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Biomedical subjects

M J Alberts

Publications and source records attributed to M J Alberts.

At least 37 records · Page 2Linked to original sources
PubMed1998

Acute hemodynamic changes during carotid artery stenting.

To determine the clinical significance of acute hemodynamic disturbances during stenting in the carotid sinus region, we assessed the relation between intraprocedural changes in heart rate (HR) and blood pressure (BP) and adverse neurologic and cardiac outcomes. Eighteen patients underwent carotid stenting with the Wallstent (Schneider Inc). Suitable candidates had at least 60% diameter stenosis of the carotid artery by angiography. Initial and nadir HR and BP were recorded during the predilatation, stent delivery, and postdilatation periods. Bradycardia was defined as HR < or =60 beats/min and hypotension as systolic BP < or =100 mm Hg. Nineteen Wallstents were successfully deployed in all 19 carotid arteries. Some degree of bradycardia or hypotension occurred in 68% of carotid stent procedures, but administration of vasoactive medications was necessary in only 7 patients (37%) with more persistent hemodynamic disturbances. Hypotension or the need for continuous vasopressor therapy was significantly more common during postdilatation (32%) than in the predilatation period (5%) (p = 0.02). Bradycardia was not reduced by prophylactic atropine. In 1 patient the hemodynamic response to stenting may have contributed to an adverse neurologic and cardiac outcome. Thus, despite frequent fluctuations in HR and BP, most carotid stenting procedures were performed with excellent overall results, even in patients at high risk.

Aged↗
PubMed1998

Acute stroke teams: results of a national survey. National Acute Stroke Team Group.

BACKGROUND AND PURPOSE: The sensitivity of the brain to brief periods of profound ischemia or prolonged periods of modest ischemia mandates an aggressive approach to acute stroke care. Past studies have shown that many stroke patients do not receive acute care in an urgent and timely fashion. The formation of acute stroke teams (AST) is one approach that can be used to accelerate the delivery of acute stroke care. METHODS: We conducted a survey of major stroke program directors and neurovascular experts throughout the United States. The survey focused on issues related to the presence of AST, their staffing, operational features, and utilization at the surveyed programs and hospitals. RESULTS: Surveys were returned from 45 of 60 centers. Ninety-one percent of the respondents indicated that they currently had an AST, with 66% formed between 1995 and 1997. Staffing of ASTs consisted of attending physicians (95%), nurses or study coordinators (73%), fellows (49%), and residents (46%). In almost all cases (98%), the AST was led by a neurologist or neurosurgeon, and 98% of the ASTs operated on a 24-hours-per-day, 7-days-per-week basis. The most common call frequency was 2 to 3 times per week (41%), followed by >5 calls per week (29%). In 59% of the cases, the teams cost </=$5000 per year to operate. The vast majority (78%) of ASTs responded within 10 minutes of receiving a call. CONCLUSIONS: The formation of ASTs is quite common at the surveyed programs. Although staffing patterns vary, most teams are led by neurologists or neurosurgeons. The utilization of ASTs varies by facility, but they appear to be useful, with only a modest incremental financial cost. The use of ASTs may assist in providing more rapid medical care to stroke patients and increase the use of some acute therapies. Extension of the AST concept to nonacademic hospitals appears feasible.

Academic Medical Centers↗
PubMed1998

tPA in acute ischemic stroke: United States experience and issues for the future.

The approval of tissue plasminogen activator (tPA) for treatment of patients with ischemic stroke in the United States marked the first therapy proven to reverse or limit the effects of an acute stroke. Despite this approval and the lack of an alternative therapy, the use of tPA in stroke has been quite low. Several explanations for this underutilization have been identified, including lack of patient awareness, potential complications, infrastructure deficiencies, and physician concerns. This article explores these issues and suggests strategies for improving the use of tPA as an acute therapy in stroke.

Acute Disease↗
PubMed1997

Hyperacute stroke therapy with tissue plasminogen activator.

The past year has seen tremendous progress in developing new therapies aimed at reversing the effects of acute stroke. Thrombolytic therapy with various agents has been extensively studied in stroke patients for the past 7 years. Tissue plasminogen activator (t-PA) received formal US Food and Drug Administration approval in June 1996 for use in patients within 3 hours of onset of an ischemic stroke. Treatment with t-PA improves neurologic outcome and functional disability to such a degree that, for every 100 stroke patients treated with t-PA, an additional 11-13 will be normal or nearly normal 3 months after their stroke. The downside of t-PA therapy is a 6% rate of symptomatic intracerebral hemorrhage (ICH) and a 3% rate of fatal ICH. Studies are under way to determine whether t-PA can be administered with an acceptable margin of safety within 5 hours of stroke, to evaluate the therapeutic benefits of intraarterial pro-urokinase, and to assess the use of magnetic resonance spectroscopy to identify which patients are most likely to benefit from thrombolysis. Combination thrombolytic-neuroprotectant therapy is also being studied. In theory, patients could be given an initial dose of a neuroprotectant by paramedics and receive thrombolytic therapy in the hospital. We are now entering an era of proactive, not reactive, stroke therapies. These treatments may reverse some or all acute stroke symptoms and improve functional outcomes.

Acute Disease↗
PubMed1997

Endoglin gene polymorphism as a risk factor for sporadic intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a common and serious type of stroke. Recent studies have shown that inherited factors that affect the development of the vessel wall can increase the risk of ICH. We studied endoglin as a candidate gene in patients with sporadic ICH, since mutations in this gene can cause telangiectasia formation. One hundred three patients with sporadic ICH and 202 controls were studied. The polymerase chain reaction and single-strand conformational polymorphism analysis were used to screen for mutations in exon 7 of the endoglin gene. No coding mutations in exon 7 were identified in the ICH patients or controls. A 6-base intronic insertion was found 26 bases beyond the 3' end of exon 7. The homozygous form of the insertion was present in 9 of 103 (8.7%) ICH patients compared with 4 of 202 (2.0%) controls, p = 0.012 (odds ratio 4.8 [95% confidence interval, 1.28, 21.60]). Analysis of the endoglin transcript around the insertion did not reveal any changes in the RNA sequence. There were no obvious clinical features that distinguished the ICH patients with the homozygous insertion from the other patients. The pathophysiologic mechanism underlying this association remains to be determined.

Adult↗
PubMed1997

Emergency brain resuscitation.

With the discovery of new and effective acute stroke therapies, health care professionals now have the means to reverse the effects of an acute stroke. These advances must be aggressively applied to the acute stroke population using the EBR concept. It is clear from all of the issues and studies reviewed in this article that an organized approach and team concept are necessary for the efficient and effective care of acute stroke patients. Health care professionals currently treat acute myocardial infarction and trauma patients with a similar organization and sense of urgency. This paradigm should be translated and modified for the acute stroke population. Improved public and professional education are a vital part of this effort, and will have to be ongoing for its success. The approval of TPA as the first acute stroke therapy provides an opportunity to reverse the effects of a stroke. However, patients must present and be treated soon after stroke onset for this therapy to be safe and effective.

Cerebrovascular Disorders↗
PubMed1996

Specificity, sensitivity, and predictive value of apolipoprotein-E genotyping for sporadic Alzheimer's disease.

BACKGROUND: We aimed to determine the specificity, sensitivity, and predictive value of apolipoprotein E (APOE) genotyping in 67 consecutive patients with clinical diagnoses of sporadic Alzheimer's disease (AD) who underwent necropsy. METHODS: We studied patients who attended the Duke Memory Disorders Clinic and were diagnosed as having probable AD. These patients were followed up until they died. APOE genotyping was done during life in most cases, but in some brain tissue obtained at necropsy was used. Members of known AD families were excluded. FINDINGS: After neuropathological examination 57 (85%) of 67 of our patients were confirmed as having AD including all 43 who had at least one APOE-epsilon 4 allele. None of the patients found not to have AD carried an epsilon 4 allele. In this series, the specificity of the epsilon 4 allele was 100%, the sensitivity 75%, the positive predictive value 100%, and the negative predictive value 42%. In this necropsy-confirmed series, the epsilon 4/epsilon 4 genotype predicted AD with 100% accuracy. The epsilon 3/epsilon 4 and epsilon 2/epsilon 4 genotypes were also unexpectedly highly specific for AD. INTERPRETATION: Data from hundreds of necropsy-confirmed non-AD patients in other longitudinal necropsy series will allow the predictive value of APOE genotypes to be assessed with useful confidence limits.

Alleles↗
PubMed1996

Hospital charges for stroke patients.

BACKGROUND AND PURPOSE: Stroke is a common disease with a yearly cost in the United States of approximately $30 billion. The increasing prevalence of managed care and cost-containment measures may affect the delivery of stroke care now and in the future. This study was performed to determine (1) hospital charges and test utilization for stroke patients and (2) the effectiveness of educational efforts in modifying test utilization and related hospital charges. METHODS: Patients with a diagnosis of stroke who were discharged from either the neurology service or another service of the Department of Medicine (DOM) were identified. Data on test utilization and hospital charges were collected and analyzed. Following this analysis, educational sessions were held in an effort to reduce the use of specific diagnostic tests. The effectiveness of these methods was studied in a second group of stroke patients. RESULTS: In the baseline period there were 303 stroke patients, of which 262 (86%) were discharged from the neurology service and 41 (14%) were discharged from other services of the DOM. Patients on the neurology service had a lower mean length of stay than patients on the other services of the DOM (9.2 days versus 10.5 days) and lower mean total charges per case ($13,149 versus $15,727), although the respective differences were not statistically significant. Patient on the neurology service were more likely to have both brain CT and MRI performed (82 of 262 patients, 31.3%) than patients on the other services of the DOM (4 of 41, 9.8%, P = .005). In addition, patients on the neurology service were more likely to undergo a transthoracic echocardiogram than patients on the other services of the DOM (71.8% versus 53.7%, P = .025). After educational sessions, the percentage of stroke patients on the neurology service having both CT and MRI fell from 31.3% to 17.7% (P = .005), and the number of stroke patients having a transthoracic echocardiogram fell from 71.8% to 60.3% (P = .025). However, the overall charges for stroke patients on the neurology services did not decrease. CONCLUSIONS: Education can be successful in reducing the utilization of and associated charges for specific diagnostic tests for some stroke patients. A multidisciplinary approach to case management, using tools such as care maps, may be necessary to realize significant cost savings in certain groups of stroke patients.

Aged↗
PubMed1996

Transcranial doppler sonography to monitor cerebral vasculitis.

We describe a patient with cerebral vasculitis treated with prednisone and cyclophosphamide and followed by serial transcranial Doppler sonography and arteriography. Proximal cerebral angiographic abnormalities correlated with transcranial Doppler abnormalities. The abnormalities gradually normalized with treatment and correlated with the findings of followup arteriography, which also showed improvement in the vascular morphology. Transcranial Doppler sonography is useful in following proximal cerebral vascular abnormalities in some cases of cerebral vasculitis.

Angiography↗
PubMed1995

Risk of intracranial aneurysms in families with subarachnoid hemorrhage.

BACKGROUND: Genetic factors may be important in the etiology of subarachnoid hemorrhage (SAH) and intracranial aneurysm (IA) formation. Several studies have reported the familial occurrence of SAH and IA, although in most cases asymptomatic family members were not studied with elective angiography. The examination of data from large sibships could provide important information about the frequency of IA occurrence in at-risk individuals and the mode of inheritance for familial SAH/IA. METHODS: We reviewed published case series of sibships with SAH and at least four siblings, in which at least one sibling underwent elective angiography. Data were collected on age-of-onset, clinical events, presence of hypertension, angiographic findings, and outcome. Patients were classified as "affected" if they had a SAH or if an IA was detected by elective angiography, and "unaffected" if they were asymptomatic and had a negative angiogram. RESULTS: Seven case series with 52 individuals (26 men and 26 women) met our inclusion criteria. The sibships ranged from 6 to 13 members. Most of the siblings (32 of 52, 61%) were asymptomatic, 18 (35%) had a SAH, and 2 (4%) had focal symptoms but no SAH. Elective angiography of 34 siblings showed an IA in 11 (32%) and was negative in 23 (68%). The overall rate of affecteds (SAH or IA) was 56%. CONCLUSIONS: Based on data from these sibships, angiography of asymptomatic at-risk siblings demonstrated an IA in almost one-third of cases. Familial SAH/IA segregated with a pattern that was consistent with an autosomal dominant trait in this selected series of sibships, although other factors could produce these findings.

Adult↗
PubMed1995

Undergraduate and postgraduate medical education for cerebrovascular disease.

BACKGROUND AND PURPOSE: There is a perception among some physicians that medical students and house officers receive little or no training in the diagnosis and treatment of patients with cerebrovascular disease. However, there is a paucity of data addressing the issue of medical education in this area. This study was performed to determine the quantity and type of undergraduate and postgraduate medical education on cerebrovascular disease that is presented to medical students and house officers. METHODS: This was a prospective questionnaire study sent to 40 mainly academic medical centers in the United States and Canada. Data were collected on the percentage of programs offering stroke education, percentage of medical students and house officers taking such courses, and the duration of teaching programs. RESULTS: Sixty-one percent of the programs had dedicated stroke teaching efforts during clinical rotations, averaging a total of 13.1 hours of didactic and clinical teaching. Medical students received approximately 5 hours of preclinical stroke instruction. Only 35% of the programs offered stroke training for house officers in their internal medicine program. Most programs (81%) offered stroke conferences and computer-based instruction. CONCLUSIONS: At some institutions, medical students received a modest amount of stroke education during their clinical rotations. However, almost 40% of programs did not have required stroke education programs for medical students. Most internal medicine programs that we surveyed did not have specific stroke education efforts for house officers. Increased educational efforts in this area may be indicated.

Academic Medical Centers↗
PubMed1995

Cystatin C mutation in an elderly man with sporadic amyloid angiopathy and intracerebral hemorrhage.

BACKGROUND: Cerebral amyloid angiopathy (CAA) with intracerebral hemorrhage (ICH) occurs both sporadically and as a result of mutations in either cystatin C or the amyloid precursor protein. ICH due to cystatin C mutations typically occurs in young people of Icelandic origin. CASE DESCRIPTION: We report a case of sporadic CAA with ICH in an elderly Croatian man with a mutation in cystatin C identical to that found in Icelandic hereditary cerebral hemorrhage with amyloidosis. CONCLUSIONS: This is the first case report of sporadic CAA associated with the same mutation causing hereditary cerebral hemorrhage with amyloidosis of the Icelandic type. Sporadic CAA may thus be associated with genetic mutations in some patients. The frequency of these mutations is yet to be determined.

Cerebral Amyloid Angiopathy↗
PubMed1995

The genetics of cerebrovascular disease.

Genetics contribute to all aspects of cerebrovascular disease from the underlying pathology, through acute neuronal injury, to recovery and long-term prognosis. By understanding better the genetic contribution to the risk for cerebrovascular disease we can work toward the day when simple genetic tests can be used to assess an individual's risk for stroke (and cardiovascular disease) in the same way that we now use routine screening of blood pressure or cholesterol (Harrap, 1994b). Finally, it is worth noting that genetic effects do not work 'in vacuo'. They are subject to environmental influences which impact on the individual's phenotypic characteristics. Modification of these environmental factors may have a significant effect on the action of certain expressed genes and their putative mutations.

Cerebrovascular Disorders↗
PubMed1994

A molecular genetic study of intracerebral hemorrhage.

BACKGROUND: Two forms of inherited intracerebral hemorrhage (ICH) are associated with an amyloid angiopathy caused by mutations in the genes for the amyloid precursor protein or cystatin C. The purpose of this study was to determine whether patients with sporadic ICH have mutations in the amyloid precursor protein or cystatin C genes. METHODS: Consecutive patients with ICH admitted to the neurology or neurosurgery services at Duke University Hospital, Durham, NC, were studied. Using the polymerase chain reaction, we amplified exons 16 and 17 of the amyloid precursor protein and exon 2 of cystatin C and sequenced the products. Twenty-six men and 22 women were studied. The ICH location was deep in 29 patients, lobar in 16, cerebellar in two, and brain stem in one. There were 30 patients (63%) with a positive family history of stroke; seven of them (15%) had a family history of ICH. CONCLUSIONS: Mutations previously reported to cause familial forms of ICH were not found in this group of patients.

Adult↗
PubMed1994

Hypothesis: microtubule instability and paired helical filament formation in the Alzheimer disease brain are related to apolipoprotein E genotype.

A genetic classification of Alzheimer disease(s) (AD) is presented. We describe a potential metabolic process in individuals who inherit apolipoprotein E-epsilon 4 (APOE4, gene; apoE4, protein) alleles, leading to increased risk and earlier age of onset of late-onset Alzheimer disease. Apolipoprotein E-epsilon 3 (apoE3) binds to tau protein, possibly slowing the initial rate of tau phosphorylation and self-assembly into paired helical filaments (PHFs); apoE4 does not bind tau. Tau promotes microtubule assembly and stabilizes microtubules; hyperphosphorylated tau does not bind, thereby destabilizing microtubules. Hyperphosphorylated tau may self-assemble into PHFs. Over time a bias toward destabilization of microtubules and the formation of neurofibrillary tangles may occur in individuals who inherit APOE4 alleles, leading to a shorter functional neuronal life span. This hypothesis focuses attention on two important aspects of AD research design: (1) Although the inheritance of APOE4 is associated with increased risk and decreased age of onset, apoE4 does not directly cause the disease. Our data point to the absence of an important function of apoE3 or apoE2 in individuals who do not inherit these alleles as the genetically relevant metabolic factor. This has important implications for design of experiments directed toward understanding the relevant neuronal metabolism. (2) Should this hypothesis be proven and confirmed, targets for pharmaceutical therapy designed to mimic the metabolic function of apoE3 or apoE2 become a realistic preventive strategy.

Alzheimer Disease↗