Abstract TMP76: Ischemic Stroke Location and Vascular Risk in Dizziness Visits and The Follow-up Period: A Population-based Study

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Kevin A Kerber ◽  
James Burke ◽  
Lewis Morgenstern ◽  
Devin Brown ◽  
Thomas McLaughlin ◽  
...  

Objective: Prior studies found a concerning frequency of missed ischemic stroke among Emergency Department (ED) dizziness visits. We aim to describe details about the location of infarction (identified at ED dizziness visits or in the follow-up time period) and vascular risk. These data could inform opportunities to identify index strokes or reduce the risk of subsequent events. Methods: From October 2016 to April 2018, ED visits for dizziness, vertigo, or imbalance were identified in Nueces County, Texas. Validated index or subsequent 90-day ischemic stroke events were identified by linkage to the Brain Attack Surveillance in Corpus Christi (BASIC) project. Infarct locations were classified using imaging reports. The proportion of the events associated with Atherosclerotic cardiovascular disease (ASCVD) score ≥0.10, a common trigger for preventive therapy, was summarized. Results: There were 55 ischemic strokes identified at the time of the ED dizziness visit and 33 ischemic strokes identified in the subsequent 90-days. The Figure displays infarct location, days since ED visit, and ASCVD score. Posterior fossa infarction comprised 47% (26/55) (17 cerebellar, 9 brainstem) of the strokes identified at the dizziness visit and 39% (13/33) (11 cerebellar, 5 brainstem) of the strokes in the follow-up period. Baseline ACSVD scores were ≥0.10 in 78% (43/55) of patients with stroke identified at the dizziness visit and 79% (26/33) of patients with stroke identified in the subsequent 90-days. Conclusions: Posterior fossa lesions account a minority of the ischemic strokes that present to the ED with dizziness or occur in the subsequent 90-days. A substantial majority of these strokes have ASCVD scores higher than a common threshold for preventative therapies. Vascular risk assessment during ED dizziness visits might help providers to both diagnose acute strokes and to prompt preventative strategies in presumed non-stroke cases at increased risk for short-term stroke.

2017 ◽  
Vol 176 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Olaf M Dekkers ◽  
Erzsébet Horváth-Puhó ◽  
Suzanne C Cannegieter ◽  
Jan P Vandenbroucke ◽  
Henrik Toft Sørensen ◽  
...  

Objective Several studies have shown an increased risk for cardiovascular disease (CVD) in hyperthyroidism, but most studies have been too small to address the effect of hyperthyroidism on individual cardiovascular endpoints. Our main aim was to assess the association among hyperthyroidism, acute cardiovascular events and mortality. Design It is a nationwide population-based cohort study. Data were obtained from the Danish Civil Registration System and the Danish National Patient Registry, which covers all Danish hospitals. We compared the rate of all-cause mortality as well as venous thromboembolism (VTE), acute myocardial infarction (AMI), ischemic and non-ischemic stroke, arterial embolism, atrial fibrillation (AF) and percutaneous coronary intervention (PCI) in the two cohorts. Hazard ratios (HR) with 95% confidence intervals (95% CI) were estimated. Results The study included 85 856 hyperthyroid patients and 847 057 matched population-based controls. Mean follow-up time was 9.2 years. The HR for mortality was highest in the first 3 months after diagnosis of hyperthyroidism: 4.62, 95% CI: 4.40–4.85, and remained elevated during long-term follow-up (>3 years) (HR: 1.35, 95% CI: 1.33–1.37). The risk for all examined cardiovascular events was increased, with the highest risk in the first 3 months after hyperthyroidism diagnosis. The 3-month post-diagnosis risk was highest for atrial fibrillation (HR: 7.32, 95% CI: 6.58–8.14) and arterial embolism (HR: 6.08, 95% CI: 4.30–8.61), but the risks of VTE, AMI, ischemic and non-ischemic stroke and PCI were increased also 2- to 3-fold. Conclusions We found an increased risk for all-cause mortality and acute cardiovascular events in patients with hyperthyroidism.


PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94027 ◽  
Author(s):  
Chia-Wei Lin ◽  
Ya-Ping Huang ◽  
Yueh-Hsia Chiu ◽  
Yu-Tsun Ho ◽  
Shin-Liang Pan

Stroke ◽  
2021 ◽  
Author(s):  
Heléne E.K. Sundelin ◽  
Torbjörn Tomson ◽  
Johan Zelano ◽  
Jonas Söderling ◽  
Peter Bang ◽  
...  

Background and Purpose: The risk of epilepsy after stroke has not been thoroughly explored in pediatric ischemic stroke. We examined the risk of epilepsy in children with ischemic stroke as well as in their first-degree relatives. Methods: In Swedish National Registers, we identified 1220 children <18 years with pediatric ischemic stroke diagnosed 1969 to 2016, alive 7 days after stroke and with no prior epilepsy. We used 12 155 age- and sex-matched individuals as comparators. All first-degree relatives to index individuals and comparators were also identified. The risk of epilepsy was estimated in children with ischemic stroke and in their first-degree relatives using Cox proportional hazard regression model. Results: Through this nationwide population-based study, 219 (18.0%) children with ischemic stroke and 91 (0.7%) comparators were diagnosed with epilepsy during follow-up corresponding to a 27.8-fold increased risk of future epilepsy (95% CI, 21.5–36.0). The risk of epilepsy was still elevated after 20 years (hazard ratio [HR], 7.9 [95% CI, 3.3–19.0]), although the highest HR was seen in the first 6 months (HR, 119.4 [95% CI, 48.0–297.4]). The overall incidence rate of epilepsy was 27.0 per 100 000 person-years (95% CI, 21.1–32.8) after ischemic stroke diagnosed ≤day 28 after birth (perinatal) and 11.6 per 100 000 person-years (95% CI, 9.6–13.5) after ischemic stroke diagnosed ≥day 29 after birth (childhood). Siblings and parents, but not offspring, to children with ischemic stroke were at increased risk of epilepsy (siblings: HR, 1.64 [95% CI, 1.08–2.48] and parents: HR, 1.41 [95% CI, 1.01–1.98]). Conclusions: The risk of epilepsy after ischemic stroke in children is increased, especially after perinatal ischemic stroke. The risk of epilepsy was highest during the first 6 months but remained elevated even 20 years after stroke which should be taken into account in future planning for children affected by stroke.


PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e68314 ◽  
Author(s):  
Ya-Ping Huang ◽  
Li-Sheng Chen ◽  
Ming-Fang Yen ◽  
Ching-Yuan Fann ◽  
Yueh-Hsia Chiu ◽  
...  

2020 ◽  
pp. 204748731989921 ◽  
Author(s):  
Mark D Danese ◽  
Peter Pemberton-Ross ◽  
David Catterick ◽  
Guillermo Villa

Aims The aims of this study were to re-estimate the international REduction of Atherothrombosis for Continued Health (REACH) risk equation using United Kingdom data and to distinguish different relative hazards for specific atherosclerotic cardiovascular disease event histories. Methods and results Patients in the UK Clinical Research Practice Datalink (CPRD) were included as of 1 January 2005 if they were 40 years or older, had 2 or more years of prior data, received one or more moderate or high-intensity statin in the previous year, and had a history of myocardial infarction, ischemic stroke, or other atherosclerotic cardiovascular disease. Patients were followed until a composite endpoint of myocardial infarction, ischemic stroke or cardiovascular death, loss to follow-up, or end of observation. We re-estimated the REACH risk equation hazard ratios (HRs) using CPRD data (re-estimated REACH model). Our event history model replaced the REACH vascular bed variables with more specific event histories. There were 60,838 patients with 5.25 years of mean follow-up. In the validation model, HRs were in the same direction, and generally greater than REACH. In the event history model, HRs compared to other atherosclerotic cardiovascular disease alone included: recurrent myocardial infarction (HR 1.19, 95% confidence interval (CI) 1.05–1.34), recurrent ischemic stroke (HR 1.36, 95% CI 1.03–1.80), myocardial infarction and other atherosclerotic cardiovascular disease (HR 1.31, 95% CI 1.23–1.38), ischemic stroke and other atherosclerotic cardiovascular disease (HR 1.40, 95% CI 1.23–1.60), myocardial infarction and ischemic stroke (HR 1.94, 95% CI 1.23–3.04), and myocardial infarction, ischemic stroke and other atherosclerotic cardiovascular disease (HR 1.93, 95% CI 1.47–2.54). Conclusion A detailed cardiovascular event history may be useful for estimating the relative risk of future cardiovascular events.


Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 362-362
Author(s):  
David Tanne ◽  
Avraham Shotan ◽  
Uri Goldbourt ◽  
Valentina Boyko ◽  
Henrietta Reicher-Reiss ◽  
...  

P126 Objective: To assess characteristics and severity of coronary heart disease (CHD) predisposing to ischemic stroke, beyond conventional vascular risk factors. Methods: We prospectively followed up 3,122 patients with documented CHD included in a secondary prevention trial of lipid modification, the Bezafibrate Infarction Prevention trial. Patients had CHD documented by a history of myocardial infarction ≥6 months and <5 years before enrollment and/or stable angina pectoris confirmed by ancillary diagnostic testing, and a selected lipid profile. Patients with severe heart failure or unstable angina upon enrollment were excluded. Results: During a mean follow-up period of 8.2 years, 186 patients developed an ischemic stroke. The rate of ischemic stroke was 8.8% among patients with an active anginal syndrome[class ≥2 according to the Canadian Cardiovascular Society angina Classification, (CCSC)]vs. 5.1% in patients with a CCSC class of 1 (p<0.001). Patients with heart failure according to class ≥2 of the New York Heart Association classification had a 7.7% rate of ischemic stroke vs. 5.5% among patients with a class of 1 (no limitation of physical activity; p=0.03). In a Cox Proportional Hazard model adjusting for conventional risk factors, CCSC angina class ≥2 remained an independent predictor of ischemic stroke (Hazard ratio 1.43; 95%CI 1.05–1.96) and hospitalization for a confirmed diagnosis of unstable angina during follow-up conferred an additional independent increased risk (Hazard ratio 1.7; 95%CI 1.04–2.87). Hazard ratios of conventional risk factors, for comparison, where 1.49 for a 10 year age increment, 2.29 for diabetes mellitus, 1.75 for current smoking, 1.81 for peripheral vascular disease, and 1.14 for a 10 mmHg increase in systolic blood pressure. Conclusion: Active angina (CCSC class ≥2)and hospitalization for unstable angina during follow-up among CHD patients,confer an independent increased risk of ischemic stroke, beyond conventional vascular risk factors.


2008 ◽  
Vol 100 (08) ◽  
pp. 308-313 ◽  
Author(s):  
Elim Y. L. Cheung ◽  
Michiel J. Bos ◽  
Frank W. G. Leebeek ◽  
Peter J. Koudstaal ◽  
Albert Hofman ◽  
...  

SummaryHaplotypes of the fibrinogen gamma and alpha (FGG and FGA) genes are associated with the structure of the fibrin network and may therefore influence the risk of stroke. We investigated the relationship between common variation in these genes with ischemic and haemorrhagic stroke. The study was based on 6,275 participants of the prospective population-based Rotterdam Study who at baseline (1990 – 1993) were aged 55 years or over, free from stroke, and had successful assessment of at least one FGG or FGA single nucleotide polymorphisms (SNP). Common haplotypes were estimated using seven tagging SNPs across a 30 kb region containing the FGG and FGA genes. Follow-up for incident stroke was complete until January 1,2005. Associations between constructed haplotypes and risk of stroke were estimated with an age- and sex-adjusted logistic regression model. We observed 668 strokes, of which 393 were ischemic and 62 haemorrhagic, during a median follow-up time of 10.1 years. FGG+FGA haplotype 3 (H3) was associated with an increased risk of ischemic stroke (odds ratio [OR] 1.36, 95% confidence interval [CI] 1.09–1.69) and the risk estimate for hemorrhagic stroke was 0.71 (95% CI 0.46–1.09) compared to the most frequent H1. The FGG and FGA genes were not associated with stroke or its subtypes when analyzed separately. In conclusion, risk of ischemic stroke was higher in FGG+FGA H3 than in H1. The results suggested that an opposite association may exist for haemorrhagic stroke.


PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94155 ◽  
Author(s):  
Jen-Yu Wang ◽  
Cheng-Yi Wang ◽  
Yung-Sung Huang ◽  
Pin-Fan Chen ◽  
Kuang-Yung Huang ◽  
...  

2021 ◽  
pp. jech-2020-214358
Author(s):  
Pekka Martikainen ◽  
Kaarina Korhonen ◽  
Aline Jelenkovic ◽  
Hannu Lahtinen ◽  
Aki Havulinna ◽  
...  

BackgroundGenetic vulnerability to coronary heart disease (CHD) is well established, but little is known whether these effects are mediated or modified by equally well-established social determinants of CHD. We estimate the joint associations of the polygenetic risk score (PRS) for CHD and education on CHD events.MethodsThe data are from the 1992, 1997, 2002, 2007 and 2012 surveys of the population-based FINRISK Study including measures of social, behavioural and metabolic factors and genome-wide genotypes (N=26 203). Follow-up of fatal and non-fatal incident CHD events (N=2063) was based on nationwide registers.ResultsAllowing for age, sex, study year, region of residence, study batch and principal components, those in the highest quartile of PRS for CHD had strongly increased risk of CHD events compared with the lowest quartile (HR=2.26; 95% CI: 1.97 to 2.59); associations were also observed for low education (HR=1.58; 95% CI: 1.32 to 1.89). These effects were largely independent of each other. Adjustment for baseline smoking, alcohol use, body mass index, igh-density lipoprotein (HDL) and total cholesterol, blood pressure and diabetes attenuated the PRS associations by 10% and the education associations by 50%. We do not find strong evidence of interactions between PRS and education.ConclusionsPRS and education predict CHD events, and these associations are independent of each other. Both can improve CHD prediction beyond behavioural risks. The results imply that observational studies that do not have information on genetic risk factors for CHD do not provide confounded estimates for the association between education and CHD.


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