Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,991 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Laura Tarko, Lauren Costa, Ashley Galloway, Yuk-Lam Ho, David Gagnon, Vasileios Lioutas, Sudha Seshadri, Kelly Cho, View ORCID ProfilePeter Wilson, View ORCID ProfileHugo J. Aparicio
First published June 1, 2022, DOI: https://doi.org/10.1212/WNL.0000000000200575
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Abstract
Background and Objectives
Racial and ethnic disparities in stroke outcomes exist, but differences
by stroke type are less understood. We studied the association of race
and ethnicity with stroke mortality, by stroke type, in a national
sample of hospitalized patients in the Veterans Health Administration.
Methods
A retrospective observational study was performed including
non-Hispanic White, non-Hispanic Black, and Hispanic patients with a
first hospitalization for stroke between 2002 and 2012. Stroke was
determined using ICD-9 codes and date of death was obtained from the
National Death Index. For each of acute ischemic stroke (AIS),
intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH), we
constructed a piecewise multivariable model for all-cause mortality,
using follow-up intervals of ≤30 days, 31–90 days, 91 days to 1 year,
and >1 year.
Results
Among 37,790 patients with stroke (89% AIS, 9% ICH, 2% SAH), 25,492
(67%) were non-Hispanic White, 9,752 (26%) were non-Hispanic Black, and
2,546 (7%) were Hispanic. The cohort was predominantly male (98%).
Compared with White patients, Black patients experienced better 30-day
survival after AIS (hazard ratio [HR] 0.80, 95% CI 0.73–0.88; 1.4% risk
difference) and worse 30-day survival after ICH (HR 1.24, 95% CI
1.06–1.44; 3.2% risk difference). Hispanic patients experienced reduced
risk for >1-year mortality after AIS (HR 0.87, 95% CI 0.80–0.94), but
had greater risk of 30-day mortality after SAH compared with White
patients (HR 1.61, 95% CI 1.03–2.52; 10.3% risk difference).
Discussion
Among US Veterans, absolute risk of 30-day mortality after ICH was 3.2%
higher for Black patients and after SAH was 10.3% higher for Hispanic
patients compared with White patients. These findings underscore the
importance of investigating stroke outcomes by stroke type to better
understand the factors driving observed racial and ethnic disparities.
Glossary
AIS=
acute ischemic stroke;
CDW=
Corporate Data Warehouse;
CMS=
Centers for Medicare & Medicaid Services;
EHR=
electronic health record;
HR=
hazard ratio;
ICD-9=
International Classification of Diseases, Ninth Revision;
It shouldn't make any difference, your hospital should have 100% recovery protocols for any stroke person that comes in. If not, they are totally incompetent.
Race, ethnicity and health insurance status all appeared to impact
receipt of treatment for ischemic stroke among patients in California,
Florida and New York, according to a retrospective analysis of more than
1 million hospitalizations.
Researchers presented their findings during the American Academy of Neurology annual meeting, which is being held virtually.
Source: Adobe Stock
“We know that racial disparities both in thrombolysis and endovascular therapy
vary across states and that low or no insurance status is associated
with a lower likelihood for receiving these treatment interventions —
regardless of race,” Alison Herman, BS (Hon), a postgraduate researcher
in neurocritical care and emergency neurology at Yale University, said
during her presentation.
Herman and colleagues sought to assess the association between race
and ethnicity and receipt of thrombolysis and endovascular therapy among
1,051,522 hospitalized patients receiving care across California
between 2006 and 2011, Florida between 2006 and 2014 and New York
between 2006 and 2014.
Overall, 39,959 patients received thrombolysis treatment alone, 2,624
received endovascular therapy alone and 2,193 received both
thrombolysis and endovascular therapy.
After adjusting for age, sex, significant comorbidities, markers of
stroke severity, insurance status and the interaction between race and
insurance status, researchers found that compared with white patients,
Black patients in Florida (OR = 0.82; P < .001) and both Black (OR = 0.65; P < .001) and Hispanic patients (OR = 0.73; P
< .001) in California were less likely to receive thrombolysis,
whereas Black (OR = 0.69; P < .01) and Hispanic (OR = 0.65; P < .01) patients in New York were less likely to receive endovascular therapy.
Moreover, Medicare and Medicaid beneficiaries across all three states
were less likely to receive thrombolysis and endovascular therapy.
Patients in Florida who were uninsured were also less likely to receive
thrombolysis and endovascular therapy.
“There are many different factors that may be contributing to these
racial disparities,” Herman said. “One argument would be whether
potential access to health care is causing these disparities or
contributing to them.”
For this reason, Herman and colleagues next conducted a geographical
analysis to see if the distance from a thrombectomy center to patients’
homes impacted the likelihood of receiving treatment for ischemic
stroke.
“Ultimately, Black patients were more likely to live closer to a
thrombectomy center compared with white patients and the same was true
for Hispanic patients in New York and Florida,” she said. “Therefore,
the distance to a thrombectomy center does not appear to impact the
likelihood of receiving treatment. Ultimately, our data show that these
disparities are not caused by physical access to treatment.”
Limitations of the study included the fact that the analysis was
limited to showing associations and generating future hypotheses, and
administrative claims data were used, which did not provide detailed
information on stroke severity, Herman noted.
“In particular, we only had data through 2014, which is a limitation
in terms of endovascular therapy since the positive trials in
thrombectomy were mostly published in 2015,” Herman said. “We therefore
considered looking at state and patient data for more recent years but
ultimately opted to look at these disparities in a nationwide sample
because this work is hypothesis-generating and we thought additional
work on future years should be conducted across all 50 states so that we
can observe racial disparities and any inconsistencies in racial
disparities across states.”
Future research should also assess whether stroke severity accounts
for any of the treatment differences observed in this study, Herman
added.
“It would also be worthwhile to assess the impact of other
socioeconomic status proxies, such as level of education and median
income,” she said. “We also want to evaluate the trends in more recent
years and throughout time. However, the most pressing need is to look at
features that account for the presence or absence of racial disparities
to develop effective policies and programs at the state level.”
Hooman Kamel, Kathleen Alwell, View ORCID ProfileBrett M. Kissela, Heidi J. Sucharew, Daniel Woo, Matthew Flaherty, Simona Ferioli, Stacie L. Demel, Charles J. Moomaw, Kyle Walsh, Jason Mackey, De Los Rios La Rosa, Felipe, View ORCID ProfileAdam Jasne, Sabreena Slavin, Sharyl Martini, Opeolu Adeoye, Tehniyat Baig, Monica L. Chen, View ORCID ProfileEmily B. Levitan, Elsayed Z. Soliman, Dawn O. Kleindorfer
First published November 25, 2020, DOI: https://doi.org/10.1212/WNL.0000000000011197
Objective:
To test the hypothesis that thrombogenic atrial cardiopathy may be
relevant to stroke-related racial disparities, we compared atrial
cardiopathy phenotypes between Black versus White ischemic stroke
patients.
Methods:
We assessed markers of atrial cardiopathy in the Greater
Cincinnati/Northern Kentucky Stroke Study, a study of stroke incidence
in a population of 1.3 million. We obtained ECGs and reports of
echocardiograms performed during evaluation of stroke during the
2010/2015 study periods. Patients with atrial fibrillation (AF) or
flutter (AFL) were excluded. Investigators blinded to patients’
characteristics measured P-wave terminal force in ECG lead V1 (PTFV1),
a marker of left atrial fibrosis and impaired inter-atrial conduction,
and abstracted left atrial diameter from echocardiogram reports. Linear
regression was used to examine the association between race and atrial
cardiopathy markers after adjustment for demographics, body mass index,
and vascular comorbidities.
Results:
Among 3,426 ischemic stroke cases in Black or White patients without
AF/AFL, 2,391 had a left atrial diameter measurement (mean, 3.65 ±0.70
cm). Black race was associated with smaller left atrial diameter in
unadjusted (β coefficient, -0.11; 95% CI, -0.17 to -0.05) and adjusted
(β, -0.15; 95% CI, -0.21 to -0.09) models. PTFV1 measurements were available in 3,209 patients (mean, 3,434 ±2,525 μV*ms). Black race was associated with greater PTFV1 in unadjusted (β, 1.59; 95% CI, 1.21 to 1.97) and adjusted (β, 1.45; 95% CI, 1.00 to 1.80) models.
Conclusions:
We found systematic Black-White racial differences in left atrial
structure and pathophysiology in a population-based sample of ischemic
stroke patients.
Classification of Evidence:
This study provides class II evidence that the rate of atrial
cardiopathy is greater among Black people with acute stroke compared to
White people.
JAMA Neurol. Published online August 21, 2020. doi:10.1001/jamaneurol.2020.3510
The killing of George
Floyd, an unarmed 46-year-old Black man by a White police officer in
Minneapolis, led to widespread protests against police brutality.
Beginning with a focus on law enforcement reforms, the protests grew in
diversity and objective, evolving into a broader call to end
institutionalized racism. For the first time in history, a diverse,
global coalition came together to protest injustice in the societal
treatment of Black lives. Perhaps it was the collision of George Floyd’s
horrific death with the disproportionate and egregiously high death
rates and coronavirus disease 2019 infection rates within communities of
color in the US that fueled this movement. Of note, precursors of
change, such as the diversity, inclusion, and equity initiatives being
spawned in all major sectors (economic, education, health), hold out
hope for meaningful progress. This Viewpoint highlights the complex role
of racism in stroke and suggests a framework for understanding its
effects.
Levels of Racism Theoretical Framework
The Levels of Racism framework delineates 3 interacting
levels of racism to guide development of interventions aimed at reducing
racial differences in health outcomes.1 These include institutionalized or structural racism, personally mediated racism, and internalized racism.1 Institutionalized racism occurs when access to goods, services, and opportunities is influenced by race.1 It is also referred to as structural racism
owing to its codification in organizational practice and policy, to the
extent that it becomes the normative behavior—a cultural
disease—without the presence of a specific transgressor. Personally
mediated racism is prejudice arising from conditioned assumptions about a
person’s intentions and abilities, based on race, causing implicit and
explicit bias.1
Internalized racism is a by-product of structural racism and personally
mediated racism, reflecting the total capitulation of the individual’s
self-worth and self-esteem. It occurs when people accept racist beliefs
about their own abilities and human value.1
Social Determinants of Health
Social determinants of health are the conditions in
which we are born, live, learn, work, and play and their impact on our
health. Differences in social determinants are linked to wealth status
and drive the powerful association between a person’s zip code and life
expectancy. But these conditions, operating across the socioecologic
spectrum of human life, are not only influenced by socioeconomic status
but also by levels of racism. They include upstream factors related to
health outcomes, such as housing conditions, school quality,
environmental conditions, employment opportunities, access to healthy
foods, and access to quality health care, all of which may be influenced
by racial inequities and moderate the downstream biological processes
responsible for health outcomes.
Stroke Disparities
A 2003 Institute of Medicine report,2
entitled “Unequal Treatment: Confronting Racial and Ethnic Disparities
in Health Care,” provided a compelling body of research highlighting
health care injustices associated with greater mortality among Black
patients. These included lower quality of health services and lower
likelihood to receive appropriate medical procedures among Black vs
White US citizens.2Poorer stroke outcomes for Black Americans compared with their White
counterparts have persisted for more than 50 years. For example, Black
individuals are twice as likely to die of stroke than White individuals,
and this disparity is not entirely explained by differences in the
prevalence of traditional risk factors (as defined by the Framingham
Stroke Risk Function). Indeed, data from Reasons for Geographic and
Racial Differences in Stroke (REGARDS) showed that only 40% of the
Black-White incidence disparity is attributable to differences in the
prevalence of traditional stroke risk factors, and that the source of
the outstanding 60% remains unclear.3
The REGARDS investigators suggest that this excess disparity may be
driven by differences in risk factor control, differential impact of
risk factors by race, and nontraditional risk factors, such as for
physical inactivity, diet, and psychosocial factors, including
depression and discrimination.3 Others have gone a step further by tracing stroke disparities to historical slavery, racism, and segregation.4
This active legacy of slavery manifests itself in the structural
inequities of American society. They cause chronic repetitive, socially
structured stressors shown to elicit physiological responses associated
with cardiovascular disease and premature death. Indeed, a growing body
of research regarding these physical consequences of social inequality
referred to as the “weathering hypothesis,” shows that its physiological
responses can be measured using markers of allostatic load.5
Structural Racism and Stroke
Social determinants of health are riddled with
race-based inequity due to the role of racial discrimination in resource
allocation that have lingered since the US government’s redlining
policies. These inequities are not only remnants of slavery and de jure
segregation, but also related to the widespread de facto segregation in
the US today. Evidence from US Census data suggests that, while the US
has become more diverse, segregation has not appreciably improved since
the era of Jim Crow. The separate social worlds between Black and White
individuals are driven in part by income, preference, the absence of
integrated experiences to help break the cycle of preference, and
discriminatory practices, such as racial steering in which real estate
brokers “steer” prospective home buyers toward or away from certain
neighborhoods based on their race. Consequently, Black individuals are
concentrated in neighborhoods excluded from mainstream resources. It is
why the variability of school quality across neighborhoods correlates
with their racial composition. Such area deprivation, captured by
economic, educational, and other environmental inequalities, is
associated with worse mortality. Although beyond the purview of
neurologists, these conditions may be drivers of stroke risk factors,
such as smoking, obesity, hypertension, and type 2 diabetes.
Personally Mediated Racism and Stroke
This form of racism influences decision-making of policy
makers and members of governing bodies responsible for resource
development and allocation, contributing to structural racism and its
indirect effects on health. But personally mediated racism is also
directly toxic to the health of those who experience it. It can be
captured and quantified by validated scales, such as the Everyday
Discrimination Scale,6
a measure of subjective experiences of discrimination. Examples of
daily race-based indignities are itemized on this measure and range from
microaggressions (eg, being treated as if you may be dishonest or as if
people may be afraid of you, or receiving poorer service than others)
to profiling and police brutality. While many of the experiences
described in the measure appear minor, their sheer volume and chronicity
have harmful consequences, including hypertension, higher levels of
inflammation, and premature mortality.6
Moreover, even the recall of these experiences, a feature of
rumination, produces adverse blood pressure responses comparable with
those that occurred when the person was exposed.7
Internalized Racism and Stroke
Internalized racism and the resulting self-devaluation, self-rejection, engagement in risky health practices, and hopelessness1
has been linked to nontraditional stroke risk factors. These include
depression, anxiety disorders, and several maladaptive behaviors in
addition to cardiovascular disease.
The hydra-headed disadvantage of being deprived and a
Black individual supports the need to include racism as a distinct
construct of health disparities. Beyond social determinants of health,
the insidious and paroxysmal health effects of racism directed at Black
people, and which begins early in life, may be underestimated,
potentially explaining some of the excess Black-White stroke disparities
observed. We call for increased funding and research that expands the
use of an “equity lens” in the design and evaluation of stroke
interventions and the role of racism in stroke outcomes. Promising areas
of study include an examination of racism’s vascular effects on stroke
risk and on differences in blood pressure control.
Corresponding Author:
Olajide Williams, MD, MS, Department of Neurology, Columbia University
Irving Medical Center, 710 W 168th St, Sixth Floor, New York, NY 10032 (ow11@cumc.columbia.edu).
Send these researchers back to the drawing board because there is no
such thing as race as far as the body is concerned. Go back and find the real reason for distinguishing them. This is just a crutch used to not do the hard work of finding out the real reason.
JAMA Neurol. Published online April 13, 2020. doi:10.1001/jamaneurol.2020.0568
Full Text
Key PointsQuestion
Do black individuals’ higher cumulative blood pressure levels
contribute to their greater risk of cognitive impairment and dementia
compared with white individuals? Findings
In this pooled cohort analysis of 19 378 participants, black
individuals, compared with white individuals, had significantly faster
declines in global cognition. Differences between black and white
individuals in global cognition decline were no longer statistically
significant after adjusting for cumulative mean systolic blood pressure. Meaning
Black individuals’ higher cumulative blood pressure levels may explain racial disparities in cognitive decline.
Abstract
Importance
Black individuals are more likely than white individuals to
develop dementia. Whether higher blood pressure (BP) levels in black
individuals explain differences between black and white individuals in
dementia risk is uncertain. Objective
To determine whether cumulative BP levels explain racial differences in cognitive decline. Design, Setting, and Participants
Individual participant data from 5 cohorts (January 1971 to
December 2017) were pooled from the Atherosclerosis Risk in Communities
Study, Coronary Artery Risk Development in Young Adults Study,
Cardiovascular Health Study, Framingham Offspring Study, and Northern
Manhattan Study. Outcomes were standardized as t scores (mean
[SD], 50 [10]); a 1-point difference represented a 0.1-SD difference in
cognition. The median (interquartile range) follow-up was 12.4
(5.9-21.0) years. Analysis began September 2018. Main Outcomes and Measures
The primary outcome was change in global cognition, and secondary outcomes were change in memory and executive function. Exposures
Race (black vs white). Results
Among 34 349 participants, 19 378 individuals who were free of
stroke and dementia and had longitudinal BP, cognitive, and covariate
data were included in the analysis. The mean (SD) age at first cognitive
assessment was 59.8 (10.4) years and ranged from 5 to 95 years. Of
19 378 individuals, 10 724 (55.3%) were female and 15 526 (80.1%) were
white. Compared with white individuals, black individuals had
significantly faster declines in global cognition (−0.03 points per year
faster [95% CI, −0.05 to −0.01]; P = .004) and memory (−0.08 points per year faster [95% CI, −0.11 to −0.06]; P < .001) but significantly slower declines in executive function (0.09 points per year slower [95% CI, 0.08-0.10]; P < .001).
Time-dependent cumulative mean systolic BP level was associated with
significantly faster declines in global cognition (−0.018 points per
year faster per each 10–mm Hg increase [95% CI, −0.023 to −0.014]; P < .001), memory (−0.028 points per year faster per each 10–mm Hg increase [95% CI, −0.035 to −0.021]; P < .001), and executive function (−0.01 points per year faster per each 10–mm Hg increase [95% CI, −0.014 to −0.007]; P < .001).
After adjusting for cumulative mean systolic BP, differences between
black and white individuals in cognitive slopes were attenuated for
global cognition (−0.01 points per year [95% CI, −0.03 to 0.01]; P = .56) and memory (−0.06 points per year [95% CI, −0.08 to −0.03]; P < .001) but not executive function (0.10 points per year [95% CI, 0.09-0.11]; P < .001). Conclusions and Relevance
These results suggest that black individuals’ higher
cumulative BP levels may contribute to racial differences in later-life
cognitive decline.
Send these researchers back to the drawing board because there is no
such thing as race as far as the body is concerned. Go back and find a separate reason for distinguishing them.
Journal of the American Heart Association — Muller CJ, et al. | June 17, 2019
By pooling data from two
cardiovascular disease cohort studies, researchers examined American
Indians (AIs; n=3,182,) aged 45 to 74 years at baseline (1988–1990) from
the SHS (Strong Heart Study) and blacks (n=3,765) and whites (n=10,413)
from the ARIC (Atherosclerosis Risk in Communities) Study, aged 45 to
64 years at baseline (1987–1989) to compare stroke incidence and
mortality in these populations. For AIs, blacks, and whites, the
incident strokes reported were 282, 416, and 613, respectively. AIs had a
lower incidence of stroke when compared to blacks, and a higher
incidence when compared to whites; differences were larger for blacks
and smaller for whites following covariate adjustment. AIs had higher
poststroke mortality vs blacks and whites.
This is completely stupid research. Knowing the sex, race, income, or education of the stroke survivors tells you nothing of why there is a gap in secondary stroke prevention. The mentors and senior researchers on this need to be fired.
Income and education play a role in significant sex and racial disparities in secondary stroke preventive measures, according to data presented at the International Stroke Conference. Paul M. Ndunda, MD, and Tabitha M. Muutu, MD,
of the department of internal medicine at the University of Kansas
School of Medicine, sought to study the sex and racial differences in
the use of secondary preventive measures in patients with stroke and
identify associated factors by analyzing data from the 2015 Behavioral Risk Factor Surveillance System
composed of 18,269 patients (mean age, 67 years; 58% women, 75% white)
with stroke. Outcomes analyzed included exercise, diet, smoking
cessation, BMI, BP medication use and alcohol intake.(So these are the real factors that cause strokes. NOT sex, race, income, or education. You had the answer right in front of you but you went to useless categories in your title and writeup.))
“In the U.S., 795,000 people suffer a stroke and 133,000 die from it
annually. Among the survivors, 185,000 get a recurrent stroke,” the
researchers wrote in an abstract. “There are gender and racial
disparities in stroke mortality, and there is need to understand the
associated factors if the [American Heart Association]’s 2020 impact
goal is to be achieved.”
Women were more likely to continue smoking (OR = 1.22; 95% CI.
1.13-1.32) and less likely to meet AHA exercise guidelines (OR = 0.87;
95% CI, 0.81-0.94). Women were also more likely to be obese or
overweight (OR = 1.45; 95% CI, 1.35-1.54) and less likely to be on
aspirin (OR = 0.57; 95% CI, 0.4-0.8) or BP medications (OR = 0.96; 95%
CI, 0.85-1.09), Ndunda and Muutu reported.
Women were like likely to eat one or more servings of fruits (OR =
1.41; 95% CI, 1.33-1.5) and vegetables (OR = 1.32; 95% CI, 1.23-1.4) and
were more likely to have medical insurance (OR = 1.21; 95% CI,
1.04-1.4) and a clinical provider (OR = 1.76; 95% CI, 1.75-1.76), the
researchers wrote. Hispanics
were more likely to continue smoking compared with white patients (OR =
1.37; 95% CI, 1.15-1.63), whereas black (OR = 0.66; 95% CI, 0.61-0.72)
and Hispanic patients (OR = 0.78; 95% CI, 0.68-0.88) were less likely to
exercise compared with white patients, according to the data.
Black patients were less likely to eat fruits (OR = 0.7; 95% CI,
0.64-0.76) and vegetables (OR = 0.56, 95% CI, 0.51-0.61), but the
effects were lessened by adjusting for income and education, the
researchers wrote. – by Earl Holland Jr. Reference:
Ndunda PM, et al. Abstract 192. Presented at: International Stroke Conference; Feb. 6-8, 2109; Honolulu.
Send these researchers back to the drawing board because there is no
such thing as race as far as the body is concerned. Go back and find the
real reason.
But they're less likely to receive tPA, analysis shows
by Judy George, Contributing Writer, MedPage Today
Asian-American stroke patients had
more severe ischemic strokes, were less likely to receive intravenous
tissue plasminogen activator (IV tPA), and had worse functional outcomes
than white patients, a retrospective analysis showed.
They also had more hemorrhagic complications after receiving tPA,
reported Sarah Song, MD, MPH, of Rush University Medical Center in
Chicago, and colleagues in JAMA Neurology.
A
study of of 64,337 Asian-American patients and 1,707,962 white patients
admitted for acute ischemic stroke to hospitals participating in the Get With The Guidelines–Stroke (GWTG-Stroke) program from 2004 to 2016 showed that, after adjusting for patient and hospital variables, Asian Americans had:
Greater stroke severity than white patients: NIH Stroke Scale (NIHSS) score ≥16 (OR 1.35, 95% CI 1.30-1.40, P<0.001)
Higher in-hospital mortality (OR 1.14, 95% CI 1.09-1.19, P<0.001), longer length of stay (OR 1.17, 95% CI 1.14-1.20, P<0.001), and less independent ambulation at discharge (OR 0.84, 95% CI 0.79-0.90, P<0.001)
Fewer IV tPA administrations (OR 0.95, 95% CI 0.91-0.98, P=0.003), but more symptomatic hemorrhage after tPA (OR 1.36, 95% CI 1.20-1.55, P<0.001), and overall post-tPA complications (OR 1.31, 95% CI 1.18-1.46, P<0.001)
"This is just one study, but it's alarming," Song told MedPage Today.
"Asian Americans are the most rapidly growing ethnic group in the
country. This study is a call to action that we need more research in
this population."
The GWTG-Stroke program, originally designed to facilitate quality
improvement activities at individual stroke centers, has grown
collectively to offer insights into questions that clinical trials are
not powered to answer, noted Cathy Sila, MD, of University Hospitals
Cleveland Medical Center in Ohio, who was not involved with the
analysis.
While the study also showed that Asian Americans were more likely to
be on Medicaid, uninsured, and arrive at the hospital without utilizing
pre-hospital providers, many questions about their outcomes remain
unanswered, Sila observed. "Why did they fare more poorly? Once they
came to the hospital, they received guidelines-driven care at excellent
rates -- across the board higher than whites -- and had greater
access to tPA," she noted.
"But interestingly, this pattern of tPA access reversed when the data was adjusted for stroke severity," Sila told MedPage Today.
"Baseline stroke severity is the most powerful predictor of outcome and
Asian Americans had a significantly higher mean NIHSS, as well as a
greater proportion of severe strokes."
"We
know that the majority were cared for in the [western U.S.] (55.2% vs
17.6%), at academic centers, and less likely to be transferred, but to
better interpret the findings, it would be helpful to know about the
specific stroke subtypes and whether tPA was not given because other
options were pursued, such as mechanical thrombectomy," she continued.
Without knowing the type of cerebrovascular disease, differences in
stroke mortality and complications can't be fully understood, added
Craig Anderson, MD, PhD, of the George Institute for Global Health at
Peking University Health Science Center in Beijing, China, who also was
not part of the study.
"Asians have more small vessel and intracranial atheroma than white
Americans, who are likely to have more cardioembolic strokes," he told MedPage Today.
"These data also suggest Asian Americans are more at risk of the
complications of thrombolysis, which may be due to dose calculation from
estimated body weight," he noted. Other studies have shown that lower
doses of tPA in mainly Asian populations were not as effective but led
to fewer intracranial hemorrhages.
Hospitals volunteer to be in the GWTG-Stroke program, and quality of
stroke care may be higher than in nonparticipating hospitals, Song and
colleagues noted. And at baseline, the Asian-American and white cohorts
in this study had differences: the white group was older and was more
likely to have specific vascular risk factors like atrial fibrillation
and coronary artery disease, while the Asian-American group was more
likely to have diabetes.
While Asian-American ethnicity in this study encompassed individuals
from multiple heritages -- Asian, Indian, Chinese, Filipino, Korean,
Japanese, Vietnamese, and other groups -- information about subgroups
was not available. Other limitations of the study included potential
residual confounding, which may account for some of the findings. In
addition, small differences became statistically significant in this
analysis because of the large sample size, possibly inflating the
importance of differences between Asian-American and white patients,
Song and colleagues added.
The
GWTG-Stroke program is sponsored by the American Heart Association
(AHA)/American Stroke Association. It is is sponsored in part by
Medtronic and has been funded in the past through support from
Boehringer-Ingelheim, Merck, a Bristol-Myers Squib/Sanofi
Pharmaceuticals partnership, Janssen Pharmaceutical Companies of Johnson
& Johnson, and the AHA Pharmaceutical Roundtable.
Song
disclosed no relevant relationships with industry. Co-authors disclosed
relevant relationships with Get With The Guidelines, the Patient
Centered Outcome Research Institute, Janssen, Cardax, the Society of
Cardiovascular Patient Care, TobeSoft, AHA, the Baim Institute for
Clinical Research, Daiichi Sankyo, the Population Health Research
Institute, the American College of Cardiology, Boehringer Ingelheim,
Bayer, Abbott, Amarin, Amgen, AstraZeneca, Bayer, Bristol-Myers Squibb,
Chiesi, Eisai, Ethicon, Forest Laboratories, Idorsia, Ironwood,
Ischemix, Lilly, Medtronic, PhaseBio, Pfizer, Regeneron, Roche, Sanofi
Aventis, Synaptic, The Medicines Company, Biotronik, Boston Scientific,
Svelte, FlowCo, Merck, Novo Nordisk, PLx Pharma, Takeda, and Genentech.
Send these researchers back to the drawing board because there is no
such thing as race as far as the body is concerned. Go back and find the
real reason.
The disparity of stroke risk in men vs. women varied by race and age, researchers reported in JAMA Neurology.
In addition, stroke risk factors varied by sex in white adults but not in black adults, according to the researchers.
“This suggests that it may not be ‘one size fits all’ when it comes to stroke prevention,” Virginia Howard, PhD,
professor of epidemiology in the School of Public Health at the
University of Alabama at Birmingham, said in a press release. “For
example, overall, black women may need better risk factor management and
more aggressive risk factor management at younger ages than white
women.”
Howard and colleagues analyzed 25,789 black and white participants
(mean age, 64 years; 55% women; 40% black) from the REGARDS cohort study
who were free from stroke at baseline.
During 222,120 person-years of follow-up, 939 strokes occurred (16.9%
in black men; 34.7% in white men; 23.1% in black women; 25.2% in white
women), Howard and colleagues wrote.
Women aged 45 to 64 years, for both races, had lower stroke risk
than men (incidence rate ratio [IRR] for white women vs. white men =
0.68; 95% CI, 0.49-0.94; IRR for black women vs. black men = 0.72; 95%
CI, 0.52-0.99), according to the researchers.
However, for women aged 65 to 74 years, the lower risk persisted in
white adults but not in black adults (IRR for white women vs. white men =
0.71; 95% CI, 0.55-0.94; IRR for black women vs. black men = 0.94; 95%
CI, 0.68-1.3), although the race-sex interaction was not significant,
Howard and colleagues wrote.
At age 75 years or older, there was no difference in stroke risk by sex for either race.
Howard and colleagues also found that there were no sex differences for any stroke risk factors in black adults.
However, for white adults, the following associations with stroke risk were greater for women than for men: systolic BP (P for interaction = .099), diabetes (P for interaction = .02) and heart disease (P
for interaction = .09), whereas the antihypertensive medication use had
a greater association with stroke risk in men than in women (P for interaction = .08), according to the researchers.
“We hope this will encourage people and their primary care physicians
to have more discussions, and to ‘target’ their discussion on risk
factors of more importance to the patient — about stroke risk factors
and what can be done to prevent the risk factor from occurring,” Howard
said in the release. “Or if someone already has risk factors, the
discussion can be geared toward better management and control of risk
factors. This is true across all race-sex-age groups.” – by Erik Swain
You mean your mentors and senior researchers don't know that race as you are using it doesn't exist? Send everyone back to the drawing board to find out the real reason for the differences. Incompetence in stroke reigns supreme.
JAMA Neurology — Howard VJ, et al. | December 12, 2018
In this prospective cohort study,
researchers investigated the incidence and risk factors for ischemic
stroke by sex for black and white individuals. They found that, for both
races, women were at lower risk of stroke at 45-64 years of age vs men,
and there was no sexual difference at age ≥ 75 years. However, the
pattern of sexual difference may vary by race from age 65-74 years. The
risk factors associated with stroke risk varied by race-sex groups. The
association of hypertension, diabetes, and heart disease with stroke
risk varied by sex for white individuals but not black individuals. Some
demographic subgroups might require earlier and more aggressive
strategies while the need for primordial prevention, optimal management,
and control of risk factors is universal across all age, racial/ethnic,
and sex groups.
Study participants included individuals aged ≥ 45 years who were
stroke-free from the Reasons for Geographic and Racial Differences in
Stroke (REGARDS) cohort, enrolled from the continental US 2003-2007 with
follow-up through October 2016.
From March 2018 to September 2018, data were analyzed.
Exposures included sex and race.
Physician-adjudicated incident ischemic stroke, self-reported
race/ethnicity, and measured and self-reported risk factors were
included main outcomes and measures.
There were a total of 25,789 participants (14,170 women [54.9%]; 10,301 black individuals [39.9%]).
Over 222,120 person-years of follow-up, there were 939 ischemic
strokes: 159 (16.9%) in black men, 326 in white men (34.7%), 217 in
black women (23.1%), and 237 in white women (25.2%).
White women aged 45-64 years had a 32% lower risk of stroke vs white men, and black women had a 28% lower risk than black men.
They observed that lower risk of stroke in women than men persisted
in white individuals at ages 65-74 but not in black individuals.
However, the race-sex interaction was not significant.
There was no sex difference in stroke risk for either race at age ≥ 75 years.
Associations of systolic blood pressure, diabetes, and heart disease
with stroke risk were greater for women than men for white individuals.
On the other hand, the association of antihypertensive medication use was greater among men vs women.
There was no evidence of a sex difference for any risk factors in black people.
Black men who sleep for a
short amount of time had a decreased risk for incident stroke, and
white men with longer sleep duration had an increased risk for incident
stroke, according to a study published in Neurology.
“These results suggest that short and long sleep duration may have
different consequences for people depending on race and sex,” Virginia J. Howard, PhD, professor
of epidemiology at the University of Alabama at Birmingham School of
Public Health, said in a press release. “More research is needed to
determine the mechanisms behind these relationships. In the meantime,
this emphasizes how important it is to better monitor and control
cardiovascular risk factors in middle-aged to older people who have long
sleep periods.”
Megan E. Petrov, PhD, assistant professor at Arizona
State University College of Nursing and Health Innovation in Phoenix,
and colleagues analyzed data from 16,733 patients (mean age, 64 years;
42% men; 37% black) from the REGARDS study
who were free from stroke and obstructive sleep apnea. Patients
completed an ancillary sleep module with questions on habitual sleep
duration. A telephone interview was conducted every 6 months to collect
information on suspected stroke events.
At baseline, 10.4% of patients reported receiving less than 6 hours of sleep and 6.8% reported sleeping at least 9 hours.
During a median follow-up of 6.1 years, 460 stroke events occurred, with 172 of them occurring in black patients.
There were significant interactions between sleep duration and race-sex groups (P = .0023) and sleep duration and race (P = .018) that were linked to incident stroke.
Black patients with short sleep duration had a decreased risk for
stroke after adjusting for stroke risk factors (HR = 0.49; 95% CI,
0.28-0.85). This was most pronounced in black men (HR = 0.21; 95% CI,
0.07-0.69).
The risk for stroke was elevated in white men with long sleep
duration after adjusting for stroke risk factors (HR = 1.71; 95% CI,
1.06-2.76).
“The underlying mechanisms that may explain the race and race by sex
differences we found in the association between sleep duration and incident stroke
are not well-understood,” Petrov and colleagues wrote. “The alleged
reduction in associated risk of incident stroke among black adults with
short sleep duration, particularly black men, is perplexing, and
conflicts with other studies examining race by sleep interactions on
cardiometabolic risk factors.” – by Darlene Dobkowski Disclosures: Howard
and Petrov report no relevant financial disclosures. Please see the
study for all other authors’ relevant financial disclosures.
Send these researchers back to the drawing board because there is no
such thing as race as far as the body is concerned. Go back and find the
real reason. Their mentors/senior researchers should have stopped this
report. This is all because we have NO fucking stroke leadership or strategy. https://www.medpagetoday.com/cardiology/prevention/73641?
Lower stem cell counts vs whites were associated with 2.8x mortality risk
saved
by Nicole Lou,
Contributing Writer, MedPage Today
This article is a collaboration between MedPage Today® and:
Fewer stem cells are mobilized from the bone marrow of black individuals, suggesting a diminished compensatory response to chronic ischemia and a potential explanation for African Americans' elevated risk of cardiovascular disease, researchers said.
Blacks had fewer CD34+ circulating progenitor cells (CPCs) overall compared with whites (-17.6%, P<0.001), Arshed Quyyumi, MD, of Emory University School of Medicine in Atlanta, and colleagues reported online in Circulation Research.
These patients also had lower CPC counts, quantified by flow cytometry, regardless of their risk factors or underlying cardiovascular disease. Lower CD34+ counts were predictive of mortality over a median of 2.2 years in both blacks (HR 2.83, 95% CI 1.12-7.20) and whites (HR 1.79, 95% CI 1.09-2.94) without significant interaction.
"Across the U.S., Blacks compared to Whites suffer from a greater burden of cardiovascular disease (CVD) including incident MI, heart failure, stroke, and other adverse cardiovascular events. This can only partly be explained by a higher prevalence of traditional risk factors such as obesity, hypertension, diabetes mellitus, or tobacco use and it has been suggested that socioeconomic factors account for the remaining disparity," Quyyumi's group wrote.
"Because Blacks have lower CPC counts, this reduced endogenous regenerative capacity may be one additional reason for the observed disparities in CVD outcomes between Blacks and Whites," they suggested.
Progenitor cells are mobilized from the bone marrow into the circulation in response to ischemia, contributing to cellular repair and regeneration, according to the authors, though they found that CPC levels decline with age, reaching on average half the levels at age 80 compared to age 20.
The study included 1,747 patients from the Emory Cardiovascular Biobank, a prospective registry of patients undergoing cardiac catheterization; the Mental Stress Ischemia Prognosis Study, which recruited patients with stable coronary artery disease; and the Emory Predictive Health Initiative, a study of individuals without overt CVD.
In all, 26% of the cohort self-reported themselves as being black.
An analysis of CPC-mobilizing factors -- stromal cell-derived factor-1α (SDF-1α), vascular endothelial growth factor (VEGF), and matrix metallopeptidase-9 (MMP-9) -- showed that blacks had significantly lower plasma MMP-9 levels, which attenuated the association between low CD34+ and black race by 19%. On other hand, VEGF and SDF-1α levels were not significantly different between the races.
Subpopulations of CD34+ cells also reduced in black versus white individuals included:
CD34+/CD133+ cells (-15.5%, P<0.001)
CD34+/CXCR4+ cells (-17.3%, P<0.001)
CD34+/VEGF2R+ cells (-27.9%, P=0.04)
"Under specific conditions such as acute MI, progenitor cell-mobilizing factors ... permit progenitor cell release from their bone marrow niches, and their subsequent proliferation, differentiation, and mobilization into the circulation," Quyyumi and colleagues wrote.
They validated the main findings of their study in a separate cohort of 411 patients recruited from Emory University-affiliated hospitals.
Among 91 individuals with acute MI, CPC levels had generally risen by the time of the angiogram (typically within 24 hours after presentation), presumably as a result of mobilization due to injury. Blacks had 30%-35% lower CPC mobilization in the setting of acute MI as well.
Nevertheless, the findings should be noted with the caveats that race was self-reported and that the researchers lacked data on sickle cell traits that could have confounded the overall results.
Quyyumi disclosed no relevant conflicts of interest.
