Cerebral aneurysms.
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Aneurysm, Ruptured↗
Biomedical subjects
David O Wiebers
Publications and source records attributed to David O Wiebers.
Unruptured intracranial aneurysms: natural history and clinical management. Update on the international study of unruptured intracranial aneurysms.
In guiding treatment decisions for all patients with unruptured intracranial aneurysms, it is important to compare size-, site-, and group-specific natural history data with size-, site- and age-specific treatment morbidity and mortality data. Because patient age has a major effect on operative morbidity and mortality, but relatively little effect on natural history, surgical treatment of an UIA patient over age 50 and any treatment of UIA patients over age 70 should be considered with particular vigilance. Optimally, patients should be evaluated and treated at high-volume centers in a setting that emphasizes neurovascular teamwork and unbiased presentation and delivery of different therapeutic option, including the option of observation, which is often appropriate for patients with UIAs.
Age Factors↗
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↗
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↗
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↗
Mitral annular calcification, aortic valve sclerosis, and incident stroke in adults free of clinical cardiovascular disease: the Strong Heart Study.
BACKGROUND AND PURPOSE: Mitral annular calcification (MAC) and aortic valve (AV) sclerosis have each been linked to cardiovascular disease. Whether MAC and AV sclerosis are risk factors for stroke independent of other echocardiographic or laboratory predictors has not been established. We evaluated the relationship between MAC, AV sclerosis, and first stroke events in a population-based cohort. METHODS: Our study cohort consisted of 2723 American Indians participating in the Strong Heart Study who were free of prevalent cardiovascular disease. Participants underwent standardized clinical, echocardiographic, and laboratory evaluation, and incident stroke was ascertained using validated methods. RESULTS: During a median follow-up of 7 years, 86 strokes occurred. Age- and sex-adjusted incidence rates of stroke were significantly increased for MAC (rate ratio [RR], 3.12; 95% CI, 1.77 to 5.25) but not for AV sclerosis (RR, 1.15; 95% CI, 0.45 to 2.49). MAC was also associated with a reduced time to first stroke events after adjustment for clinical variables and the inflammatory markers C-reactive protein and fibrinogen (hazard ratio [HR], 2.42; 95% CI, 1.39 to 4.21) or the echocardiographic covariates left ventricular hypertrophy and left atrial enlargement (HR, 1.89; 95% CI, 1.04 to 3.41). Individuals with and without AV sclerosis showed no significant difference in stroke-free survival in unadjusted analyses (P=0.698). Crossing of the survival curves precluded multivariable analysis using Cox models. CONCLUSIONS: In this cohort of American Indians without clinical cardiovascular disease, the presence of MAC, but not AV sclerosis, proved to be a strong risk factor for incident stroke after extensive adjustment for other predictors. Individuals exhibiting MAC may benefit from aggressive risk factor modification, but this will require further investigation.
Aged↗
The natural history of radiographically defined vertebrobasilar nonsaccular intracranial aneurysms.
BACKGROUND: Vertebrobasilar nonsaccular intracranial aneurysms (VBNIA) are characterized by dilatation, elongation, and tortuosity of the vertebrobasilar system. METHODS: The medical records and imaging of patients with vertebrobasilar fusiform aneurysms or dolichoectasia between 1989 and 2001 were reviewed. Prospective follow-up was obtained. RESULTS: One hundred and fifty-nine patients were identified (74% male) with 719 patient years of follow-up. Presenting events included: hemorrhage (3%), ischemia (28%), and compression (22%). The remainder were incidental. The 1-, 5-, and 10-year risk of cerebral infarction (CI) due toVBNIA is 2.7, 11.3, and 15.9% respectively. The risk of recurrent CI is 6.7% per patient year. Median survival was 7.8 years and death was most commonly due to ischemia. CONCLUSIONS: VBNIA are more common in men and typically present in the 6-7th decade. Recurrent CI is more common than hemorrhage risk.
Adult↗
Patients with small, asymptomatic, unruptured intracranial aneurysms and no history of subarachnoid hemorrhage should generally be treated conservatively: for.
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Aged↗
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↗
Neuroepidemiology of unruptured intracranial aneurysms: implications for decision making regarding patient management.
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Aneurysm, Ruptured↗
Enlarging vertebrobasilar nonsaccular intracranial aneurysms: frequency, predictors, and clinical outcome of growth.
OBJECT: Vertebrobasilar nonsaccular intracranial aneurysms (NIAs) are characterized by elongation, dilation, and tortuosity of the vertebrobasilar arteries. The goal of this study was to define the frequency, predictors, and clinical outcome of the enlargement of vertebrobasilar NIAs. METHODS: Patients with vertebrobasilar fusiform or dolichoectatic aneurysms demonstrated on imaging studies between 1989 and 2001 were identified. In particular, patients who had undergone serial imaging were included in this study and their medical records were retrospectively reviewed. Prospective information was collected from medical records or death certificates when available. Both initial and serial imaging studies were reviewed. The authors defined NIA enlargement as a change in lesion diameter greater than 2 mm or noted on the neuroradiologist's report. A Cox proportional hazards regression was used to model time from diagnosis of the vertebrobasilar NIA to the first documented enlargement as a function of various predictors. The Kaplan-Meier method was used to study patient death as a function of aneurysm growth. Of the 159 patients with a diagnosis of vertebrobasilar NIA, 52 had undergone serial imaging studies including 25 patients with aneurysm enlargement. Lesion growth significantly correlated with symptomatic compression at the initial diagnosis (p = 0.0028), lesion type (p < 0.001), and the initial maximal lesion diameter (median 15 mm in patients whose aneurysm enlarged compared with median 8 mm in patients whose aneurysm did not enlarge; p < 0.001). The mortality rate was 5.7 times higher in patients with aneurysm growth than in those with no enlargement after adjustment for patient age (p = 0.002). CONCLUSIONS: Forty-eight percent of vertebrobasilar NIAs demonstrated on serial imaging enlarged, and this growth was associated with significant morbidity and death. Significant risk factors for aneurysm enlargement included symptomatic compression at the initial diagnosis, transitional or fusiform vertebrobasilar NIAs, and initial lesion diameter. Further studies are necessary to determine appropriate treatments of this disease entity once enlargement has been predicted or occurs.
Adult↗
The risk of rupture of unruptured cerebral aneurysms in the Japanese population: a systematic review of the literature from Japan by Morita, et al.
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Aneurysm, Ruptured↗
Outcomes among valvular heart disease patients experiencing ischemic stroke or transient ischemic attack in Olmsted County, Minnesota.
OBJECTIVE: To estimate the rates and predictors of survival and recurrence among residents of Olmsted County, Minnesota, who received an Initial diagnosis based on 2-dimensional color Doppler echocardiography of moderate or severe mitral or aortic stenosis or regurgitation and who experienced a first ischemic stroke, transient ischemic attack (TIA), or amaurosis fugax. PATIENTS AND METHODS: At the Mayo Clinic in Rochester, Minn, we used the resources of the Rochester Epidemiology Project to identify Individuals who met the criteria for inclusion in the study and to verify exclusion criteria. The study included all residents of Olmsted County, Minnesota, who experienced a first Ischemic stroke, TIA, or amaurosis fugax within 30 days of or subsequent to receiving a first-time 2-dimensional color Doppler echocardlography-based diagnosis of moderate or severe mitral or aortic stenosis or regurgitation between January 1, 1985, and December 31, 1992. The Kaplan-Meier product-limit method was used to estimate the rates of subsequent stroke and death after the ischemic stroke, TIA, or amaurosis fugax. The Cox proportional hazards model was used to assess the effect of several potential risk factors on subsequent stroke occurrence and death. RESULTS: For the 125 patients in the study, the Kaplan-Meier estimates of the risk of death and the risk of stroke at 2-year follow-up were 38.6% (95% confidence interval [CI], 29.9%-47.5%) and 18.5% (95% CI, 10.0%-27.0%), respectively. Compared with the general population, death rates were significantly Increased (standardized mortality ratio = 1.75; 95% CI, 1.38-2.19; P < .001) but rates of subsequent stroke occurrence were not (standardized morbidity ratio = 1.20; 95% CI, 0.75-1.84; P = .40). After adjustment for age, sex, and cardiac comorbidity, neither the type nor severity of valvular heart disease was an independent determinant of survival or subsequent stroke occurrence. CONCLUSIONS: Patients with mitral or aortic valvular heart disease who experience Ischemic stroke, TIA, or amaurosis fugax have Increased rates of death, but not recurrent stroke, compared with expected rates. Other cardiovascular risk factors are more important determinants of survival In these patients than the type or echocardiographic severity of the valvular heart disease.
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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↗
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.
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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↗
Prospective risk of hemorrhage in patients with vertebrobasilar nonsaccular intracranial aneurysm.
OBJECT: Nonsaccular intracranial aneurysms (NIAs) are characterized by dilation, elongation, and tortuosity of intracranial arteries. Dilemmas in management exist due to the limited regarding the natural history of this disease entity. The objective of this study was to determine the prospective risk of subarachnoid hemorrhage (SAH) in patients with vertebrobasilar NIAs. METHODS: All patients with vertebrobasilar fusiform or dolichoectatic aneurysms that had been radiographically demonstrated between 1989 and 2001 were identified. These patients' medical records were retrospectively reviewed. A prospective follow-up survey was sent and death certificates were requested. Based on results of neuroimaging studies, the maximal diameter of the involved artery, presence of SAH, and measurements of arterial tortuosity were recorded. Nonsaccular intracranial aneurysms were classified according to their radiographic appearance: fusiform, dolichoectatic, and transitional. Dissecting aneurysms were excluded. The aneurysm rupture rate was calculated based on person-years of follow up. Predictive factors for rupture were evaluated using univariate analysis (p < 0.05). One hundred fifty-nine patients, 74% of whom were men, were identified. The mean age at diagnosis was 64 years (range 20-87 years). Five patients (3%) initially presented with hemorrhage; four of these patients died during follow up. The mean duration of follow up was 4.4 years (692 person-years). Nine patients (6%) experienced hemorrhage after presentation; six hemorrhages were definitely related to the NIA. The prospective annual rupture rate was 0.9% (six patients/692 person-years) overall and 2.3% in those with transitional or fusiform aneurysm subtypes. Evidence of aneurysm enlargement or transitional type of NIA was a significant predictor of lesion rupture. Six patients died within 1 week of experiencing lesion rupture. CONCLUSIONS: Risk of hemorrhage in patients harboring vertebrobasilar NIAs is more common in those with evidence of aneurysm enlargement or a transitional type of aneurysm and carries a significant risk of death.
Adult↗
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↗