PubMed Health⌕ Search

Biomedical subjects

Irene Meissner

Publications and source records attributed to Irene Meissner.

At least 19 recordsLinked to original sources
PubMed2006

Update on evidence for a genetic predisposition to cerebral vasospasm.

Considerable evidence links cerebral vasospasm to the decreased bioavailability of endothelial nitric oxide synthase (eNOS) after aneurysmal subarachnoid hemorrhage (SAH). In recent studies from the cardiology literature, researchers have suggested that a genetic predisposition to coronary vasospasm might develop as the result of a T-786C single nucleotide polymorphism (SNP) in the eNOS gene. The authors of this study attempted to determine if there may be a similar genetic predisposition toward cerebral vasospasm. The authors prospectively identified 28 patients with Fisher Grade 3 SAH from a group of 51 consecutive patients with ruptured intracranial saccular aneurysms. Genomic DNA was isolated from a peripheral blood sample obtained with permission from each patient. Gene microarray technology was used to assay the samples for the presence and distribution of certain key eNOS gene polymorphisms. Clinical, radiological, and genomic data were analyzed. The finding of eNOS T-786C SNP could be used to significantly differentiate between the presence and severity of cerebral vasospasm (p = 0.04). The findings from this preliminary study support similar findings in the coronary vasospasm literature as well as the hypothesis that a predisposition toward cerebral vasospasm may be related partially to genetic factors, which needs to be confirmed in a larger study. Such gene-based information may be important in rapidly identifying patients at increased risk of vasospasm after SAH, independent of their Fisher grade. In this article, the authors review key studies in this area.

Animals↗
PubMed2006

Population-based study of the relationship between patent foramen ovale and cerebrovascular ischemic events.

OBJECTIVE: To determine whether patent foramen ovale (PFO) is a risk factor for a cryptogenic cerebrovascular ischemic event (CIE). METHODS: This case-control study of 1072 residents of Olmsted County, Minnesota, who underwent contrast transesophageal echocardiography between 1993 and 1997 included 519 controls without CIE randomly selected from the population, 262 controls without CIE referred for transesophageal echocardiography because of cardiac disease, 158 cases with incident CIE of obvious cause (noncryptogenic), and 133 cases with incident CIE of uncertain cause (cryptogenic). RESULTS: Large PFOs were detected in 108 randomly selected controls (20.8%), 22 referred controls (8.4%), 17 noncryptogenic CIE cases (10.8%), and 22 cryptogenic CIE cases (16.5%). After adjustment for age, sex, hypertension, smoking, atrial fibrillation, ischemic heart disease, and number of contrast injections, the presence of a large PFO was not significantly associated with group status (P=.07). Using the odds of the presence of large PFO in the randomly selected controls as the reference, the odds ratio (95% confidence interval) of the presence of large PFO was 0.47 (0.26-0.87) for referred controls, 0.69 (0.37-1.29) for noncryptogenic CIE cases, and 1.10 (0.63-1.90) for cryptogenic CIE cases. CONCLUSIONS: Patent foramen ovale is not a risk factor for cryptogenic ischemic stroke or transient ischemic attack in the general population. The PFO's importance in the genesis of cryptogenic CIE may have been overestimated in previous studies because of selective referral of cases and underascertainment of PFO among comparison groups of patients referred for echocardiography for clinical indications other than cryptogenic CIE.

Adult↗
PubMed2006

Population-based study of the relationship between atherosclerotic aortic debris and cerebrovascular ischemic events.

OBJECTIVE: To assess the validity of the suggestion that protruding atheromatous material in the thoracic aorta is an important cause of cerebrovascular ischemic events (CIEs) (ie, transient ischemic attack or ischemic stroke). METHODS: This case-control study of Olmsted County, Minnesota, residents who underwent transesophageal echocardiography (TEE) from 1993 to 1997 included controls without CIE randomly selected from the population, controls without CIE referred for TEE because of cardiac disease, cases with incident CIE of obvious cause (noncryptogenic), and cases with incident CIE of uncertain cause (cryptogenic). RESULTS: Of the 1135 subjects, 520 were randomly selected controls without CIE, 329 were controls without CIE referred for TEE, 159 were noncryptogenic CIE cases, and 127 were cryptogenic CIE cases. Complex atherosclerotic aortic debris in ascending and transverse segments of the arch was detected in 8 randomly selected controls (1.5%), 13 referred controls (4.0%), and 15 noncryptogenic (9.4%) and 4 cryptogenic (3.1%) CIE cases. After adjusting for age, sex, hypertension, smoking, atrial fibrillation, valvular heart disease, congestive heart failure, and atherosclerosis other than in the thoracic aorta, complex atherosclerotic aortic debris was not significantly associated with group status. With randomly selected controls as the referent group, odds ratios (95% confidence intervals) were 1.72 (0.61-4.87) for referred controls, 3.16 (1.18-8.51) for noncryptogenic CIE cases, and 1.39 (0.39-4.88) for cryptogenic CIE cases. CONCLUSIONS: Complex atherosclerotic aortic debris is not a risk factor for cryptogenic ischemic stroke or transient ischemic attack but is a marker for generalized atherosclerosis and well-established atherosclerotic and cardioembolic mechanisms of cerebral ischemia. Embolization from the aorta is not a common mechanism of ischemic stroke or transient ischemic attack.

Aged↗
PubMed2005

Patent foramen ovale: innocent or guilty? Evidence from a prospective population-based study.

OBJECTIVES: We sought to determine the association between patent foramen ovale (PFO), atrial septal aneurysm (ASA), and stroke prospectively in a unselected population sample. BACKGROUND: The disputed relationship between PFO and stroke reflects methodologic weaknesses in studies using invalid controls, unblinded transesophageal echocardiography examinations, and data that are unadjusted for age or comorbidity. METHODS: The use of transesophageal echocardiography to identify PFO was performed by a single echocardiographer using standardized definitions in 585 randomly sampled, Olmsted County (Minnesota) subjects age 45 years or older participating in the Stroke Prevention: Assessment of Risk in a Community (SPARC) study. RESULTS: A PFO was identified in 140 (24.3%) subjects and ASA in 11 (1.9%) subjects. Of the 140 subjects with PFO, 6 (4.3%) had an ASA; of the 437 subjects without PFO, 5 had an ASA (1.1%, two-sided Fisher exact test, p = 0.028). During a median follow-up of 5.1 years, cerebrovascular events (cerebrovascular disease-related death, ischemic stroke, transient ischemic attack) occurred in 41 subjects. After adjustment for age and comorbidity, PFO was not a significant independent predictor of stroke (hazard ratio 1.46, 95% confidence interval 0.74 to 2.88, p = 0.28). The risk of a cerebrovascular event among subjects with ASA was nearly four times higher than that in those without ASA (hazard ratio 3.72, 95% confidence interval 0.88 to 15.71, p = 0.074). CONCLUSIONS: These prospective population-based data suggest that, after correction for age and comorbidity, PFO is not an independent risk factor for future cerebrovascular events in the general population. A larger study is required to test the putative stroke risk associated with ASA.

Aged↗
PubMed2005

The Familial Intracranial Aneurysm (FIA) study protocol.

BACKGROUND: Subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms (IAs) occurs in about 20,000 people per year in the U.S. annually and nearly half of the affected persons are dead within the first 30 days. Survivors of ruptured IAs are often left with substantial disability. Thus, primary prevention of aneurysm formation and rupture is of paramount importance. Prior studies indicate that genetic factors are important in the formation and rupture of IAs. The long-term goal of the Familial Intracranial Aneurysm (FIA) Study is to identify genes that underlie the development and rupture of intracranial aneurysms (IA). METHODS/DESIGN: The FIA Study includes 26 clinical centers which have extensive experience in the clinical management and imaging of intracerebral aneurysms. 475 families with affected sib pairs or with multiple affected relatives will be enrolled through retrospective and prospective screening of potential subjects with an IA. After giving informed consent, the proband or their spokesperson invites other family members to participate. Each participant is interviewed using a standardized questionnaire which covers medical history, social history and demographic information. In addition blood is drawn from each participant for DNA isolation and immortalization of lymphocytes. High- risk family members without a previously diagnosed IA undergo magnetic resonance angiography (MRA) to identify asymptomatic unruptured aneurysms. A 10 cM genome screen will be performed to identify FIA susceptibility loci. Due to the significant mortality of affected individuals, novel approaches are employed to reconstruct the genotype of critical deceased individuals. These include the intensive recruitment of the spouse and children of deceased, affected individuals. DISCUSSION: A successful, adequately-powered genetic linkage study of IA is challenging given the very high, early mortality of ruptured IA. Design features in the FIA Study that address this challenge include recruitment at a large number of highly active clinical centers, comprehensive screening and recruitment techniques, non-invasive vascular imaging of high-risk subjects, genome reconstruction of dead affected individuals using marker data from closely related family members, and inclusion of environmental covariates in the statistical analysis.

Clinical Protocols↗
PubMed2005

The management of patients with patent foramen ovale and stroke.

The management of patients with patent foramen ovale (PFO) and stroke remains uncertain. What is known is that PFO is a very common finding in the general population. The risk of initial and recurrent stroke in individuals with PFO is relatively low. With the advent of transesophageal echocardiography, PFO is more commonly being diagnosed. There are insufficient data to support a benefit of warfarin over aspirin in preventing recurrent stroke in most patients with PFO. In those with PFO and a history of a procoagulant state or deep venous thrombosis, anticoagulation may be indicated after weighing the risks of anticoagulation against potential benefits in preventing recurrent stroke. PFO closure does not guarantee the prevention of future stroke and should be addressed case by case, with consideration of patients for entry into ongoing clinical trials of safety, efficacy, and durability.

Journal Article↗
PubMed2005

Clinical, laboratory, and transesophageal echocardiographic correlates of interatrial septal thickness: a population-based transesophageal echocardiographic study.

BACKGROUND: The determinants of interatrial septal (IAS) thickening ("lipomatous hypertrophy"), a common echocardiographic finding in the elderly, are poorly defined. The objective of this study was to determine the clinical, laboratory, and transesophageal echocardiographic correlates of IAS thickening in the general population. METHODS: The thickness of the IAS was measured by transesophageal echocardiography in 384 patients (median age: 66 years; range: 51-101 years; 53% men) participating in a population-based study (Stroke Prevention: Assessment of Risk in a Community). The associations between atherosclerosis risk factors, clinical cardiovascular disease, aortic atherosclerotic plaques, and IAS thickness were examined. RESULTS: Age and body surface area (BSA) were significantly associated with IAS thickness (median: 6 mm; range: 2-17 mm). IAS thickness increased by 12.6% per 10 years of age (95% confidence interval: 9.0-16.4%) adjusting for sex and BSA, and increased by 7.0% per 0.1 m 2 BSA (confidence interval: 5.0-9.2%) adjusting for age and sex. Overall, age, sex, and BSA accounted for 22.5% of the variability in IAS thickness. Current smoking (20.4% increase in IAS thickness in current smokers) and hypertension treatment (8.5% increase in treated patients) were associated with increased IAS thickness, adjusting for age, sex, and BSA ( P < .05), but these two risk factor variables jointly explained only an additional 2.3% of the variability in IAS thickness beyond the variability explained by age, sex, and BSA. Clinical coronary artery and cerebrovascular disease, atrial arrhythmias, and aortic atherosclerotic plaques were not associated with IAS thickness, adjusting for age, sex, and BSA ( P > .3). CONCLUSIONS: IAS thickening is an age-associated process. Atherosclerosis risk factors are weakly associated with IAS thickening, whereas atherosclerotic vascular disease is not.

Age Factors↗
PubMed2005

The presence of tandem endothelial nitric oxide synthase gene polymorphisms identifying brain aneurysms more prone to rupture.

OBJECT: It is becoming apparent that the presence of certain genetic variations (polymorphisms) may increase the individual's susceptibility to cardiovascular diseases, even in the absence of a family history. We hypothesized that brain aneurysms more prone to rupture may be identified on the basis of an individual's genotype for endothelial nitric oxide synthase (eNOS), a critical vasomodulatory protein found to be increasingly relevant to the pathobiology of aneurysms. METHODS: Patients' clinical data were recorded prospectively. Genomic DNA was isolated from blood samples obtained from individuals presenting consecutively to the Mayo Clinic with ruptured (58 patients) or unruptured (49 patients) intracranial saccular aneurysms. Using polymerase chain reaction and gene microarray technology, the following eNOS genetic polymorphisms were studied: intron-4 27-base pair variable number of tandem repeats (27 VNTR); promoter single nucleotide polymorphism (T-786C SNP); and exon-7 SNP (G894T SNP). Both groups of patients had similar demographic and clinical characteristics. For all three polymorphisms, variant alleles (p < or = 0.003) and their corresponding genotypes (p < or = 0.006) were found two to four times more frequently in patients with ruptured aneurysms than in patients with unruptured aneurysms. Strikingly, the odds ratio for presenting with a ruptured brain aneurysm among individuals demonstrating the copresence of all three variant alleles was 11.4 (95% confidence interval 1.7-75.9, p = 0.004). CONCLUSIONS: The authors have uniquely identified a set of tandem eNOS gene variations whose presence can be used to identify patients with aneurysms likely to rupture. We believe that if this finding is reproducible in a large multicenter study, in addition to known anatomical factors a rapid and cost-effective screening tool will become available to clinicians as a genetic aid to predict the risks of rupture in patients presenting with unruptured intracranial aneurysms.

Aneurysm, Ruptured↗
PubMed2004

Update on genetic evidence for rupture-prone compared with rupture-resistant intracranial saccular aneurysms.

OBJECT: Anecdotal evidence exists for at least two subpopulations of intracranial saccular aneurysms; those that form rapidly and rupture when small and those that enlarge slowly and are particularly prone to rupture when they are 10 mm or more in diameter. The goal in this study was to determine if there was genetic evidence to support the classification of intracranial saccular aneurysms as 'rupture-prone' or 'rupture-resistant' lesions. METHODS: The authors prospectively obtained and analyzed clinical and genetic data in a cohort of 197 individuals composed of 58 patients with ruptured intracranial saccular aneurysms, 49 with unruptured aneurysms, and 90 healthy community volunteers. Based on recent studies supporting an increasingly relevant role for the critical vasomodulatory protein endothelial nitric oxide synthase (eNOS) in aneurysm pathobiology, the authors assayed blood from all 197 participants to determine and compare their eNOS genotypes. The eNOS gene intron 4 27-base pair variable-number tandem-repeat polymorphism was significantly overrepresented in persons with ruptured intracranial saccular aneurysms compared with community volunteers (p < 0.002). When comparing eNOS genotypes among patients with ruptured or unruptured aneurysms, an approximately 10-fold increase in the odds of presenting with brain aneurysm rupture was found among individuals with multiple variant eNOS alleles (p = 0.004). CONCLUSIONS: Uniquely, the authors have identified a set of eNOS gene variations whose presence indicates patients with intracranial saccular aneurysms that are more prone to rupture. The authors conclude that if these findings are reproducible in the setting of a large multicenter study, then in addition to known anatomical factors, a rapid and costeffective genetic screening tool will become available to clinicians as an aid to predicting rupture risks in patients presenting with unruptured intracranial aneurysms.

Aneurysm, Ruptured↗
PubMed2004

C-reactive protein and atherosclerosis of the thoracic aorta: a population-based transesophageal echocardiographic study.

BACKGROUND: An association between systemic inflammatory markers and the presence and severity of atherosclerotic plaques has not been demonstrated in a nonselected population. The purpose of this study was to examine the association of inflammatory markers with aortic atherosclerotic plaques in a sample of the general population and in a subgroup free of clinical vascular disease. METHODS: Transesophageal echocardiography was performed in 386 subjects (median age, 66 years; 53% men). We examined the association between systemic inflammatory markers and aortic atherosclerotic plaques. RESULTS: Aortic plaques were present in 267 subjects (69%). Plaques at least 4 and 6 mm thick and mobile debris were present in 114, 41, and 20 subjects, respectively. High-sensitivity C-reactive protein (hs-CRP) level was associated with the presence of aortic plaques, adjusting for age, sex, smoking status, and additional atherosclerosis risk factors. Among subjects with plaques, hs-CRP level was independently associated with plaques at least 6 mm thick; similar trends were observed for the associations of hs-CRP level with plaques at least 4 mm thick and mobile debris. In subjects with aortic plaques who were free of clinically apparent coronary artery or cerebrovascular disease, hs-CRP level was independently associated with plaques at least 6 mm thick. CONCLUSIONS: Level of hs-CRP is independently associated with the presence and severity of aortic atherosclerotic plaques. These observations establish the association of systemic inflammation with anatomically defined atherosclerosis in the general population.

Age Distribution↗
PubMed2004

Atherosclerosis of the aorta: risk factor, risk marker, or innocent bystander? A prospective population-based transesophageal echocardiography study.

OBJECTIVES: The goal of this study was to investigate whether complex aortic atherosclerosis is associated with increased risk of vascular events in a non-selected population. BACKGROUND: In selected high-risk patients, aortic atherosclerosis is associated with increased risk of vascular events. METHODS: We describe the relationship between simple versus complex (>4-mm thick or mobile debris) aortic atherosclerotic plaques and vascular events during follow-up in a random sample of 585 persons (age > or =45 years) using 1993 to 2000 data from the Stroke Prevention: Assessment of Risk in a Community (SPARC), a prospective population-based longitudinal study. RESULTS: At five-year median follow-up (range, 0.5 to 6.5 years), cardiac events (death, non-fatal myocardial infarction, coronary revascularization, heart failure associated with coronary artery disease) and cerebrovascular events (ischemic fatal and non-fatal strokes, transient ischemic attacks) had occurred in 95 subjects and 41 subjects, respectively. Age, male gender, prior coronary artery disease, higher pulse pressure, and diabetes were significant cardiovascular predictors. Age, prior myocardial infarction, and a history of atrial fibrillation were significant cerebrovascular predictors. Simple aortic plaques (253 persons) were not independently associated with either cardiac or cerebrovascular events. Complex plaques (44 persons) were marginally associated with cardiac events, adjusting for age and gender (hazard ratio [HR], 2.28; 95% confidence interval [CI], 1.11 to 4.68; p = 0.053 for two degrees of freedom [complex and simple plaques vs. no plaques]) but not after adjusting for additional clinical risk factors (HR, 1.22; 95% CI, 0.57 to 2.62; p = 0.64). Complex plaques were associated with cerebrovascular events only univariately. CONCLUSIONS: Aortic atherosclerotic plaques are not associated with future cardiac or cerebrovascular events. Aortic atherosclerosis may not be an independent risk factor for vascular events in the general population.

Aged↗
PubMed2004

Inflammation, infection, and aortic valve sclerosis; Insights from the Olmsted County (Minnesota) population.

Atherosclerosis-related mechanisms, including inflammation and possibly infection, are likely to be involved in the pathogenesis of calcific aortic valve disease. The purpose of this study was to examine whether systemic inflammatory markers and Chlamydia pneumoniae seropositivity are associated with aortic valve sclerosis (AVS) in a sample of the general population. Transesophageal echocardiography was performed in 381 subjects (median age: 67 years, range: 51-101; 52% men), a sample of the adult population in Olmsted County, Minnesota. The associations between systemic inflammatory markers (blood counts, including white blood cells differential counts, fibrinogen, and high-sensitivity C-reactive protein [hs-CRP]), C. pneumoniae immunoglobulin G (IgG) antibody titers, and AVS were examined. AVS was present in 140 subjects (37% of the population). After adjustment for age, sex, and smoking status: (1). hs-CRP was associated with AVS (odds ratio: 1.20 per two-fold increase in hs-CRP; 95% confidence interval: 1.01-1.43; P = 0.04) but this association was not significant after adjustment for additional risk factors for AVS, including body mass index (P = 0.52). (2). Blood counts and fibrinogen were not associated with AVS (P-values >0.30). (3). C. pneumoniae IgG antibody titers (low [1:16-1:32], intermediate [1:64-1:128], or high [>or=1:256] titers, compared with titers <1:16) were not associated with AVS (P = 0.21). In conclusion, hs-CRP is weakly associated with AVS, an association that is not independent of other AVS risk factors. Blood counts, fibrinogen, and C. pneumoniae seropositivity are not associated with AVS. These findings suggest that other non-inflammatory non-infectious mechanisms are likely to have a role in the pathogenesis of calcific aortic valve disease.

Age Distribution↗
PubMed2004

Electrophoretic measurement of lipoprotein(a) cholesterol in plasma with and without ultracentrifugation: comparison with an immunoturbidimetric lipoprotein(a) method.

OBJECTIVES: Elevated plasma lipoprotein(a) [Lp(a)] is a significant risk factor for vascular disease. Standardization of Lp(a) mass measurement is complicated by the heterogeneity of apolipoprotein(a) [apo(a)]. We investigated whether Lp(a) cholesterol measurement, which is not influenced by apo(a) size, is a viable alternative to measuring Lp(a) mass. DESIGN AND METHODS: Plasma Lp(a) cholesterol was measured electrophoretically, with and without ultracentrifugation, and results were compared to each other and to immunoturbidimetrically measured Lp(a) mass in 470 subjects. RESULTS: Ultracentrifuged and whole plasma Lp(a) cholesterol levels demonstrated high correlation (R = 0.964). All samples with detectable (>/=2.0 mg/dl) Lp(a) cholesterol had Lp(a) mass >30 mg/dl (the clinically relevant cutpoint), while 59 samples with Lp(a) mass >30 mg/dl did not have detectable Lp(a) cholesterol. CONCLUSIONS: Lp(a) cholesterol can be measured in whole plasma without interference from VLDL lipoproteins. The relative clinical merits of measuring Lp(a) cholesterol vs. Lp(a) mass or both in combination deserves investigation.

Blotting, Western↗
PubMed2004

Endothelial nitric oxide synthase gene polymorphisms predict susceptibility to aneurysmal subarachnoid hemorrhage and cerebral vasospasm.

Rupture of an intracranial aneurysm (subarachnoid hemorrhage) is a potentially devastating condition frequently complicated by delayed cerebral ischemia from sustained contraction of intracranial arteries (cerebral vasospasm). There is mounting evidence linking the formation of intracranial aneurysms and the pathogenesis of post-subarachnoid hemorrhage vasospasm to aberrant bioavailability and action of the vasodilator molecule nitric oxide generated by isoforms of nitric oxide synthase. In humans, the gene encoding the endothelial isoform of nitric oxide synthase (eNOS) is known to be polymorphic, with certain polymorphisms associated with increased cardiovascular disease susceptibility. In this prospective clinical study involving 141 participants, we used gene microarray technology to demonstrate that the eNOS gene intron-4 27-base pair variable number tandem repeat polymorphism (eNOS 27 VNTR) predicts susceptibility to intracranial aneurysm rupture, while the eNOS gene promoter T-786C single nucleotide polymorphism (eNOS T-786C SNP) predicts susceptibility to post-subarachnoid hemorrhage vasospasm. We believe that genetic information such as this, which can be obtained expeditiously at the time of diagnosis, may be used as a helpful adjunct to other clinical information aimed at predicting and favorably modifying the clinical course of persons with intracranial aneurysms.

Adult↗
PubMed2004

Pathogenesis, natural history, and treatment of unruptured intracranial aneurysms.

Unruptured intracranial aneurysms (UIAs) are a major public health issue. These lesions have become increasingly recognized in recent years with the advent of advanced cerebral imaging techniques. Epidemiological evidence from multiple sources suggests that most intracranial aneurysms do not rupture. Therefore, it is desirable to identify which UIAs are at greatest risk of rupture when considering which to repair. It is important to compare size-, site-, and group-specific natural history rates with size-, site-, and age-specific morbidity and mortality associated with UIA repair because increased natural history risk often is associated with increased risk of aneurysm repair. Patient age is crucial in decision making because of its major effect on operative morbidity and mortality; however, it does not substantially affect natural history. The effect of age is most notable in patients about 50 years of age and older for open surgery and about 70 years of age and older for endovascular procedures. In general, rupture risk is lowest for patients in asymptomatic group 1 (no history of subarachnoid hemorrhage) with UIAs less than 7 mm in diameter in the anterior circulation. Surgical morbidity and mortality are most favorable for asymptomatic patients younger than 50 years who have UIAs less than 24 mm in diameter in the anterior circulation and no history of ischemic cerebrovascular disease. Endovascular morbidity and mortality may be less age dependent, and this could favor endovascular procedures, particularly in patients aged 50 to 70 years. An important issue is determining immediate vs long-term risk regarding treatment effectiveness and durability. This issue emphasizes the importance of long-term follow-up in patients after surgical and endovascular procedures.

Adult↗
PubMed2004

Evaluation and management of asymptomatic carotid artery stenosis.

Internal carotid artery stenosis (ICAS) is responsible for approximately 30% of ischemic strokes. Internal carotid artery stenosis of greater than 50% is present in about 4% to 8% of the population aged 50 to 79 years. Natural history studies and clinical trials have shown a small increase in stroke risk in patients with increasing degrees of ICAS, especially in those with greater than 80% reduction in carotid artery diameter. Randomized, prospective multicenter trials have revealed the superiority of carotid endarterectomy (CEA) over medical therapy in recently symptomatic patients with severe ICAS. However, the evidence from several randomized controlled trials of CEA in asymptomatic patients does not support the use of CEA in most of these patients; also, the role of noninvasive screening in this patient population remains uncertain and controversial. Furthermore, there is considerable uncertainty about whether the statistical benefit of avoiding a nondisabling stroke is worth the overall cost and risk of the procedure. Clinicians continue to struggle with treatment decisions for patients with asymptomatic ICAS. Carotid endarterectomy for asymptomatic ICAS should be considered only for medically stable patients with 80% or greater stenosis who are expected to live at least 5 years, and only in centers with surgeons who have a demonstrated low (<3%) perioperative complication rate. We outline the prevalence and natural history of ICAS, the evidence for CEA in patients with asymptomatic ICAS, the roles of screening and monitoring for ICAS, the methods of evaluating ICAS, and the implications for practicing clinicians.

Carotid Artery, Internal↗
PubMed2003

Durability of carotid endarterectomy.

BACKGROUND AND PURPOSE: We sought to determine the incidence of recurrent stenosis after carotid endarterectomy. METHODS: One thousand consecutive carotid endarterectomy patients were followed prospectively. The surgery was performed in a standard fashion. Cerebral protection was provided with intraoperative electroencephalographic monitoring and selective shunting. All arteriotomies were repaired with a patch graft. Each patient was seen 3 months after surgery and then yearly, with a duplex ultrasound obtained at each visit. Evidence for new ischemic events or recurrent stenosis of >or=70% was recorded. RESULTS: The 30-day combined minor and major stroke and death rate was 1.9%. At 7.1-year follow-up, 0.1% of patients had recurrent stenosis >or=70%, the majority of which were asymptomatic. CONCLUSIONS: Carotid endarterectomy is a low-risk procedure for the treatment of carotid occlusive disease, with excellent long-term durability. Although less invasive, carotid angioplasty must demonstrate equal robustness in long-term follow-up before it is considered a routine alternative to surgery.

Aged↗