Age At Menopause: A Female Risk Factor of Stroke?

Stroke ranks as the third leading cause of death in the United States. It is now estimated that there are more than 700 000 incident strokes annually and 4.4 million stroke survivors.1 2 The economic burden of stroke was estimated by the American Heart Association to be $51 billion (direct and indirect costs) in 1999.3 Despite the advent of treatment of selected patients with acute ischemic stroke with tissue plasminogen activator and the promise of other experimental therapies, the best approach to reducing the burden of stroke remains prevention.4 5 High-risk or stroke-prone individuals can be identified and targeted for specific interventions.6 This is important because epidemiological data suggest a substantial leveling off of prior declines in stroke-related mortality and a possible increase in stroke incidence.7 8 The Stroke Council of the American Heart Association formed an ad hoc writing group to provide a clear and concise overview of the evidence regarding various established and potential stroke risk factors. The writing group was chosen based on expertise in specific subject areas, and it used literature review, reference to previously published guidelines, and expert opinion to summarize existing evidence and formulate recommendations (Table 1⇓). View this table: Table 1. Levels of Evidence and Grading of Recommendations As given in Tables 2 through 4⇓⇓⇓, risk factors or risk markers for a first stroke were classified according to potential for modification (nonmodifiable, modifiable, or potentially modifiable) and strength of evidence (well documented, less well documented).5 The tables give the estimated prevalence, population attributable risk, relative risk, and risk reduction with treatment for each factor when known. Population attributable risk reflects the proportion of ischemic strokes in the population that can be attributed to a particular risk factor and is given by the formula 100×[prevalence(relative risk−1)/prevalence(relative risk−1)+1]). …

Pulmonary Aspergillosis in Critically Ill Coronavirus Disease 2019 Patients– A Multinational Observational Study by the European Confederation of Medical Mycology

Acta Neurologica ScandinavicaVolume 65, Issue S90 p. 154-155 EVIDENCE OF AN ISCHEMIC PENUMBRA IN COLLATERALLY PERFUSED BRAIN TISSUE. A rCBF STUDY OF ACUTE STROKE PATIENTS: T. Skyhoj Olsen, T. Skyhoj Olsen Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorB. Larsen, B. Larsen Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorM. Herning, M. Herning Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorE. Bech Skriver, E. Bech Skriver Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorN. A. Lassen, N. A. Lassen Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this author T. Skyhoj Olsen, T. Skyhoj Olsen Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorB. Larsen, B. Larsen Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorM. Herning, M. Herning Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorE. Bech Skriver, E. Bech Skriver Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this authorN. A. Lassen, N. A. Lassen Departments of Neurology, Clinical Physiology and Radiology, Bispebjerg Hospital and Department of Neuroradiology, Hvid- ovre Hospital, Copenhagen, Denmark.Search for more papers by this author First published: March 1982 https://doi.org/10.1111/j.1600-0404.1982.tb03428.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume65, IssueS90March 1982Pages 154-155 RelatedInformation

Background: Atrial fibrillation (AF) is the most common sustained heart arrhythmia. Difficulties in diagnosing AF - particularly when paroxysmal and asymptomatic - and lack of routine screening contribute to underdiagnoses. Efficient, cost-effective detection of the undiagnosed may be supported by risk-prediction models relating patient factors to AF risk. However, there exists a need for an implementable risk model that is contemporaneous and informed by routinely collected patient data, reflecting the real-world pathology of AF. Methods: Machine learning and conventional statistical models were evaluated using patients identified from UK healthcare records, aged ≥30 years, without a history of AF, from January-2006 to December-2016. A matched case-control study evaluated published risk models (Framingham, ARIC, CHARGE-AF), machine learning models using baseline and time-updated information (neural network, LASSO, random forests, support vector machines) and Cox regression. Models were ranked with maximal discrimination between AF and non-AF cases (area under the receiver operating characteristic curve, AUROC) and potential number-needed-to-screen (NNS) to detect a case of AF. Findings: Analysis of 2,994,837 patients (3.2% AF) identified time-varying neural networks as the optimal model. Compared to the best existing model CHARGE-AF, the optimal model achieved an AUROC of 0.827 vs. 0.725, with NNS of 9 vs. 13 patients at 75% sensitivity. The optimal model confirmed known baseline risk factors (age, previous cardiovascular disease, antihypertensive medication usage) and identified additional time-varying predictors previously unknown (recency of cardiovascular events, body mass index (both levels and changes), pulse pressure, and the frequency of blood pressure measurements). Interpretation: The optimal time-varying machine learning model exhibited greater predictive performance than existing AF risk models and reflected known and new relationships between patient risk factors for AF. If utilised, the model may help improve the precision of AF screening, leading to better patient outcomes and cost-effective use of healthcare resources. Funding: Bristol-Myers Squibb and Pfizer. Declaration of Interest: NR Hill, U Farooqui, & S Lister are employees of Bristol-Myers Squibb Company. M Lumley is an employee of Pfizer Inc. D Ayoubkhani, P McEwan, D M Sugrue, J Gordon are employed by HEOR ltd., which provides consulting and other research services to pharmaceutical, medical device, and related organizations. In their salaried positions, they work with a variety of companies and organizations, and are precluded from receiving payments or honoraria directly from these organizations for services rendered. AT Cohen reports grants and personal fees from Bristol-Myers Squibb Company and Pfizer Inc. during the conduct of the study; personal fees from Boehringer Ingelheim, grants and personal fees from Bristol-Myers Squibb Company, grants and personal fees from Daiichi-Sankyo Europe, personal fees from Johnson & Johnson, grants and personal fees from Pfizer, Inc., personal fees from Portola, personal fees from Sanofi, personal fees from XO1, personal fees from Janssen, personal fees from ONO Pharmaceuticals, and grants and personal fees from Bayer AG, outside the submitted work. A Bakhai reports personal fees from Bristol-Myers Squibb Company and Pfizer Inc. during the conduct of the study; personal fees from Boehringer Ingelheim, personal fees from Bristol-Myers Squibb Company, personal fees from Daiichi-Sankyo Europe, personal fees from Johnson & Johnson, personal fees from Pfizer, Inc., personal fees from Novartis, personal fees from Sanofi, personal fees from MSD, personal fees from Janssen, personal fees from Roche, and personal fees from Bayer AG, outside the submitted work. DA Clifton reports personal fees from Bristol-Myers Squibb Company during the conduct of the study; and outside the submitted work, personal fees from Drayson Health (now Sensyne Health), personal fees from Ferrovial plc., personal fees from Quanta Dialysis, and personal fees from BioBeats Ltd. M O’Neill reports personal fees from Bristol-Myers Squibb Company and Pfizer Inc. during the conduct of the study; grants and personal fees from Biosense Webster, grants and personal fees from Abbott, personal fees from Siemens, personal fees from Vytronus, personal fees from Medtronic outside the submitted work. Ethical Approval: The study protocol was reviewed and approved by the Independent Scientific Advisory Committee for MHRA database research (ISAC, reference number 17_151).

Contraceptive conundrums: A case report of a woman with migraine.

Given the potential therapeutic effect of vascular disease control timing to reduce dementia risk, we investigated the age-related influences of vascular risk factor burden on brain structure throughout the lifespan. We studied participants from the community-based prospective Framingham Heart Study. Overall vascular risk factor burden was calculated according to the Framingham Stroke Risk Profile, a validated algorithm that predicts stroke risk. Brain volume was estimated by MRI. We used cross-sectional data to examine how the strength of association between vascular risk factor burden and brain volume changed across each age decade from age 45-54 years through to 85-94 years (N = 2,887). Second, we leveraged up to 40 years of longitudinal data to determine how the strength of association between vascular risk factor burden and brain volume changed when vascular risk factors were examined at progressively earlier ages (N = 7,868). In both cross-sectional and longitudinal analyses, higher vascular risk factor burden was associated with lower brain volume across each age decade. In the cross-sectional analysis, the strength of this association decreased with each decade of advancing age (p for trend < 0.0001). In longitudinal analysis, the strength of association between vascular risk factor burden and brain volume was stronger when vascular risk factors were measured at younger ages. For example, vascular risk factor burden was most strongly associated with lower brain volume in later life when vascular risk factors were measured at age 45 years. Vascular risk factors at younger ages appear to have detrimental effects on current and future brain volume.

Trends in American Indian/Alaskan native self-reported stroke prevalence and associated modifiable risk factors in the United States from 2011-2021

In the accompanying article, Arenillas and colleagues1 furnish new evidence that a persistently elevated level of CRP after a first cerebrovascular event (ischemic stroke or TIA) is associated with an increased risk of vascular events (both cerebral and cardiac) in a population of patients with documented intracranial large-artery occlusive disease. The evolving concept of using a high-sensitivity CRP assay as a marker of cerebrovascular risk is enticing, and the message suggested by the results of this study is both provocative and in accord with the increasing body of literature rapidly accumulating in the exciting field of stroke preventive medicine. The theory behind this association is fascinating: patients with high-risk lesions may be expected to manifest signs of increased inflammatory activity. Such inflammation appears to occur not only locally (in the affected vessel wall) but also systemically, as suggested by increased circulating levels of CRP. The use of an easily measurable systemic marker of inflammation (such as high-sensitivity CRP) may hold the key for determining which patients with intracranial large-artery occlusive disease are most at risk. In fact, the patients at highest risk manifest evidence of surprisingly widespread inflammatory response. Although the full relation between CRP elevation and cardiovascular risk is not yet completely known, the inflammatory status may be a marker for individuals with an exaggerated inflammatory response that may in turn accelerate atheroma progression and facilitate thrombogenesis. Studying the effect that a general inflammatory marker, such as CRP, has on cerebrovascular risk prediction is far from a simple task. Methodological problems are inherent in design, implementation, and analysis of any such study. The role of elevated high-sensitivity CRP as a risk marker for cardiovascular diseases, including coronary heart disease, …

The burden of stroke to the health care system in the United States continues to increase. Stroke-related hospital admissions grew from 580 000 in 1988 to 820 000 in 1997, an 18.6% increase after age adjustment.1 More effective stroke prevention provides the primary means of reducing these alarming statistics. This can be accomplished through better implementation of known preventive strategies2 and through research into new approaches to stroke prevention. Diet can affect stroke risk, with epidemiological studies indicating an inverse relationship between fruit and vegetable consumption and cardiovascular events.2 For example, one study including individuals free of cardiovascular disease at baseline found that the relative risk (RR) of stroke was reduced by 31% (RR, 0.69; 95% CI, 0.52 to 0.92) for persons in the highest quintile of fruit and vegetable intake.3 Analysis of data from the National Health and Nutrition Examination Survey (NHANES) Epidemiologic Follow-up Study supports these results.4 The study included 9608 adults aged 25 to 74 years who were free of cardiovascular disease at a baseline evaluation between 1971 and 1975. Consumption of fruits and vegetables ≥3 times per day compared with <1 time per day was associated with a 27% lower stroke incidence (RR, 0.73; 95% CI, 0.57 to 0.95) after adjustment for potential confounders, suggesting the benefit is not attributable to a healthy-user effect. The results reinforce present recommendations for an intake of 5 servings of fruits and vegetables daily. Because fruits and vegetables contain antioxidants, antioxidant food supplements might be expected to have similar benefits. However, a 3-year study of patients with coronary heart disease, low levels of high-density lipoprotein cholesterol, and normal levels of low-density lipoprotein cholesterol found no reduction in cardiovascular end points (death, myocardial infarction, stroke, and revascularization procedures) with the use of antioxidant supplements (800 IU …

Establishing new approaches for the prevention and treatment of stroke relies on identifying modifiable risk factors that contribute to the development of this complex disease. Mendelian randomization (MR) studies, analogous to naturally occurring randomized trials, can assess causality of potentially modifiable biomarkers and offer new insights into biological pathways. Stroke is the second leading cause of death worldwide and the chief determinant of long-term disability. Stroke is a heterogeneous disease arising from several distinct underlying pathologies and is typically classified as ischemic or hemorrhagic, and further subclassified using imaging data. Ischemic stroke (IS), including its 3 main subtypes: small vessel disease, large vessel disease, and cardioembolic stroke, accounts for ≈80% of stroke and is the result of an interrupted blood supply, leading to localized areas of ischemia in the brain. Small vessel disease may be a consequence of nonatherosclerotic, as well as atherosclerotic, mechanisms that result in an occlusion of the small perforating arteries, whereas large vessel disease results from occlusions or emboli from plaque rupture in larger vessels, such as a carotid artery. Cardioembolic stroke arises typically from emboli from the heart. By contrast, hemorrhagic stroke is a consequence of intracerebral hemorrhage (bleeding into the brain) or subarachnoid hemorrhage (bleeding into the subarachnoid space). These diverse stroke subtypes have distinct underlying pathologies reflecting different risk factor distributions. MR studies, using genetic variants as instrumental variables, afford a powerful approach to assessing causality of risk factors and avoid biases inherent in observational studies, including confounding and reverse causation. This review considers the contribution of MR studies to stroke epidemiology and their relevance to understanding risk factors and new therapeutic targets for stroke. Meta-analyses of large prospective studies have enhanced our knowledge of classical and emerging risk factors for stroke.1–4 Classical risk factors for stroke include nonmodifiable characteristics, …

Clinical Prediction Rules to Stratify Short-Term Risk of Stroke Among Patients Diagnosed in the Emergency Department With a Transient Ischemic Attack

Evaluating Outcomes for Autologous Hematopoietic Cell Transplantation for Diffuse Large B-Cell Lymphoma in the CAR-T Era

The causes of stroke in patients with asymptomatic carotid-artery stenosis have not been carefully studied. Information about causes might influence decisions about the use of carotid endarterectomy in such patients. We studied patients with unilateral symptomatic carotid-artery stenosis and asymptomatic contralateral stenosis from 1988 to 1997. The causes, severity, risk, and predictors of stroke in the territory of the asymptomatic artery were examined and quantified. The risk of stroke at five years after study entry in a total of 1820 patients increased with the severity of stenosis. Among 1604 patients with stenosis of less than 60 percent of the luminal diameter, the risk of a first stroke was 8.0 percent (1.6 percent annually), as compared with 16.2 percent (3.2 percent annually) among 216 patients with 60 to 99 percent stenosis. In the group with 60 to 99 percent stenosis, the five-year risk of stroke in the territory of a large artery was 9.9 percent, that of lacunar stroke was 6.0 percent, and that of cardioembolic stroke 2.1 percent. Some patients had more than one stroke of more than one cause. In the territory of an asymptomatic occluded artery (as was identified in 86 patients), the annualized risk of stroke was 1.9 percent. Strokes with different causes had different risk factors. The risk factors for large-artery stroke were silent brain infarction, a history of diabetes, and a higher degree of stenosis; for cardioembolic stroke, a history of myocardial infarction or angina and hypertension; for lacunar stroke, age of 75 years or older, hypertension, diabetes, and a higher degree of stenosis. The risk of stroke among patients with asymptomatic carotid-artery stenosis is relatively low. Forty-five percent of strokes in patients with asymptomatic stenosis of 60 to 99 percent are attributable to lacunes or cardioembolism. These observations have implications for the use of endarterectomy in asymptomatic patients. Without analysis of the risk of stroke according to cause, the absolute benefit associated with endarterectomy may be overestimated.

The aim of this study was to determine whether pulse wave velocity (PWV), a marker of vascular endothelial impairment and arteriosclerosis, predicts future ischemic stroke in patients who developed acute lacunar infarction. Patients with a first-ever ischemic stroke due to acute lacunar infarction were enrolled in this study. An oscillometric device (Form PWV/ABI; Omron Colin, Tokyo, Japan) was used to measure brachial-ankle PWV 1 week after stroke onset. Patients were followed for at least 5 years. The main end point of the study was recurrent ischemic stroke. Event-free survival was analyzed using Kaplan-Meier plots and log-rank tests. The risk of recurrent ischemic stroke was estimated using the Cox proportional-hazards model. Of the 156 patients (61% male, mean age: 69.2±11.3 years) assessed in this study, 29 developed recurrent ischemic stroke. The median brachial-ankle PWV value was 20.4 m s-1. Patients with high PWV values had a greater risk of recurrent ischemic stroke than patients with low PWV values (28% vs. 15%, P=0.08). Kaplan-Meier curve analysis showed that patients with high PWV values had a less favorable (that is, free of recurrent ischemic stroke) survival time (P=0.015). A multivariate Cox proportional-hazards model identified high PWV as an independent predictor of recurrent ischemic stroke after adjusting for age, sex and blood pressure (hazard ratio 2.35, 95% confidence interval, 1.02-5.70, P=0.044). In patients with acute lacunar infarction, a high PWV predicts a twofold greater risk of future ischemic stroke, independent of patient age, sex and blood pressure levels.

Surgery and Smoking at First and Second Hand