Abstract TP177: Long-term Stroke Risk in Patients Diagnosed with Hypertensive Encephalopathy

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Michael P Lerario ◽  
Alexander E Merkler ◽  
Gino Gialdini ◽  
Neal S Parikh ◽  
Gary L Bernardini ◽  
...  

Introduction: The long-term cerebrovascular consequences of hypertensive encephalopathy (HE) are poorly understood. Therefore, we aimed to measure the risk of stroke following HE. Methods: We identified all adult patients discharged from nonfederal acute care hospitals between 2005 and 2013 in New York with a primary ICD-9-CM discharge diagnosis of HE (437.2). Only patients who underwent magnetic resonance imaging were included to reduce the likelihood of misclassification error. Patients with all other forms of hypertension (401-405), without concomitant codes for HE or cerebrovascular disease (430-438), served as controls. The primary outcome was incident stroke (431, 433.x1, 434.x1, or 436 in the absence of hemorrhage, trauma, or rehabilitation codes). Kaplan-Meier survival analysis was used to calculate cumulative rates of incident stroke and Cox proportional hazards analysis was used to determine the association between HE and incident stroke while adjusting for demographics, vascular risk factors, and the Elixhauser comorbidity index. Results: We identified 1,386 patients with HE and 2,869,873 with hypertension. Over a mean follow-up period of 3.3 (+/-1.8) years, we identified 66,594 ischemic and 12,343 hemorrhagic strokes. After 5 years, the cumulative rate of stroke was 7.8% (95% CI, 6.2-9.9%) in patients with HE and 3.2% (95% CI, 3.2-3.2%; P<0.001 for the log-rank test) in patients with any other hypertensive disease. After adjusting for demographics, vascular risk factors, and the Elixhauser comorbidity index, HE was independently associated with incident stroke (hazard ratio, 1.9; 95% CI, 1.5-2.4) as compared to controls. This association was similar when considering ischemic and hemorrhagic stroke separately. Conclusions: Patients discharged after HE face a higher long-term risk of subsequent stroke than patients without prior neurological complications of hypertension.

2021 ◽  
pp. 1-12
Author(s):  
Jagan A. Pillai ◽  
Kou Lei ◽  
James Bena ◽  
Lisa Penn ◽  
James B. Leverenz

Background: There is significant interest in understanding the role of modifiable vascular risk factors contributing to dementia risk across age groups. Objective: Risk of dementia onset was assessed in relation to vascular risk factors of hypertension and hypercholesterolemia among cognitively normal APOE ɛ4 carriers and non-carriers. Methods: In a sample of prospectively characterized longitudinal cohort from the National Alzheimer’s Coordinating Center database, 9,349 participants met criteria for normal cognition at baseline, had a CDR-Global (CDR-G) score of zero, and had concomitant data on APOE ɛ4 status and medical co-morbidities including histories of hypertension and hypercholesterolemia. Multivariable Cox proportional hazards models adjusted for well-known potential confounders were used to compare dementia onset among APOE ɛ4 carriers and non-carriers by young (≤65 years) and old (>  65 year) age groups. Results: 519 participants converted to dementia within an average follow up of 5.97 years. Among older APOE ɛ4 carriers, hypercholesterolemia was related to lower risk of dementia (HR (95% CI), 0.68 (0.49–0.94), p = 0.02). Among older APOE ɛ4 non-carriers, hypertension was related to higher risk of dementia (HR (95% CI), 1.44 (1.13–1.82), p = 0.003). These results were corroborated among a subset with autopsy data characterizing underlying neuropathology. Among younger participants, vascular risk factors did not impact dementia risk, likely from a lower frequency of vascular and Alzheimer’s as etiologies of dementia among this cohort. Conclusion: A history of hypercholesterolemia related to a lower risk of dementia among older APOE ɛ4 carriers, while hypertension related to a higher risk of dementia among older APOE ɛ4 non-carriers.


Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Benjamin R Kummer ◽  
Ashley E Aaroe ◽  
Hooman Kamel ◽  
Costantino Iadecola ◽  
Babak B Navi

Introduction: Cerebral ischemia and vascular risk factors are associated with the development of Alzheimer disease (AD). While Parkinson disease (PD) is also a common neurodegenerative condition, the relationship between ischemic stroke and PD remains unclear. Some evidence suggests a shared pathogenic pathway between both diseases. Methods: We used inpatient and outpatient claims data from 2008-2014 in a 5% sample of Medicare beneficiaries ≥66 years of age. Our variables of interest were: 1) a hospital-based diagnosis of ischemic stroke and 2) an outpatient or hospital-based diagnosis of idiopathic PD. Previously validated ICD-9-CM code algorithms were used to identify all diagnoses. We used Cox proportional hazards modeling to characterize the relationship between ischemic stroke and PD, while adjusting for demographics and vascular risk factors. We assessed both the association between PD and subsequent stroke, as well as stroke and subsequent PD. In a separate but identically designed set of analyses, we characterized the relationship between ischemic stroke and AD as a point of comparison. Results: Our analysis encompassed nearly 1.6 million patients with a mean age of 73(+/- 8) years, of whom 57% were female. The annual incidence of ischemic stroke was 1.75% (95% confidence interval [CI], 1.67-1.85%) after a diagnosis of PD versus 0.96% (95% CI, 0.96-0.97%) in those without PD (adjusted hazard ratio [aHR], 1.25; 95% CI, 1.19-1.32). In contrast, the annual incidence of ischemic stroke was 1.96% (95% CI, 1.89-2.03%) after a diagnosis of AD versus 0.96% (95% CI, 0.96-0.97%) in those without AD (aHR, 0.98; 95% CI, 0.95-1.02). The annual incidence of PD was 0.97% (95% CI, 0.92-1.03%) after ischemic stroke versus 0.39% (95% CI, 0.38-0.39%) in those without ischemic stroke (aHR, 1.62; 95% CI, 1.53-1.72). In contrast, the annual incidence of AD was 3.66% (95% CI, 3.56-3.78%) after a diagnosis of ischemic stroke versus 1.17% (95% CI, 1.16-1.17%) in those without ischemic stroke (aHR, 1.67; 95% CI, 1.61-1.72). Conclusions: Among Medicare beneficiaries, the relationships between stroke and PD were similar to those between stroke and AD. As in AD, a link may exist between cerebrovascular disease and PD.


Neurology ◽  
2019 ◽  
Vol 92 (14) ◽  
pp. e1624-e1633 ◽  
Author(s):  
Ruth Ann Marrie ◽  
Allan Garland ◽  
Stephen Allan Schaffer ◽  
Randy Fransoo ◽  
Stella Leung ◽  
...  

ObjectiveTo compare the risk of incident acute myocardial infarction (AMI) in the multiple sclerosis (MS) population and a matched population without MS, controlling for traditional vascular risk factors.MethodsWe conducted a retrospective matched cohort study using population-based administrative (health claims) data in 2 Canadian provinces, British Columbia and Manitoba. We identified incident MS cases using a validated case definition. For each case, we identified up to 5 controls without MS matched on age, sex, and region. We compared the incidence of AMI between cohorts using incidence rate ratios (IRR). We used Cox proportional hazards regression to compare the hazard of AMI between cohorts adjusting for sociodemographic factors, diabetes, hypertension, and hyperlipidemia. We pooled the provincial findings using meta-analysis.ResultsWe identified 14,565 persons with MS and 72,825 matched controls. The crude incidence of AMI per 100,000 population was 146.2 (95% confidence interval [CI] 129.0–163.5) in the MS population and 128.8 (95% CI 121.8–135.8) in the matched population. After age standardization, the incidence of AMI was higher in the MS population than in the matched population (IRR 1.18; 95% CI 1.03–1.36). After adjustment, the hazard of AMI was 60% higher in the MS population than in the matched population (hazard ratio 1.63; 95% CI 1.43–1.87).ConclusionThe risk of AMI is elevated in MS, and this risk may not be accounted for by traditional vascular risk factors.


Gerontology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Feng Cheng Lin ◽  
Chih Yin Chen ◽  
Chung Wei Lin ◽  
Ming Tsang Wu ◽  
Hsuan Yu Chen ◽  
...  

<b><i>Introduction:</i></b> Dementia is one of the major causes of disability and dependency among older people worldwide. Alz­heimer’s disease (AD), the most common cause of dementia among the elderly, has great impact on the health-care system of developed nations. Several risk factors are suggestive of an increased risk of AD, including APOE-ε4, male, age, diabetes mellitus, hypertension, and low social engagement. However, data on risk factors of AD progression are limited. Air pollution is revealed to be associated with increasing dementia incidence, but the relationship between air pollution and clinical AD cognitive deterioration is unclear. <b><i>Methods:</i></b> We conducted a case-control and city-to-city study to compare the progression of AD patients in different level of air-polluted cities. Clinical data of a total of 704 AD patients were retrospectively collected, 584 residences in Kaohsiung and 120 residences in Pingtung between 2002 and 2018. An annual interview was performed with each patient, and the Clinical Dementia Rating score (0 [normal] to 3 [severe stage]) was used to evaluate their cognitive deterioration. Air pollution data of Kaohsiung and Pingtung city for 2002–2018 were retrieved from Taiwan Environmental Protection Administration. Annual Pollutant Standards Index (PSI) and concentrations of particulate matter (PM<sub>10</sub>), sulfur dioxide (SO<sub>2</sub>), ozone (O<sub>3</sub>), nitrogen dioxide (NO<sub>2</sub>), and carbon monoxide (CO) were obtained. <b><i>Results:</i></b> The PSI was higher in Kaohsiung and compared with Pingtung patients, Kaohsiung patients were exposed to higher average annual concentrations of CO, NO<sub>2</sub>, PM<sub>10</sub>, and SO<sub>2</sub>. AD patients living in Kaohsiung suffered from faster cognitive deterioration in comparison with Pingtung patients (log-rank test: <i>p</i> = 0.016). When using multivariate Cox proportional hazards regression analysis, higher levels of CO, NO<sub>2</sub>, PM<sub>10</sub>, and SO<sub>2</sub> exposure were associated with increased risk of AD cognitive deterioration. Among all these air pollutants, high SO<sub>2</sub> exposure has the greatest impact while O<sub>3</sub> has a neutral effect on AD cognitive deterioration. <b><i>Conclusions:</i></b> Air pollution is an environment-related risk factor that can be controlled and is associated with cognitive deterioration of AD. This finding could contribute to the implementation of public intervention strategies of AD.


2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 4048-4048
Author(s):  
Y. Yeh ◽  
Q. Cai ◽  
J. Chao ◽  
M. Russell

4048 Background: NCCN guidelines recommend assessment of =12 lymph nodes (LN) to improve accuracy in colorectal cancer (CRC) staging. Previous studies have used various cut-points to assess the relationship between the number of LN sampled and survival. The association between NCCN guideline-compliant nodal sampling and survival is assessed, while controlling for other risk factors. Methods: We selected 145,485 adult patients newly diagnosed with stage II or III from SEER during 1990–2003. Kaplan-Meier curves were compared using the log-rank test. Cox proportional hazards models were constructed to determine the effect of sampling ≥ 12 LN on survival. Results: Median patient follow-up was 5.7 years. The table shows overall survival rates in CRC patients with < 12 versus =12 LN assessed: After adjusting for age, sex, tumor size and grade, sampling ≥ 12 LN was independently associated with improved survival. For patients with =12 versus <12 LN assessed, survival increased by 13% for stage IIa [HR=0.75; 95%CI 0.72–0.78; p< .001], 16% for stage IIb [HR=0.69; 95%CI 0.67- 0.71; p< .001], 12% for stage IIIb [HR=0.75; 95%CI 0.72–0.77], and 10% for stage IIIc [HR=0.85, 95%CI 0.81–0.89]. The association was not statistically significant for stage IIIa patients. Conclusion: Consistent with previous reports, this analysis found that optimal nodal sampling increased survival across stage II and III, specifically when ≥ 12 LN are sampled and when controlling for other risk factors. Furthermore, the results underscore the need for adhering to the NCCN guidelines. The lack of a statistically significant association in stage IIIa patients may be due to small cohort size. [Table: see text] [Table: see text]


2019 ◽  
Vol 8 (11) ◽  
pp. 1924
Author(s):  
Abecassis ◽  
Wainstock ◽  
Sheiner ◽  
Pariente

The aim of this study was to evaluate perinatal outcome and long-term offspring gastrointestinal morbidity of women with celiac disease. Perinatal outcomes, as well as long-term gastrointestinal morbidity of offspring of mothers with and without celiac disease were assessed. The study groups were followed until 18 years of age for gastrointestinal-related morbidity. For perinatal outcomes, generalized estimation equation (GEE) models were used. A Kaplan–Meier survival curve was used to compare cumulative incidence of long-term gastrointestinal morbidity, and Cox proportional hazards models were constructed to control for confounders. During the study period, 243,682 deliveries met the inclusion criteria, of which 212 (0.08%) were to mothers with celiac disease. Using GEE models, maternal celiac disease was noted as an independent risk factor for low birth weight and cesarean delivery. Offspring born to mothers with celiac disease had higher rates of gastrointestinal related morbidity (Kaplan–Meier log rank test P < 0.001). Using a Cox proportional hazards model, being born to a mother with celiac disease was found to be an independent risk factor for long-term gastrointestinal morbidity of the offspring. Pregnancy of women with celiac disease is independently associated with adverse perinatal outcome as well as higher risk for long-term gastrointestinal morbidity of offspring.


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Rebecca F Gottesman ◽  
Aozhou Wu ◽  
Josef Coresh ◽  
Clifford R Jack ◽  
David S Knopman ◽  
...  

Background: Midlife vascular risk factors (MVRF) are associated with incident dementia. Similarly, amyloid β(Aβ) and neurodegeneration (e.g.brain volumes), as parts of the Alzheimer’s Disease (AD) ATN framework, are associated with cognition. Whether vascular and AD-associated factors contribute to dementia independently or interact synergistically to reduce cognitive ability is not well understood. Methods: Recruited from 3 U.S. communities, ARIC-PET participants were followed from 1987-89 (45-64 yo) through 2016-17 (74-94 yo). Cognition was evaluated in 2011-13 (ages 69-88), and twice more, every 2-3 years. In 2011-13, nondemented ARIC-PET participants had a brain MRI, with measurement of white matter hyperintensities (WMH) and brain volumes, with florbetapir (Aβ) PET scans in 2012-14; global cortical standardized uptake value ratio (SUVR) was log-transformed and standardized. Dementia was classified by expert review, as well as phone and medical record surveillance. The relative contributions of vascular risk (MVRF, WMH volume) and AD pathology (elevated Aβ SUVR, smaller AD signature region volumes) to incident dementia were evaluated with Cox proportional hazards regression. Results: In 298 individuals, 36 developed dementia. In models with key MVRF, demographics, and Aβ SUVR, hypertension and Aβ each independently predicted dementia risk (per SD of Aβ SUVR: HR 2.57, 95% CI 1.72-3.84; hypertension: HR 2.57, 95% CI 1.16-5.67), but didn’t interact on dementia risk. WMH (per SD: HR 1.51, 95% CI 1.03-2.20) and Aβ SUVR (per SD: HR 2.52, 95% CI 1.83-3.47) each contributed to incident dementia but WMH lost significance when MVRF were added to the model. Smaller AD signature regions were associated with incident dementia, independent of Aβ SUVR, and remained significant after adjustment for MVRF (HR per SD 2.18, 95% CI 1.18-4.01). Conclusions: Midlife hypertension and late-life Aβ independently contribute to dementia risk, but don’t synergize on a multiplicative scale. Neurodegeneration (e.g.smaller AD signature region volume) is also associated with incident dementia, independent of Aβ and MVRF. Multiple pathways leading to dementia should be considered when evaluating risk factors and interventions to reduce the burden of dementia.


Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Silvia Koton ◽  
James R Pike ◽  
Michelle C Johansen ◽  
David Knopman ◽  
Kamakshi Lakshminarayan ◽  
...  

Background: Ischemic Stroke (IS) is associated with an increased risk of dementia, but the relative contribution of IS severity or recurrence to cognition is not known. We aimed to determine the risk of dementia after incident IS and how it varies by stroke severity and recurrence in the Atherosclerosis Risk in Communities (ARIC) study. Methods: 15,405 ARIC participants free of stroke and dementia at baseline (1987-9) were followed for IS and dementia through 2019. Incident and recurrent IS were classified by expert review of hospital records, with stroke severity by the National Institutes of Health Stroke Scale (NIHSS) classified as NIHSS≤5, 6-10, 11-15, ≥16. Dementia cases were adjudicated through expert review of in-person evaluations, informant interviews, phone assessments, hospitalization code or death certificates. Poisson regression models with robust error variance were used to estimate dementia incidence in participants with and without IS, and associations between time-dependent IS incidence (excluding dementia in the first year after stroke), frequency and severity, and dementia were studied with Cox proportional hazards models, adjusting for demographics, APOE ε4 and vascular risk factors . Results: 1151 IS (970 incident) and 2807 dementia cases were identified. NIHSS was available for 877 IS (76%). Adjusted incidence rates (95% CI) of dementia per 100 person-years were 0.45 (0.42-0.49) in participants without IS vs. 1.33 (1.15-1.55) in those with IS. Compared to no IS, risk of dementia (adjusted HR, 95% CI) increased with IS number and severity from 1.71 (1.47-1.99) for participants with one IS to 6.68 (3.58-12.46) for those with ≥3 events, and from 1.64 (1.36-1.98) for NIHSS≤5 to 4.43 (1.84-10.68) for NIHSS≥16 ( Table ). Conclusion: Risk of dementia is significantly increased after stroke, independent of vascular risk factors. These data suggest a dose-response relationship between number of stroke events and stroke severity, and risk of dementia.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Mazidi ◽  
D P Mikhailidis ◽  
N Katsiki ◽  
D Pella ◽  
M Banach

Abstract Background The long-term effect of potato consumption on mortality and cardiometabolic risk factors is still largely unknown. Purpose Using the National Health and Nutrition Examination Surveys (NHANES) 1999–2010, we evaluated the long-term impact of potato intake on total and cause-specific (cardiovascular disease [CVD],cerebrovascular disease and cancer] mortality, and the results were next validated in the systematic review and meta-analysis of cohort studies investigating pooled associations of potato consumption with all-cause and cause-specific death. Methods Vital status through December 31, 2011 was ascertained. Cox proportional hazards were applied to determine the hazard ratios (HRs) and 95% confidence intervals (95% CIs) of mortality for each quartile of the potato intake, with the lowest quartile (Q1 – with the lowest intake) used as reference. We used adjusted Cox regression to determine the risk ratio (RR) and 95% CI, as well as random effects models and generic inverse variance methods to synthesize quantitative and pooled data, followed by a leave-one-out method for sensitivity analysis. Results Among the 24,856 participants included, 3433 deaths occurred during the mean follow-up of 6.4 years. In multivariate adjusted Cox models, total (42%), CVD (65%), cerebrovascular (26%) and cancer (52%) mortality risk was greater in individuals with higher potato consumption than those with the lowest intake (p<0.001 for all comparisons). However this link disappeared after adjustment for confounding factors (see Table below). Results from pooling current prospective studies with 73,717 participants revealed a non-significant association between total (RR: 1.25, 0.98–1.60, p=0.066), CVD (RR: 0.99, 0.90–1.08, p=0.845) and stroke mortality (RR: 0.94, 0.85–1.03, p=0.214) with potato consumption. Individuals with a higher potato intake had a less favorable profile of cardiometabolic factors, including greater WC (97.2 vs. 99.5 cm, p<0.001) and a less favorable profile of systolic and diastolic blood pressure, levels of triglycerides (TGs), high-density lipoprotein-cholesterol (HDL-C) and TG/HDL-C ratio (p<0.001 for all comparisons). HRs for mortality across potato intake. Conclusions Our results highlighted the neutral effect of potato intake on long-term mortalities; whereas potato consumption was adversely related to cardiometabolic risk factors. These findings should be taken into consideration for public health strategies, establishing the position for potatoes in the food pyramid. Acknowledgement/Funding None


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