59. ©1998 Blackwell Science Ltd.
Background The aim of this study was to investigate whether the introduction of routine transcranial Doppler (TCD) ultrasonography during carotid endarterectomy reduces the incidence of microembolization by altering operative technique.
Methods The number and nature of microemboli detected during the first 75 consecutive carotid endarterectomies performed with TCD monitoring during 1992–1993 (group 1) were compared with those in a similar series of 75 consecutive patients undergoing carotid endarterectomy in 1995 (group 2), after substantial experience (210 patients) with TCD monitoring. Emboli were classified as either particulate or gaseous.
Results In patients with evidence of particulate emboli during the dissection phase of the operation, the total number of particulate emboli fell significantly in patients in group 2 (P=0.019). Similarly, in patients in whom microembolization was detected on immediate opening of the shunt, the total number of microemboli also fell significantly in group 2 (P=0.003). Overall, the median (95 per cent confidence interval) number of particulate emboli detected during the entire procedure fell significantly from 21 (16–29) in group 1 to 9 (7–14) in group 2 (P=0.0008).
Conclusion TCD monitoring plays an important role in the training and quality control of carotid endarterectomy and helps significantly to reduce the amount of microembolization.
Key Words: ultrasonography, Doppler, carotid endarterectomy
Comparison of Transcranial Power Dopple and Contrast-Enhanced Color-Coded Sonography in the Identification of Intracranial Arteries—Postert T (Dept of Neurology, St Josef Hospital, Ruhr-Univ Bochum, Gudrunstr, 56, 44791 Bochum, Germany), Federlein J, Przuntek H, Büttner T—J Ultrasound Med. 1998;17:91–96. ©by the American Institute of Ultrasound in Medicine.
Power-based transcranial color-coded sonography and contrast-enhanced transcranial color-coded sonography are ultrasonographic techniques that allow improved visualization of vascular structures. The present study was designed to investigate and compare the diagnostic capacity and applicability of both methods in the assessment of intracranial vessels of the circle of Willis (33 patients) and the vertebrobasilar system (21 patients). Compared to conventional transcranial color-coded sonography, both power-based and contrast-enhanced transcranial color-coded sonography improved the diagnostic sensitivity in identifying peripheral segments and small vessels of the circle of Willis. Contrast-enhanced transcranial color-coded sonography was significantly superior to power-based transcranial color-coded ultrasonography in the depiction of the second segment of the middle cerebral artery (66 of 66 versus 60 of 66, P<0.005), both segments of the anterior cerebral artery (66 of 66 versus 56 of 66 for the A1 segment, P<0.005; 61 of 66 versus 44 of 66 for the A2 segment, P<0.005), the first segment of the posterior cerebral artery (66 of 66 versus 55 of 66, P<0.005), and the basilar artery using the transtemporal approach (21 of 21 versus 15 of 21, P<0.05). Using the transforaminal approach contrast-enhanced transcranial color-coded real-time sonography did not increase fine resolution of the vertebrobasilar system compared to power Doppler sonography. In conclusion, contrast-enhanced transcranial color-coded real-time sonography further improves the diagnostic potential of power Doppler sonography in the identification of vascular structures of the circle of Willis. Contrast-enhanced transcranial color-coded sonography and power Doppler sonography are equally effective in visualizing the vertebrobasilar system with branches.
Key Words: ultrasonics, cerebral arteries
Electromyographic Biofeedback to Improve Lower Extremity Function After Stroke: A Meta-Analysis—Moreland JD, Thomson MA, Fuoco AR (reprints are not available from the authors)—Arch Phys Med Rehabil. 1998;79:134–140. ©1998 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation.
Objective: To examine the efficacy of electromyographic (EMG) biofeedback compared with conventional physiotherapy for improving lower extremity function in stroke patients.
Data Sources: A literature search covering the years 1976 to 1995 in MEDLINE, CINAHL, and EXCERPTA MEDICA.
Study Selection: Studies of adults after stroke, in which the treatment group received biofeedback alone or with conventional physical therapy and the control group received conventional physical therapy. Outcomes included functional measures related to the lower extremity. The study design criterion was that all must be randomized controlled trials.
Data Extraction: Study quality was assessed independently by two observers using eight criteria. Data for analysis were extracted by two observers to ensure accuracy.
Data Synthesis: For outcomes that were analyzed in more than one study, meta-analyses were done. Seventy-nine studies were identified as potentially relevant and eight studies met the selection criteria. The mean effect sizes were: for ankle dorsiflexion muscle strength, 1.17 (95% CI, .50–1.85; p=.0006); for gait quality, .48 (95% CI, −.06–1.01; p=.08); for ankle range of motion, .07 (95% CI, −.42–0.57; p=.78); for ankle angle during gait, .52 (95% CI, −.18–1.21; p=.14); for stride length, .09 (95% CI, −.56–.73; p=.80); and for gait speed, .31 (95% CI, −.16–.78; p=.20).
Conclusions: The results indicate that EMG biofeedback is superior to conventional therapy alone for improving ankle dorsiflexion muscle strength.
Key Words: stroke outcome, rehabilitation
Clinical and Ultrasonic Long-term Results of Percutaneous Transluminal Carotid Angioplasty—Schoser BGH (Dept of Neurology, Univ Hospital Hamburg-Eppendorf, Martinistr 52, D-20246 Hamburg, Germany), Becker VU, Eckert B, Zeumer H, Thie A—Cerebrovasc Dis. 1998;8:38–41. ©1998 S. Karger AG, Basel.
Experience of the long-term outcome of patients treated with carotid balloon angioplasty is limited. Therefore, we prospectively analyzed the ultrasonic and clinical features of 29 patients with complete follow-up data beyond 24 months, evaluated from 1989 through 1996 from our carotid angioplasty cohort of 106 patients. Mean follow-up time was 33 months. For up to 78 months postangioplasty, 23 patients with 24 angioplasties (77%) had no further neurological sequelae. Single ipsilateral amaurosis fugax or TIA events occurred in 3 patients. Recurrent ipsilateral amaurosis fugax or TIA events were noted twice in 2 patients. No patient suffered an ipsilateral stroke. Fifteen angioplasties (50%) remained with normal ultrasound (stenosis <50%), mild restenosis (50–70%) occurred in 12 angioplasties (40%), and severe restenosis (>70%) in 3 angioplasties (10%). Only in 2 of 15 patients clinical complications were related to the occurrence of ipsilateral restenosis above 50%. Until now, rigorous and careful evaluation of patients and clinical and ultrasonic follow-up have been essential for the estimation of the long-term efficacy of carotid angioplasty. It should be noted that carotid angioplasty is a new technique in evolution, with a high potential improving the technical results.
Key Words: angioplasty, transluminal, carotid artery diseases
Intravenous t-PA for Acute Ischemic Stroke: Therapeutic Yield of a Stroke Code System—Zweifler RM (USA Stroke Center, 10th Floor, Suite I, 2451 Fillingim St, Mobile, AL 36617), Brody ML, Graves GC, Drinkard R, Cunningham S, Rothrock JF—Neurology. 1998;50:501–503. ©1998 by the American Academy of Neurology.
Subsequent to publication of the NINDS t-PA Stroke Study results, we sought to determine the proportion of patients eligible for and receiving intravenous tissue plasminogen activator (t-PA) at an active acute stroke treatment center. Over a 12-month period there were 185 stroke code activations. Of these, 134 involved patients with ischemic stroke, and 48 of these (36%) were potentially eligible for treatment with t-PA by the time criterion (i.e., interval from stroke onset to hospital presentation <3 hours). Nine of the 48 potentially eligible patients (19%) and 9 of 134 ischemic stroke patients (7%) overall received t-PA. In our patient population only a small proportion of all patients with acute ischemic stroke presently are eligible for treatment with t-PA.
Key Words: stroke, acute, plasminogen activator, tissue-type
Carotid Endarterectomy Does Not Affect Long-Term Blood Pressure: Observations From the NASCET—Eliasziw M, Spence JD, Barnett HJM (John P. Robarts Research Institute, 100 Perth Dr, London, Ont N6A 5K8, Canada)—Cerebrovasc Dis. 1998;8:20–24. ©1998 S. Karger AG, Basel.
The aim of the study was to examine how blood pressure is affected by carotid endarterectomy over a 2-year period. We analyzed the data from 997 patients who received best medical care alone and 999 patients who received best medical care plus carotid endarterectomy (CE). All patients were recruited by the North American Symptomatic Carotid Endarterectomy Trial and were followed at regular clinic visits. The mean blood pressure at baseline was 145.2/81.2 mm Hg for medically treated patients and 146.2/81.9 mm Hg for surgically treated patients. The mean systolic and diastolic pressures increased by approximately 2.5% in the first month following randomization, then decreased over the next year and then remained relatively uniform. Throughout follow-up, surgical patients had slightly higher blood pressures than medically treated patients. At the end of 2 years, the mean systolic pressures in the two treatment groups converged to 147.6 mm Hg. The mean diastolic pressure in the medical patients returned to its baseline value, whereas the surgical patients’ blood pressure remained slightly elevated by 0.5 mm Hg. The percentage of patients on antihypertensive medications mirrored the rise and fall in blood pressures. A sharp decrease in medication (from 56 to 43%) was observed in both treatment groups at 1 month. The percentage of patients on medication increased subsequently, with approximately 63% taking medication at the end of 2 years. CE does not affect long-term blood pressure. The use of antihypertensive medications appears to be the key component in blood pressure management. As hypertension is related to neurologic morbidity and mortality, strict regulation of blood pressure is extremely important in patients with cerebrovascular disease.
Key Words: carotid endarterectomy, blood pressure
Radiosurgery for Cavernous Malformations—Karlsson B (Dept of Neurosurgery, Karolinska Hospital, S-171 76 Stockholm, Sweden), Kihlström L, Lindquist C, Ericson K, Steiner L—J Neurosurg. 1998;88:293–297.
Object. The authors examined 22 patients with cavernous malformations (CMs) who had undergone gamma knife radiosurgery (GKRS) to assess the value of this procedure in treating these lesions.
Methods. At the Karolinska Hospital, GKRS was used to treat 23 patients with CMs during the period of 1985 through 1996. One of the patients was lost to follow up and the treatment results of the 22 remaining patients were analyzed. In the first half of the series, the CMs were treated with high doses of radiation (>15-Gy dose to the periphery); in the second half of the series, lower doses were used.
Nine of the 22 patients suffered a post-GKRS hemorrhage and six developed a radiation-induced complication (two of these patients experienced both). Some time after GKRS was performed, surgical removal of the CM had to be undertaken in four patients because of hemorrhage and in two patients because of radiation-induced complications. Four of the nine patients who experienced no post-GKRS hemorrhage or radiation-induced complication were treated before 1990; recent magnetic resonance imaging revealed a decrease in the size of the CM in three of these individuals and no size change in the other.
The annual post-GKRS hemorrhage rate was 8% in this group. There was a trend in the hemorrhage rate to decrease 4 years postsurgery. There was also a trend for higher radiation doses administered to the periphery of the lesion to result in a lower risk of posttreatment hemorrhage. However, it could not be concluded whether GKRS affects the natural course of a CM. The incidence of radiation-induced complications was approximately seven times higher than that expected if the same number of patients had been treated by GKRS with the same radiation dose distributions for arteriovenous malformations instead of CMs.
Conclusions. The high incidence of radiation-induced complications does not seem to justify the limited protection the treatment may afford in only exceptional cases. A prospective randomized study is needed before the role of radiosurgery in the management of these lesions can be defined. Until such a study has proved differently, a caveat must be raised for the treatment of CM with GKRS.
Key Words: radiosurgery, cavernous malformations
Improving the Cost-Effectiveness of Carotid Endarterectomy—Back MR, Harward TRS, Huber TS, Carlton LM, Flynn TC, Seeger JM (Section of Vascular Surgery, Univ of Florida College of Medicine, PO Box 100286, Gainesville, FL 32610-0286)—J Vasc Surg. 1997;26:456–464. ©1997 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter.
Purpose: Carotid endarterectomy (CEA) has been shown to significantly reduce the risk of stroke caused by carotid artery stenosis. Limiting the costs of CEA without increasing the risks will improve the cost-effectiveness of this procedure.
Methods: Results were prospectively collected from 63 consecutive CEAs performed in 60 patients who were entered into a clinical pathway for CEA that included avoidance of cerebral arteriography, preferential use of regional anesthesia, selective use of the intensive care unit (ICU), and early hospital discharge. The mortality rate, complications, hospital costs, and net income in these patients were then compared with results from 45 CEAs performed in 42 consecutive patients immediately before beginning the CEA pathway. Age, comorbid risk factors, incidence of symptoms, and degree of carotid artery stenosis were similar in both patient groups.
Results: The rates of mortality and complications associated with CEA were low (mortality rate, 0%; stroke, 0.9%; transient ischemic attack, 2.8%) and did not vary between the two groups. Implementation of the CEA pathway resulted in significant (p<0.001) reductions in the use of arteriography (74% to 13%), general anesthesia (100% to 24%), ICU use (98% to 30%), and mean hospital length of stay (5.8 days to 2.0 days). These changes resulted in a 41% reduction in mean total hospital cost ($9652 to $5699) and a 124% increase in mean net hospital income ($1804 to $4039) per CEA (p<0.01). For the 39 patients (62%) who achieved all elements of the CEA pathway, the mean hospital length of stay was 1.3 days, the mean hospital cost was $4175, and the mean hospital income was $4327.
Conclusion: Costs associated with CEA can be reduced substantially without increased risk. This makes CEA an extremely cost-effective treatment of carotid disease against which new therapeutic approaches must be measured.
Key Words: carotid endarterectomy, costs and cost analysis
Items of Interest
Perfusion-Weighted Imaging Defects During Spontaneous Migrainous Aura—Cutrer FM, Sorensen AG, Weisskoff RM, Østergaard L, Sanches del Rio M, Lee EJ, Rosen BR, Moskowitz MA (Massachusetts General Hospital, 149 13th St, CNY 6403, Charlestown, MA 02129)—Ann Neurol. 1998;48:25–31. ©1998 by the American Neurological Association.
Neuroprotection as Initial Therapy in Acute Stroke: Third Report of an Ad Hoc Consensus Group Meeting—The European Ad Hoc Consensus Group (Prof. Dr. Werner Hacke, Dept of Neurology, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany)—Cerebrovasc Dis. 1998;8:59–72. ©1998 S. Karger AG, Basel.
Guidelines for Carotid Endarterectomy: A Statement for Healthcare Professionals From A Special Writing Group of the Stroke Council, American Heart Association—Biller J, Feinberg WM, Castaldo JE, Whittemore AD, Harbaugh RE, Dempsey RJ, Caplan LR, Kresowik TF, Matchar DB, Toole JF, Easton JD, Adams HP Jr, Brass LM, Hobson RW, Brott TG, Sternau L (American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596; Reprint No. 71-0133)—Circulation. 1998;97:501–509. ©1998 American Heart Association, Inc.
Cardiac Disorders and Stroke—Sen S, Oppenheimer SM (Cerebrovascular Program, Johns Hopkins Hospital, Meyer 5-185, 600 N Wolfe St, Baltimore, MD 21287)—Curr Opin Neurol. 1998;11:51–56. ©1998 Rapid Science Ltd.
Molecular Biology of Atherosclerosis—Libby P (Cardiovascular Division, Dept of Medicine, Brigham and Women’s Hospital, 221 Longwood Ave, Boston, MA 02115), Sukhova G, Lee RT, Liao JK—Int J Cardiol. 1997;62:S23–S29. ©1997 Elsevier Science Ireland Ltd.
Carotid Stenting and Angioplasty: A Statement for Healthcare Professionals From the Councils on Cardiovascular Radiology, Stroke, Cardiovascular Surgery, Epidemiology and Prevention, and Clinical Cardiology, American Heart Association—Bettmann MA, Katzen BT, Whisnant J, Brant-Zawadzki M, Broderick JP, Furlan AJ, Hershey LA, Howard V, Kuntz R, Loftus CM, Pearce W, Roberts A, Roubin G (American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596, Reprint No. 71-0131)—JVIR. 1998;9:3–5. ©1998 American Heart Association, Inc.
Susac Syndrome—Papo T (Internal Medicine Unit, Hôpital Pitié-Salpêtrière, 83 Boulevard de l’Hôpital, 75651 Paris Cedex 13, France), Biousse V, Lehoang P, Fardeau C, N’Guyen N, Huong DLT, Aumaitre O, Bousser M-G, Godeau P, Piette J-C—Medicine. 1998;77:3–11. ©1998 by William & Wilkins.
Ischemic Stroke: From Basic Mechanisms to New Drug Development—Series: Monographs in Clinical Neuroscience; 1998:16—Editor: Hsu Cy. Publisher: Karger, Postfach (CH-4009 Basel, Switzerland).
The abstracts in this section have been typeset for consistency with journal format but otherwise appear as in the original articles.
- Copyright © 1998 by American Heart Association