Stroke prevention

Secondary Stroke Prevention - Recent Advances: B Vitamins and Cerebral Ischemia

Deutsches Aerzteblatt Online ◽

10.3238/arztebl.2008.0128c ◽

2008 ◽

Author(s):

Stefan Lorenzl ◽

Michael Linnebank ◽

Olaf Stanger

Keyword(s):

Cerebral Ischemia ◽

Stroke Prevention ◽

B Vitamins ◽

Secondary Stroke Prevention ◽

Recent Advances

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Stroke ◽

10.1161/strokeaha.120.029679 ◽

2020 ◽

Vol 51 (7) ◽

pp. 2255-2262

Author(s):

J. David Spence

Keyword(s):

Risk Factors ◽

Stroke Prevention ◽

Genetic Research ◽

Egg Yolk ◽

B Vitamins ◽

Intestinal Microbiome ◽

Plaque Burden ◽

Black Patients ◽

Risk Patients ◽

Total Homocysteine

In 44 years of practicing stroke prevention, I have learned many lessons; in this article, I hope to impart some of them. Three areas of my research are discussed. Controlling resistant hypertension is markedly improved by physiologically individualized therapy based on renin/aldosterone phenotyping; this is particularly important in black patients. Measurement of carotid plaque burden strongly predicts cardiovascular risk and is useful for genetic research and for a process called treating arteries instead of risk factors. Doing so in high-risk patients with asymptomatic carotid stenosis was associated with a >80% reduction in the 2-year risk of stroke and myocardial infarction. It also permitted the identification of extremes of atherosclerosis that are useful for studying both the genetics and the biology of atherosclerosis. Patients with very high plaque burden despite low levels of risk factors have an unexplained phenotype; those with little or no plaque despite high levels of risk factors are protected. Patients with unexplained atherosclerosis have higher plasma levels of toxic metabolites produced by the intestinal microbiome largely from egg yolk, red meat, and protein, and those metabolites are renally excreted. This has important dietary implications for stroke prevention. Lowering of plasma total homocysteine with B vitamins significantly reduces the risk of stroke. That was not apparent in early studies because harm from cyanocobalamin among participants with renal failure obscured the benefit among those with good renal function. We should be using B vitamins to prevent stroke but should use methylcobalamin or oxocobalamin instead of cyanocobalamin.

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Stroke Associated with SARS-CoV-2 Infection and its Pathogenesis:A Systematic Review

Basic and Clinical Neuroscience Journal ◽

10.32598/bcn.2021.3277.1 ◽

2021 ◽

Author(s):

Samaneh Kazemi ◽

◽

Arash Pourgholaminejad ◽

Alia Saberi ◽

◽

...

Keyword(s):

Systematic Review ◽

Hemorrhagic Stroke ◽

Endothelial Damage ◽

Therapeutic Approaches ◽

Stroke Incidence ◽

Small Vessels ◽

New Therapeutic Approaches ◽

Coagulation Abnormalities ◽

Therapeutic Anticoagulation ◽

Almost All

In this systematic review, in addition to pluralization of almost all reports of stroke cases from the outbreak of the SARS-CoV-2 pandemic to 2 July 2020, we will discuss the change of stroke incidence during the pandemic period as well as the proposed mechanisms of this relationship between SARS-CoV-2 and stroke. Web of Science, PMC/Medline and Scopus databases were searched up to July 2020 without any time and language limitation. After quality assessment, 22 articles were included in this study. Based on the results of all studies, it is certainly impossible to conclude the rising or decreasing stroke frequency or the shift in the ischemic and hemorrhagic ratio. It appears that SARS-CoV-2 infection has some correlation with stroke. The supposed mechanisms for the SARS-CoV-2-related hemorrhagic stroke include 1) SARS-CoV-2-related vasculopathy with the endothelial damage of small vessels, 2) viral infection induced platelet dysfunction or thrombocytopenia, and 3) activation of the pro-inflammatory cascade leading to coagulopathy. Receiving therapeutic anticoagulation for high D-dimer or for a known thrombus due to SARS-CoV-2 infection as well as using extracorporeal membrane oxygenation (ECMO) in some patients are intended helpful strategies. Furthermore, the possible mechanisms for ischemic stroke include 1) dysregulation of ACE2 (key host cellular receptor for SARS-CoV-2) -related physiologic functions, 2) endothelial cell damages, 3) thrombo-inflammation, 4) coagulopathy and coagulation abnormalities related to SARS-CoV-2 infection. A better understanding of the SARS-CoV-2 pathogenesis and its relation to neurologic abnormalities such as stroke can be considered to prevent SARS-CoV-2 and improve new therapeutic approaches.

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Incidence and Case Fatality at the County Level as Contributors to Geographic Disparities in Stroke Mortality

Neuroepidemiology ◽

10.1159/000449102 ◽

2016 ◽

Vol 47 (2) ◽

pp. 96-102 ◽

Cited By ~ 10

Author(s):

Darwin R. Labarthe ◽

George Howard ◽

Monika M. Safford ◽

Virginia J. Howard ◽

Suzanne E. Judd ◽

...

Keyword(s):

Racial Differences ◽

Stroke Prevention ◽

Case Fatality ◽

Stroke Care ◽

The United States ◽

Hazard Ratio ◽

Mortality Data ◽

Stroke Mortality ◽

Stroke Incidence ◽

Stroke Case

Background: Is the high stroke mortality in the Southeastern parts of the United States driven by differences in stroke incidence or case-fatality? This question remains unanswered. Differences in incidence would underscore the need for stroke prevention, while differences in case fatality would call for improved stroke care. Methods: Quartiles of US counties were defined by stroke mortality, and this gradient was related with stroke incidence and stroke case fatality in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study, where 1,317 incident stroke events (of which 242 were fatal) occurred among 29,650 participants. Results: There was a significant (p = 0.0025) gradient of fatal stroke events in REGARDS (quartile 4 vs. quartile 1 (Q4/Q1) hazard ratio 1.95, 95% CI 1.35-2.81), demonstrating the consistency of REGARDS with national mortality data. The gradient for incident stroke (fatal + nonfatal) was also significant (p = 0.0023; Q4/Q1 hazard ratio 1.29, 95% CI 1.10-1.52). The gradient for stroke case-fatality was marginally significant (p = 0.058), though the OR for Q4/Q1 (1.71, 95% CI 1.13-2.25) was large. Conclusions: Both stroke incidence and case-fatality in REGARDS appear to be contributing, underscoring the need for strengthening both stroke prevention and acute stroke care in order to reduce the disparity.

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B vitamins for stroke prevention

Stroke and Vascular Neurology ◽

10.1136/svn-2018-000156 ◽

2018 ◽

Vol 3 (2) ◽

pp. 51-58 ◽

Cited By ~ 12

Author(s):

Graeme J Hankey

Keyword(s):

Clinical Trials ◽

Folic Acid ◽

Stroke Prevention ◽

Stroke Risk ◽

Folic Acid Supplementation ◽

Adverse Outcomes ◽

B Vitamins ◽

Vitamin B ◽

Folate Supplementation ◽

Acid Supplementation

Supplementation with B vitamins (vitamin B9(folic acid), vitamin B12 and vitamin B6) lowers blood total homocysteine (tHcy) concentrations by about 25% and reduces the relative risk of stroke overall by about 10% (risk ratio (RR) 0.90, 95% CI 0.82 to 0.99) compared with placebo. Homocysteine-lowering interventions have no significant effect on myocardial infarction, death from any cause or adverse outcomes. Factors that appear to modify the effect of B vitamins on stroke risk include low folic acid status, high tHcy, high cyanocobalamin dose in patients with impaired renal function and concurrent antiplatelet therapy. In regions with increasing levels or established policies of population folate supplementation, evidence from observational genetic epidemiological studies and randomised controlled clinical trials is concordant in suggesting an absence of benefit from lowering of homocysteine with folic acid for prevention of stroke. Clinical trials indicate that in countries which mandate folic acid fortification of food, folic acid supplementation has no significant effect on reducing stroke risk (RR 1.05, 95% CI 0.90 to 1.23). However, in countries without mandatory folic acid food fortification, folic acid supplementation reduces the risk of stroke by about 15% (RR 0.85, 95% CI 0.77 to 0.94). Folic acid alone or in combination with minimal cyanocobalamin (≤0.05 mg/day) is associated with an even greater reduction in risk of future stroke by 25% (RR 0.75, 95% CI 0.66 to 0.86), whereas the combination of folic acid and a higher dose of cyanocobalamin (≥0.4 mg/day) is not associated with a reduced risk of future stroke (RR 0.95, 95% CI 0.86 to 1.05). The lack of benefit of folic acid plus higher doses of cyanocobalamin (≥0.4 mg/day) was observed in trials which all included participants with chronic kidney disease. Because metabolic B12 deficiency is very common and usually not diagnosed, future randomised trials of homocysteine-lowering interventions for stroke prevention should probably test a combination of folic acid and methylcobalamin or hydroxocobalamin instead of cyanocobalamin, and perhaps vitamin B6.

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Efficacy of Supplementation with B Vitamins for Stroke Prevention: A Network Meta-Analysis of Randomized Controlled Trials

PLoS ONE ◽

10.1371/journal.pone.0137533 ◽

2015 ◽

Vol 10 (9) ◽

pp. e0137533 ◽

Cited By ~ 14

Author(s):

Hongli Dong ◽

Fuhua Pi ◽

Zan Ding ◽

Wei Chen ◽

Shaojie Pang ◽

...

Keyword(s):

Randomized Controlled Trials ◽

Stroke Prevention ◽

Meta Analysis ◽

B Vitamins ◽

Controlled Trials ◽

Randomized Controlled

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Declining stroke rates in Californian children with sickle cell disease

Blood ◽

10.1182/blood-2004-02-0636 ◽

2004 ◽

Vol 104 (2) ◽

pp. 336-339 ◽

Cited By ~ 120

Author(s):

Heather J. Fullerton ◽

Robert J. Adams ◽

Shoujun Zhao ◽

S. Claiborne Johnston

Keyword(s):

Sickle Cell Disease ◽

Sickle Cell ◽

Stroke Prevention ◽

Incidence Rates ◽

Cell Disease ◽

Stroke Incidence ◽

The Impact ◽

Discharge Database ◽

High Risk Children

Abstract Although the Stroke Prevention Trial in Sickle Cell Anemia (STOP) demonstrated the efficacy of blood transfusions for primary stroke prevention in high-risk children with sickle cell disease (SCD) in 1998, the impact of this trial on public health has not been studied. Our objective was to determine whether stroke rates in Californian children with SCD have declined since 1998. Using a California-wide hospital discharge database, we identified all first admissions for stroke in children with SCD from 1991 through 2000. Annual stroke incidence rates were calculated as the number of admissions divided by the estimated population of Californian children with SCD in that year. For 1991-2000, 93 children with SCD were admitted to Californian hospitals with a first stroke during 12 030 person-years of follow-up; 92.5% were ischemic and 7.5% hemorrhagic. Overall, the rate of first stroke was 0.77/100 person-years. For the study years 1991-1998, the rate for first stroke was 0.88/100 person-years compared to 0.50 in 1999 and 0.17 in 2000 (P < .005 for trend). Since the publication of the STOP study in 1998, annual rates of admissions for first stroke for Californian children with SCD have declined. (Blood. 2004;104:336-339)

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Incidence of Silent Stroke in the United States

Stroke ◽

10.1161/str.32.suppl_1.363-b ◽

2001 ◽

Vol 32 (suppl_1) ◽

pp. 363-363

Author(s):

Megan C Leary ◽

Jeffrey L Saver

Keyword(s):

United States ◽

Stroke Prevention ◽

The United States ◽

Population Based ◽

Incidence Rates ◽

Health Study ◽

Cardiovascular Health Study ◽

Stroke Incidence ◽

Age Cohorts ◽

The Us

P134 Background: Recent estimates of stroke incidence in the US range from 715,000–750,000 annually. These estimates, however, do not reflect silent infarcts and hemorrhages. Since population-based studies have found that prevalence of silent stroke is 10–20 times that of symptomatic, estimates of stroke incidence based solely on symptomatic events may substantially underestimate the annual burden of stroke. Silent strokes contribute to vascular dementia, gait impairment, and other major adverse patient outcomes. Methods: Incidence of silent infarcts for different age strata were derived from two US population-based studies of the prevalence of silent infarct-like lesions on MRI, Atherosclerosis Risk In Communities and Cardiovascular Health Study. Prevalence observations in these studies and age-specific death rates from the US Census Bureau were inputted to calculate silent infarct incidence (method of Leske et al). Similarly, incidence rates of silent hemorrhage at differing ages were extrapolated from population-based prevalence observations employing MR GRE imaging in the Austrian Stroke Prevention Study. Age-specific incidence rates were projected onto age cohorts in the 1998 US population to calculate annual burden of silent stroke. Results: Derived incidence rates per 100,000 of silent infarct ranged from 6400 in the age 50–59 strata to 16400 at ages 75–79. Extrapolated incidence rates of silent hemorrhage ranged from 230 in the age 30–39 strata to 7360 at ages > 80. Incidence rates of both subclinical infarcts and hemorrhage increased exponentially with age. Overall estimated annual US occurrence of silent infarct was 9,039,000, and of silent hemorrhage 2,130,000. Conclusion: In 1998, nearly 12 million strokes occurred in the United States, of which ∼750,000 were symptomatic and over 11 million were subclinical. Among the silent strokes, ∼81% were infarcts and ∼19% hemorrhages. These findings demonstrate that the annual burden of stroke is substantially higher than suggested by estimates based solely on clinically manifest events, and suggest that greater research and clinical resources should be allocated to stroke prevention and treatment.

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