One Gout Medication Comes Out on Top for CV Risk

Once again 12 years out of date(WHO - 2006) in not knowing that strokes are no longer cardiovascular they are neurological diseases.  Symptomatic in stroke, no one knows anything.
Bad research since they didn't include the colchicine drug in the comparison. 
But do you want gout because of this?

Gout may lessen Alzheimer risk

Or take this for gout?

Could Old Gout Drug Offer New CV Benefits?

https://www.medpagetoday.com/rheumatology/arthritis/71372?

Allopurinol the loser in retrospective comparison of two drugs

• by Nicole Lou, Contributing Writer, MedPage Today February 26, 2018

A retrospective comparison of two established gout medications suggested that patients receiving probenecid (Probalan) have a lower cardiovascular risk than peers on the standard therapy of allopurinol (Zyloprim), researchers reported from a government-funded study.
Already at higher risk of cardiovascular disease, patients with gout nonetheless did have fewer myocardial infarctions (MIs) and strokes when they took probenecid in lieu of allopurinol (2.36 per 100 person-years versus 2.83 per 100-person years, HR 0.80, 95% CI 0.69-0.93), according to Seoyoung Kim, MD, ScD, MSCE, of Brigham and Women's Hospital in Boston, and colleagues.
As reported online in the Journal of the American College of Cardiology, the rates of other adverse outcomes similarly favored probenecid recipients. These were as follows:

• MI: 1.40 per 100-person years versus 1.64 per 1oo-person years (HR 0.81, 95% CI 0.67-0.99)
• Stroke: 0.96 per 100 person-years versus 1.27 per 100 person-years (HR 0.72, 95% CI 0.57-0.90)
• Heart failure exacerbation among those with baseline heart failure: 36.88 per 100 person-years versus 37.05 per 100 person-years (HR 0.91, 95% CI 0.83-0.997)
• Mortality: 2.91 per 100 person-years versus 3.25 per 100 person-years (HR 0.87, 95% CI 0.76-1.00)

"These results were consistent in the subgroup analyses of patients without baseline cardiovascular disease or those without baseline chronic kidney disease [CKD]," the authors noted.
Writing in an accompanying editorial, Michael Givertz, MD, also of Brigham and Women's Hospital, added that the findings "were observed on top of background cardioprotective therapy with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (61%), beta-blockers (43%), and statins (54%)."
Kim and colleagues said that although both probenecid and allopurinol have been available for a long time for the management of gout, to the best of their knowledge, this is the first study that has evaluated the cardiovascular effect of probenecid in a direct comparison with allopurinol in a population-representative cohort of gout patients.
The study included gout patients enrolled in Medicare who started probenecid (n=9,722) or allopurinol (n=29,166) from 2008 to 2013. Participants had a mean age of 76, and 54% of the total were males. All were required to have been off the medications for at least 1 year before the index dispensing date.
Median follow-up was 118 days for the patients treated with probenecid and 358 days for those on allopurinol. Out of 180 days, the median number of days covered for the probenecid arm was 39.8% and 87.3% for allopurinol; by 365 days, these rates fell to 26.1% and 82.2%, respectively.
That the probenecid group was much less adherent to prescribed therapy is one reason to raise questions about the biological plausibility of the study's primary results, suggested Givertz.
"More importantly, these observational data are hypothesis-generating only. Although it might be tempting to use the data by Kim et al to alter clinical practice (e.g., prescribe probenecid rather than allopurinol to older patients with gout), there remain practical hurdles of uricosuric therapy including renal contraindications (CKD and nephrolithiasis), dosing, and gastrointestinal side effects."
The researchers acknowledged that probenecid is known to increase the concentration of some drugs such as antibiotics and NSAIDs when used concomitantly, but drug interactions between probenecid and statins or other cardiovascular drugs were not reported.
In addition, the team said, their retrospective study was subject to residual confounding despite propensity-score matching for baseline differences -- i.e., the probenecid group started off with less CKD and heart failure, for example. Moreover, the study groups took relatively low doses of their gout medication.

The study was supported by NIH grants.
Kim reported institutional research grants from Roche/Genentech, Pfizer, Bristol-Myers Squibb, Merck, and AstraZeneca for unrelated studies.
Givertz reported having no competing interests.

last updated 02.26.2018

• Primary Source

  Journal of the American College of Cardiology

  Source Reference: Kim SC, et al "Cardiovascular risks of probenecid versus allopurinol in older patients with gout" J Am Coll Cardiol 2018; DOI: 10.1016/j.jacc.2017.12.052.

• Secondary Source

  Journal of the American College of Cardiology

  Source Reference: Givertz MM "Treating gout in patients with cardiovascular disease: mutual benefit or unintended consequences?" J Am Coll Cardiol 2018; DOI: 10.1016/j.jacc.2018.01.006.

How Your Neck Size Affects Your Heart Health

Well mine always was 16.5 until after the stroke it increased to 17.5. I can't tell what it really is right now since it takes two useable hands to measure it.
https://www.menshealth.com/health/neck-circumference-and-heart-disease

If your neck circumference is greater than this number, there may be a problem brewing in your chest

If you can’t button your dress shirt’s collar, you might have a bigger issue than looking sloppy: Guys with big necks may be at higher risk of heart disease, a new study from Brazil found.
After analyzing nearly 4,000 men, the researchers determined the average neck circumference for a guy was about 15 inches. 

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For each 1-inch increase in neck circumference—say, comparing average-necked guys with those with a 16-inch neck—men were 32 percent more likely to have insulin resistance, 24 percent more likely to have raised blood pressure, 50 percent more likely to have high triglycerides, and 22 percent more likely to have low HDL, or “good” cholesterol.

Related: The Men’s Health Better Man Project—2,000+ Scientific Tricks For Always Looking and Feeling Your Best

Fat deposits around your neck can produce inflammatory substances that lead to plaque buildup in the carotid arteries in your neck, which hampers your heart health, says study author Cristina Baena, Ph.D.
Because the relationship is likely due to excess fat hanging out above your shoulders, men with thick necks due to strong, developed trap muscles likely wouldn’t face the same risk.
Your move: Grab a tape measure and see how your neck stacks up.
If your number is larger than 15.3 inches, see your doctor as a preventive measure, Baena says.
Related: 10 Health Numbers You Can Hit This Year
He may want to check your BP and run blood sugar or cholesterol tests. In Baena’s study, men with a neck circumference greater than that were more likely to have 3 or more heart disease risk factors.

Open Access Anxiety After Stroke The Importance of Subtyping

Treat anxiety by having a defined protocol getting you to 100% recovery.  Treat the primary problem not the secondary problems. 
http://stroke.ahajournals.org/content/49/3/556?etoc=

Ho-Yan Yvonne Chun, William N. Whiteley, Martin S. Dennis, Gillian E. Mead, Alan J. Carson

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https://doi.org/10.1161/STROKEAHA.117.020078

Stroke. 2018;49:556-564

Originally published February 6, 2018

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Abstract

Background and Purpose—Anxiety after stroke is common and disabling. Stroke trialists have treated anxiety as a homogenous condition, and intervention studies have followed suit, neglecting the different treatment approaches for phobic and generalized anxiety. Using diagnostic psychiatric interviews, we aimed to report the frequency of phobic and generalized anxiety, phobic avoidance, predictors of anxiety, and patient outcomes at 3 months poststroke/transient ischemic attack.

Methods—We followed prospectively a cohort of new diagnosis of stroke/transient ischemic attack at 3 months with a telephone semistructured psychiatric interview, Fear Questionnaire, modified Rankin Scale, EuroQol-5D5L, and Work and Social Adjustment Scale.

Results—Anxiety disorder was common (any anxiety disorder, 38 of 175 [22%]). Phobic disorder was the predominant anxiety subtype: phobic disorder only, 18 of 175 (10%); phobic and generalized anxiety disorder, 13 of 175 (7%); and generalized anxiety disorder only, 7 of 175 (4%). Participants with anxiety disorder reported higher level of phobic avoidance across all situations on the Fear Questionnaire. Younger age (per decade increase in odds ratio, 0.64; 95% confidence interval, 0.45–0.91) and having previous anxiety/depression (odds ratio, 4.38; 95% confidence interval, 1.94–9.89) were predictors for anxiety poststroke/transient ischemic attack. Participants with anxiety disorder were more dependent (modified Rankin Scale score 3–5, [anxiety] 55% versus [no anxiety] 29%; P<0.0005), had poorer quality of life on EQ-5D5L, and restricted participation (Work and Social Adjustment Scale: median, interquartile range, [anxiety] 19.5, 10–27 versus [no anxiety] 0, 0–5; P<0.001).

Conclusions—Anxiety after stroke/transient ischemic attack is predominantly phobic and is associated with poorer patient outcomes. Trials of anxiety intervention in stroke should consider the different treatment approaches needed for phobic and generalized anxiety.

Stroke Risk Factors Unique to Women

Be careful out there
http://stroke.ahajournals.org/content/49/3/518?etoc=

Stacie L. Demel, Steven Kittner, Sylvia H. Ley, Mollie McDermott, Kathryn M. Rexrode

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https://doi.org/10.1161/STROKEAHA.117.018415

Stroke. 2018;49:518-523

Originally published February 8, 2018

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• contraception
• estrogens
• postmenopause
• pregnancy
• stroke

Stroke is the third leading cause of death in women in the United States and is a leading cause of disability. Each year 55 000 more women than men have a stroke, a discrepancy largely driven by longer life expectancy in women (www.stroke.org). Although the majority of stroke incidence can be attributed to traditional vascular risk factors that occur in both men and women, including hypertension, hyperlipidemia, diabetes mellitus, smoking, and atrial fibrillation, there are several stroke risk factors that are specific to women. Specifically, differences in sex hormones, exogenous estrogens, and pregnancy exposures are factors exclusively experienced by women. In this review, we will summarize the current state of the literature with regards to women-specific factors, such as endogenous hormone levels, exogenous hormone therapy, pregnancy, parity, timing of age at menarche, and menopause in relation to stroke risk.

Methods

The following terms were searched with women and stroke in PubMed and Google Scholar, mainly for original articles and meta-analysis/systematic reviews: estrogens, estradiol, testosterone, DHEAS, menarche, menopause, oophorectomy, postmenopausal hormone therapy, oral contraception, transgender, transmen, transwomen, pregnancy, peripartum, postpartum, and parity The following search was also performed: therapy OR treatment OR secondary prevention AND pregnancy AND stroke. The resultant literature was reviewed by the authors, and the data covering the topics outlined below were reviewed in this manuscript.

Endogenous Estrogen State

Endogenous Hormone Levels

Data on the relationship of endogenous sex hormones and risk of stroke in women are relatively limited. Estrogen levels fluctuate dramatically in women with the menstrual cycle and then drop dramatically in the menopausal transition and in post-menopause. In data from the Copenhagen City Study, neither high nor low estradiol levels were associated with increased risk of ischemic stroke.¹ In premenopausal women, those in the lowest 10th percentile of estradiol had a >2-fold increased risk of ischemic stroke, but this was based on small case numbers. There was no relationship observed for postmenopausal estradiol levels and risk of ischemic stroke. Similarly, the authors of a study of French women over the age of 65 years found no association between estradiol levels and risk of ischemic stroke.² In the Study of Osteoporotic Fractures, women in the highest category of free estrogen index had a higher age-adjusted risk of ischemic stroke, but this was not independent of standard stroke risk factors, including hypertension, diabetes mellitus, and adiposity.³ Subsequently, a meta-analysis of the 3 available studies found no association, further supporting the lack of a relationship between estradiol levels and risk of ischemic stroke.¹

Testosterone levels are more stable than estrogen levels across the lifespan in women, with relatively constant levels from ages 30 to 70 years.¹ Although low testosterone levels have been associated with increased stroke risk in men, no clear relationship has been seen for testosterone levels and risk of stroke in women.¹ The investigators of the aforementioned study of French women over the age of 65 years found no association between high or low testosterone levels and risk of stroke.²

Dehydroepiandrosterone, an adrenal hormone which can also be used for the synthesis of estrogen and testosterone, has also been investigated. Low dehydroepiandrosterone levels have been associated with increased risk of ischemic stroke, with women in the lowest quartile having a relative risk (RR) of 1.41 (95% confidence interval [CI], 1.03–1.92) for ischemic stroke after adjustment for other risk factors.⁴ Dehydroepiandrosterone levels at presentation of acute stroke were also inversely associated with stroke severity in a hospital-based study of stroke in postmenopausal women.⁵ Another study of women undergoing coronary angiography provided evidence that lower dehydroepiandrosterone levels were associated with increased cardiovascular mortality, including death from stroke.⁶

Additional prospective studies of endogenous sex hormones and risk of stroke in women are needed, particularly with more sensitive measures of hormones, and in high-risk groups including black and Hispanic women.

Age at Menarche

Earlier age at menarche has been associated with greater cardiovascular disease (CVD) morbidity and mortality in some,^7–9 but not all studies,^10–12 and data specific for stroke are limited. In the Million Women Study from the United Kingdom, a U-shaped relationship between age at menarche and cerebrovascular disease was observed.⁹ Women who experienced menarche at age ≤10 years were at higher risk of developing stroke in later life compared with those with age at menarche at 13 years (RR, 1.16 [95% CI, 1.09–1.23]); however, women who experienced menarche at age ≥17 years were also at higher risk of developing stroke compared with those with age at menarche at 13 years (RR, 1.13 [95% CI, 1.03–1.24]).⁹ Women with extremely early age at menarche may experience hormonal disturbances, such as higher exposure to estradiol, potentially mediated through childhood obesity.¹³ The timing of menarche is associated with type 2 diabetes mellitus risk,^14,15 an association which may be influenced by childhood adiposity and endocrinopathies.^13,16 Although the Million Women Study attempted to control for potential confounding factors, such as body mass index, through statistical adjustment,⁹ obesity may have been present before the onset of menarche, complicating inferences about cause and effect.

Age at Natural Menopause and Surgical Menopause

Women of reproductive age are at a lower risk of CVD compared with men of similar age and lifestyle, but women who experience early menopause have increased cardiovascular risk.¹⁷ In a recent meta-analysis, investigators reported that early age at natural menopause (menopause onset before 45 years) was associated with a slightly higher risk of total CVD mortality (RR, 1.12 [95% CI, 1.03–1.21]) than onset at age 45 years or later; however, this association was not observed for stroke mortality risk independently.¹⁸ Surgical menopause, bilateral oophorectomy with or without hysterectomy, has also been associated with higher risk of CVD.^19,20 In the Nurses’ Health Study, bilateral oophorectomy before age 50 years was associated with increased CVD mortality in women and especially in women who did not use hormone therapy.²¹ When a sensitivity analysis of stroke mortality was conducted, the CI of this association widened potentially because of low numbers although the risk estimate remained elevated (RR, 1.15 [95% CI, 0.85–1.56]).²¹ Therefore, further investigations are warranted to examine these potential associations for early menopause and stroke.

Specific mechanisms responsible for the association between the timing of age at menopause and CVD are unclear. However, CVD incidence rising sharply after menopause suggests protective benefits of ovarian hormones.²² Estrogen inhibits hepatic lipase,²³ thus decline in endogenous estrogens in the menopausal transition may adversely affect lipid levels and subsequently cardiovascular risk.²⁴ The menopausal transition is associated with declines in high-density lipoprotein cholesterol and increases in low-density lipoprotein cholesterol,²⁴ as well as changes in high-density lipoprotein composition, with higher number of small high-density lipoprotein particles, which confer less cardiovascular protection than large high-density lipoprotein particles.²⁵ Hence, decreased estrogen concentrations over the menopause transition and effects on lipoprotein profiles may subsequently contribute to atherosclerosis. In a cross-sectional, population-based study, longer duration of reproductive lifespan and years from menarche to menopause, were associated with a lower 10-year CVD risk assessed by the Framingham Risk Score in postmenopausal women.²⁶ In the prospective cohort Nurses’ Health Study, a shorter duration of reproductive lifespan was associated with a higher risk of stroke, as well as CVD, which was likely driven by earlier age at menopause (either naturally or surgically).²⁷

Exogenous Estrogens and Stroke Risk

Hormone-Containing Birth Control and Stroke

Hormonal contraceptives, including oral, transdermal, and vaginal formulations, are effective and are used worldwide by >100 million women (World Health Organization 2014). There are various formulations containing either combined estrogen and progestogen or progestogen alone, administered as pills, patches, and rings. Combined oral contraceptives (COC), comprised both estrogen and progestogen, are thrombogenic²⁸ and, historically, have been associated with increased risk of CVD.^29,30 Oral estrogens have a dose–response association with risk, and doses have declined since their introduction in the 1960s. Most COCs now contain <50 μg and some contain as low as 15 μg of estrogen. Authors who evaluated the risk of second- and third-generation estrogen-containing oral contraceptives continued to find a 60% to 80% increased odds (95% CI, 1.2–2.8) of the combined end point of myocardial infarction or ischemic stroke among COC users compared with nonusers.^30–33 In a separate study, second-generation COCs were associated with an odds ratio=2.54 (95% CI, 1.96–3.28) and third-generation oral contraceptives with an odds ratio=2.03 (95% CI, 1.15–3.57) of stroke.³⁴ Progestogen-only hormonal contraceptives have not been associated with increased risk of ischemic stroke although data are limited.^30,35 Nonoral methods of delivering combined hormonal contraceptives, including the vaginal ring and contraceptive patches, seem to have the same risk as oral contraceptives.³⁶

Risk of stroke with COC use rises in the presence of other cardiovascular risk factors (ie, smoking, age [>35 years], and history of migraine with aura). Migraine with aura is a common condition in younger women, and the risk of stroke in patients with migraine with aura is increased ≈2-fold.³⁷ Women with migraine who also use COCs have a further increased risk of ischemic stroke (7.02 [95% CI, 1.51–32.68]) where women with migraine with aura, COC use, and who are active smokers have a dramatically elevated risk for stroke (RR, 10 [95% CI, 1.4–73.7]).³⁷ Guidelines from the International Headache Society Task Force on COC prescribing recommendations have been published previously.³⁸ Women who have migraine with aura should be advised to control all modifiable risk factors, including tobacco use and hypertension, and birth control methods other than COCs should be considered.³¹

Hormonal contraceptives are used by millions of women, and for most low-risk women, the risk of stroke associated with COC is lower than the risk of stroke during pregnancy. However, there is a clear association between hormone-containing birth control methods and ischemic stroke. This is magnified by stroke risk factors. Although a COC pill containing 30 μg of estrogen is considered safe and effective hormonal contraception,³⁰ careful attention to stroke risk should be made before prescribing. Nonhormonal and progestogen-only methods of contraception should also be considered in high-risk patients. Further research to evaluate the risk of progestogen-only methods (depot injection, pills, implants, and intrauterine devices) is needed.

Postmenopausal Hormone Therapy and Stroke Risk

Prospective observational studies and randomized trials consistently demonstrate an increased risk of stroke, particularly ischemic stroke, with oral postmenopausal hormone therapy.

In prospective cohort studies, data suggest that postmenopausal users of oral estrogens with or without progestin have a 27% to 39% increased risk of stroke compared with nonusers.³⁹ In the Women’s Health Initiative, women randomized to combined estrogen plus progestin had a hazard ratio of 1.31 (95% CI, 1.02–1.68) for total stroke and 1.44 (95% CI, 1.09–1.90) for ischemic stroke.⁴⁰ In the Women’s Health Initiative trial of unopposed estrogen, women randomized to active therapy had a hazard ratio of 1.37 (95% CI, 1.09–1.73) for total stroke and 1.55 (95% CI, 1.19–2.01) for ischemic stroke.⁴¹

Although some data suggest an association between timing of hormone therapy and coronary heart disease, time since menopause is not associated with differences in stroke incidence in either observational studies³⁹ or clinical trials.⁴² The incidence of stroke is relatively low in younger women (age, 50–59 years), with ≈2 additional cases of stroke per 10 000 women per year taking postmenopausal hormones.⁴² In addition, there is a dose–response relationship between dose of oral conjugated estrogen and stroke, with RRs of 0.93 for a dose of 0.3 mg, 1.54 at 0.625 mg, and 1.62 at 1.25 mg (P for trend, <0.001).³⁹

Similar results have been found in secondary cardiovascular prevention. Both the HERS (Heart and Estrogen/Progestin Replacement Study) in women with prior coronary heart disease⁴³ and the WEST (Women’s Estrogen for Stroke Trial) in women with recent mild ischemic stroke or transient ischemic attack⁴⁴ found no significant effect of treatment with oral estrogen or combined oral estrogen and progestin on risk of stroke, with a trend toward harm.

Limited data are available for transdermal estrogens, which have been associated with lower risk of venous thromboembolism. In a population-based nested case–control study, current use of transdermal hormone therapy was not associated with an increased risk of stroke (hazard ratio, 0.95 [0.75–1.20]).⁴⁵ However, when the dose was examined, low-dose transdermal estrogen (≤50 μg/d estradiol) was not associated with risk while high-dose transdermal estrogen (>50 μg/d) was associated with increased stroke risk.⁴⁵

Transgender Medicine

Transgender individuals are people whose sex identity differs from their sex assigned at birth. The prevalence of self-identified transgender adults in the United States is estimated to be ≈0.5% of the population.⁴⁶ Some transgender people pursue hormonal therapy or sex-affirming surgery to assume secondary sex characteristics consistent with their sex identity. The use of certain hormonal therapies has implications for the incidence of cerebrovascular disease in these individuals.

Transwomen are people with an assigned male sex and a female sex identity. Transwomen may undergo medical treatment with estrogens, antiandrogens, or a combination of both.⁴⁷ Those who have undergone orchiectomy may pursue only estrogen therapy.

Antiandrogen therapies do not seem to increase stroke risk in transwomen. Spironolactone is the antiandrogen most commonly prescribed to transwomen in the United States.⁴⁷ Spironolactone, a potassium-sparing diuretic, may lower blood pressure but does not increase thrombotic risk. Similarly, finasteride, a less commonly used antiandrogen, does not seem to increase thrombotic risk.

Direct data on the effect of exogenous estrogens in transwomen are scant. Much of our knowledge about the effects of exogenous estrogen is derived from studies of the increased risk of thrombotic complications, including stroke among postmenopausal women using postmenopausal hormone therapy.^48,49 Prospective trials of thrombotic risk in transwomen receiving estrogen therapy are lacking.⁵⁰ A 1997 Dutch single-center retrospective descriptive study of 816 transwomen treated for a mean 9.5 patient-years with ethinyl estradiol and the antiandrogen cyproterone acetate found that 45 (5.5%) developed deep vein thrombosis or pulmonary embolism, 5 (0.6%) experienced a transient ischemic attack, and none experienced ischemic stroke.⁵¹ A 2013 Belgian single-center case–control study evaluated 214 transwomen who were maintained on estrogen therapy for a median of 6 years.⁵² Eleven of the 214 transwomen (5.1%) developed deep vein thrombosis or pulmonary embolism during hormonal treatment. Five of the 214 transwomen (2.3%) were diagnosed with transient ischemic attack or cerebrovascular disease during treatment, a higher prevalence than in the age-matched control men. In a 2011 Dutch retrospective single-clinic cohort mortality study of 966 transwomen on estrogen with or without antiandrogen therapy with a mean follow-up of 19.4 years, no difference was found in the incidence of fatal stroke in transwomen compared with the incidence in the general population.⁵³

As we await prospective studies of estrogen therapy in transwomen, we recommend that medical providers maintain a high index of suspicion for deep vein thrombosis/pulmonary embolism and cerebral venous thrombosis in transwomen receiving estrogen therapy. Cardiovascular risk should be evaluated, and transwomen who smoke should be encouraged to quit smoking and provided with appropriate pharmacological and psychosocial supports.

Transmen are individuals with an assigned female sex and male sex identity. Transmen may undergo treatment with testosterone to promote development of male secondary sex characteristics. Testosterone is available via transdermal and intramuscular routes. Unlike estrogen, testosterone does not seem to be associated with an increased risk of thromboembolic complications. The majority of existing studies of transmen do not suggest an increased risk of cardiovascular morbidity with exogenous testosterone therapy.^51–54

In general, providers should be aware that transgender people may be less likely to seek medical attention than their cisgender peers because of previous negative interactions with the medical community, poor psychosocial wellbeing, and fear of stigma.^55,56 This has direct implications for delay of appropriate stroke care. Health systems and medical providers can improve the medical care of transgender people by asking about sex identity and preferred pronouns on intake forms⁵⁷; promoting an explicitly supportive and inclusive clinic or unit culture for transgender patients and their families; and pursuing research into the unique health needs of transmen and transwomen.

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Table.

Summary of Female-Specific Stroke Risk Factors

Issues of Pregnancy, Parity, and Stroke

Pregnancy and the peripartum are associated with increased risk of stroke. The peripartum period from 2 days before to 1 day after delivery and, to a lesser extent, up to 6 weeks postpartum is associated with an increased risk of ischemic stroke and intracerebral hemorrhage.^58–60 In a large population-based study of women in England (age, 15–49 years), authors found that the baseline incidence of stroke was 25.0/100 000 person-years in women when they were not pregnant. The incidence rate dropped during early pregnancy but was 9-fold higher in the peripartum period (161.1/100 000 person-years) and 3-fold higher in the early postpartum period (47.1/100 000 person-years; 95% CI, 31.3–70.9).⁶¹ For subarachnoid hemorrhage, only the peripartum period confers increased risk^60,61; nonaneurysmal subarachnoid hemorrhage is likely a major contributor to this risk. The risk of any thrombotic event that includes ischemic stroke remains increased to a lesser extent until 12 weeks postpartum,⁶² but it is not established that the risk of stroke remains increased beyond 6 weeks postpartum.⁶¹ Eclampsia and preeclampsia are the strongest risk factors for both ischemic stroke and intracerebral hemorrhage accounting for 24% to 48% of all pregnancy-associated strokes^58,59; this risk is potentiated by preexisting genitourinary tract infection, chronic hypertension, prothrombotic states, and coagulopathies.⁶³

Complications of pregnancy, specifically pregnancy-inducted hypertension, gestational diabetes mellitus, and preeclampsia are also associated with long-term risk of stroke.⁶⁴ There is evidence that women with pregnancy outcomes of preterm birth and small for gestational age infants have higher rates of cerebrovascular events even after adjusting for other pregnancy complications.⁶⁵

For women with prior stroke, the risk of recurrent stroke is increased in the peripartum and postpartum periods. Limited data from case series^66–68 suggest an absolute risk of recurrent arterial ischemic stroke associated with pregnancy of 0.7%, similar to the <1% yearly risk of recurrent stroke among young adults who have no vascular risk factors⁶⁹; however, the 95% CI is wide, 0.04% to 4.4%, indicating the need for further study. In addition, the absolute risk depends on clinical circumstances, with the presence of vascular risk factors or a definite cause of stroke, including thrombophilic disorders, conferring an increased risk. Similarly, there is a paucity of information on the excess risk of pregnancy complications to mother and child among women with prior ischemic stroke.⁷⁰

The role of pregnancy on risk of intracranial hemorrhage from preexisting arteriovenous malformations is uncertain. The 2 largest case-crossover studies of arteriovenous malformations, single-center studies from China⁷¹ and Baltimore,⁷² yielded conflicting results. The preponderance of available evidence suggests that pregnancy and delivery does not increase the risk of aneurysm rupture.^73,74

Conclusions

It is important to be aware of stroke risk factors specific to women. The Table summarizes the associations for stroke risk factors unique to women. Specific considerations that include endogenous hormone levels, exogenous hormone therapy, pregnancy and the peripartum period, and pregnancy-related complications change the risk of stroke for women as well as the optimal stroke prevention strategies. Special attention and further research are also needed in the area of transgender individuals. Further research to determine whether risk prediction models should include risk factors specific to women, including hormonal and reproductive exposures, is needed.

2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke

What a fucking pile of shit, GUIDELINES, not protocols, or efficacy with results. They never say how godawful the recovery percentage is for these guidelines.
http://stroke.ahajournals.org/content/49/3/509?etoc=

Karen L. Furie, Mahesh V. Jayaraman

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https://doi.org/10.1161/STROKEAHA.118.020176

Stroke. 2018;509-510

Originally published January 24, 2018

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creatinine

thrombectomy

workflow

Given the seismic changes we have seen in stroke care over the past 5 years, the stroke community has been eagerly anticipating the 2018 updated Acute Ischemic Stroke Guideline.¹ This comprehensive document defines state-of-the-art acute stroke management. We highlight a few selected areas of change relevant to stroke systems of care, imaging, thrombectomy eligibility, postprocedure management, and secondary prevention.

Most current stroke systems of care are designed to have Emergency Medical Services transport suspected stroke patients to the closest stroke center, regardless of its infrastructure and subspecialty expertise. Unlike intravenous alteplase, the successful delivery of mechanical thrombectomy requires specialized services unavailable at most hospitals. An important area of future study will be if there is a benefit to bypassing a closer hospital without thrombectomy capabilities to transport patients directly in the field to a Comprehensive Stroke Center, where thrombectomy can be performed more expeditiously. As the authors summarize, there is insufficient evidence to recommend one field severity scale over another, but the implementation of a severity-based algorithm such as the Mission: Lifeline Severity-Based Stroke Triage Algorithm for Emergency Medical Services (http://www.heart.org/missionlifelinestroke) has the potential to increase access to thrombectomy. Hopefully, future research can determine the optimal methods for triaging patients appropriately from the field.

Imaging is central to the management of the acute stroke patient. Historically, parenchymal imaging with noncontrast CT scan has been the mainstay of imaging. However, as the authors report, there has recently been an increasing use of vessel imaging with CT angiography (CTA). Moving forward, the use of vessel imaging should become routine at most centers. An important new recommendation is that it is reasonable to expect that all Primary Stroke Centers are able to perform CTA on stroke patients, and do so without delaying alteplase administration. The availability of CTA is more widespread, and most community hospitals have the capability to perform CTA in a rapid fashion. As the authors summarize, in most cases, the combination of the noncontrast CT and CTA provides sufficient information to determine eligibility for thrombectomy in the first 6 hours from stroke onset. An additional benefit of performing vessel imaging with CTA at the Primary Stroke Center would be to more efficiently triage transfers for endovascular therapy. In some series, less than half of transferred patients receive thrombectomy because of lack of intracranial vessel occlusion. Such futile transfers are resource intensive and may overwhelm Comprehensive Stroke Centers. We also commend the authors for reaffirming the low incidence of contrast-induced nephropathy, and suggesting that waiting for a serum creatinine should not delay CTA in patients who would be potential thrombectomy candidates.

Two important trials, DAWN (Diffusion Weighted Imaging [DWI] or Computerized Tomography Perfusion [CTP] Assessment With Clinical Mismatch in the Triage of Wake Up and Late Presenting Strokes Undergoing Neurointervention) and DEFUSE-3 (Endovascular Therapy Following Imaging Evaluation for Ischemic Stroke 3), have shed light on the benefit of mechanical thrombectomy in anterior circulation large-vessel occlusion stroke beyond 6 hours from symptom onset. Both trials showed that in patients who are carefully selected using advanced imaging, using either CT perfusion or magnetic resonance imaging, thrombectomy dramatically improves outcomes even up to 24 hours from onset. These results also have implications for patients at Primary Stroke Centers and Acute Stroke Ready Hospitals. These centers will need to ensure that their workflow can identify potential candidates for thrombectomy beyond 6 hours and rapidly transfer them to a Comprehensive Stroke Center. Again, using CTA at the Primary Stroke Center or Acute Stroke Ready Hospitals to ensure that there is a vessel occlusion before transfer would likely be an optimal workflow and could minimize futile transfers.

There has been a palpable shift toward more focused cost-effective recommendations for laboratory and cardiac testing. The message is clear: more is not necessarily better. The new Guideline emphasizes a targeted approach to the diagnostic evaluation and the institution of secondary stroke preventive interventions. Although the role of antiplatelet agents and statins remains relatively unchanged in this update, consideration of dual antiplatelet agents has been added as a new recommendation, albeit with limited evidence.

To quote Thoreau, “When any real progress is made, we unlearn and learn anew what we thought we knew before.”² The stroke field has made enormous progress in the past 5 years, and this Guideline will elegantly serve as a primer for updating our knowledge.

Disclosures

None.

Footnotes

• The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.

• © 2018 American Heart Association, Inc.

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Discovery Reveals Way to Stop Inflammation in Alzheimer's, Arthritis, More

You probably want this to prevent your likely dementia, so ask your doctor for followup. 
https://www.rdmag.com/news/2018/02/discovery-reveals-way-stop-inflammation-alzheimers-arthritis-more?

A new discovery about the immune system may allow doctors to treat harmful inflammation that damages the brain in neurodegenerative diseases such as Alzheimer's. It might also let doctors save patients from the potentially deadly inflammation of sepsis, a full-body infection that kills a quarter-million Americans every year.

The finding "opens up a whole new research area to look at neuroinflammation in the context of Alzheimer's and Parkinson's," said lead researcher Bimal Desai, PhD, of the University of Virginia School of Medicine. "But the clinical impact will be in many, many different areas."

Neurological Treatments

Traditional treatments for neurological inflammation, such as in Alzheimer's and Parkinson's disease, are largely ineffective because biological drugs are blocked by what is known as the blood-brain barrier. That barrier protects the brain from dangers such as bacteria or toxins in the blood, but it also makes it very difficult to get drugs into the brain. "A lot of the drugs we use right now to treat inflammation, [known as] biologicals, don't work in the brain because they can't get through," explained Desai, of UVA's Department of Pharmacology and UVA's Carter Immunology Center.

His new finding, involving important immune cells known as macrophages (and microglia), could offer a way around that. He and his team have identified a specific electrical switch, known as an ion channel, within macrophages that controls the flow of calcium into the cells. Without calcium, the cells can't cause inflammation. By targeting this switch with tiny molecules, researchers could deny the macrophages calcium and prevent inflammation - even in the brain.

A Better Way to Battle Inflammation

That could let researchers develop a new and better way to stop inflammation. "Small molecules are perhaps more affordable as treatments and can hit things like this ion channel switch, TRPM7," said researcher Michael Schappe, a graduate student in Desai's lab. "We could use that to address inflammation in a bunch of contexts, but particularly in instances like neuroinflammation, where [current] treatments are particularly ineffective."

Desai noted that drug companies are already at work on drugs that could target this type of switch. And that could be good news for patients with many inflammatory diseases. "Right now, you have conditions like arthritis or IBD [inflammatory bowel disease], where inflammation plays a huge role. They do have very good drugs for them, but these drugs are extremely expensive and cannot be taken orally by the patients. They can cost as much as $20,000 a year," he said. "The reason for that is that they're biologicals. They're protein molecules that are very difficult to make and distribute. But having identified an ion channel as a target in this context allows you to use small molecules, which are ridiculously cheap compared to biologicals and can be taken orally by the patients."

The discovery of the new drug target, the researchers noted, was made possible by something very unusual about UVA. To learn more, visit the Making of Medicine blog at https://makingofmedicine.virginia.edu/2018/02/26/the-switch-that-could-shut-down-inflammation-even-in-the-brain/

GEMS: the Gait Enhancing Mobile Shoe

Interesting, video at link.  Does your therapy department even have a split belt treadmill? Or know about it?

GEMS: the Gait Enhancing Mobile Shoe

Project Background

A Split-belt treadmill as part of the USF CAREN system.

Walking requires precise coordination between the legs. This interlimb coordination is often impaired in individuals with central nervous system lesion, such as stroke, resulting in an asymmetric walking pattern and a slower walking velocity. Walking on a split-belt treadmill, which has two belts moving the legs at different speeds, has been shown to correct walking asymmetries in people with stroke. One distinct drawback is that learning on the treadmill does not transfer completely to walking over the ground. Although regular and more frequent training leads to greater rehabilitation, another drawback of a split-belt is that people cannot practice in their more natural everyday environment, such as at home. Walking on a treadmill is a stationary task, so the sensory information experienced while walking over ground, such as the optic/visual flow of motion, is not the same as that while walking on a treadmill. It has been hypothesized that the limited transfer to over-ground walking is due to the conflicting sensory experiences between the treadmill training environment and the over-ground environment. The perceptual change gives the individual cues that the new environment is not the same as that in which he was trained. Mimicking the effects of the split-belt treadmill while walking over ground can alleviate the dynamic and psychological differences of walking on a treadmill and, thus, increase the transfer of the new walking pattern from treadmill to over-ground walking.

Gait Enhancing Mobile Shoe (GEMS)

Our innovative Gait Enhancing Mobile Shoe (GEMS) can impose a motion to a foot that is capable of changing interlimb coordination and the resulting walking velocity while walking over ground. The GEMS creates a motion similar to that felt when walking on a split-belt treadmill, but while walking over ground where the sensory information of the real world task will be experienced. The objective of this proposed research and development is to validate the use of the GEMS for long-term correction of the wearer's gait. The GEMS design uses no external power since the shoe mechanically converts the wearer's downward and horizontal forces into a horizontal motion. This shoe design is completely mobile, which opens up the doors to enabling long-term continuous rehabilitation outside the rehabilitation clinic. We anticipate that both the longer use of the device and experiencing gait modifications in real world environments will aid in achieving better rehabilitation outcomes.

Several Gait Enhancing Mobile Shoe prototypes have been developed and tested. The first GEMS was passive and completely mechanical, but it had no control of the backward foot motion. Although it moved the wearer's foot backward, it did so in a jerky and fairly unpredictable motion comparable to sliding on ice or a slippery surface. The second GEMS provided a smooth motion by controlling the generated horizontal motion. However, because of the various motion controls, this version ended up being too high off the ground and too heavy for actual subject testing. The third and fourth prototypes built upon the third being purely passive and completely mechanical, while introducing a rotary damper to regulate the backward motion of the foot. The fifth (not shown here) is currently undergoing a clinical trial.

GEMS Testing

While the research and development of the Gait Enhancing Mobile Shoe is centered in the REED Lab at the University of South Florida, the GEMS project works in collaboration with Erin Vasudeven at the Moss Rehab Einstein rehabilitation facility in Philadelphia, PN. Moss Rehab allows more extensive and comprehensive testing of prototype devices.

Future Work

Asymmetric Passive Dynamic Walker

The GEMS design is always evolving. While there have been several prototypes, the design and manufacture of the GEMS is an ongoing process toward finding an optimum design that realistically can be comfortably and safely implemented by gait asymmetry patients for rehabilitation.

A Passive Dynamic Walker (PDW) Model has also implemented to help in the analysis and optimization of the GEMS. A PDW is a passive mechanical device that walks in a human-like manner down an incline by using only the force of gravity. Such virtual modeling is very useful and a crucial step in the design process of a physical GEMS prototype and the prediction of the body dynamics of a person using a GEMS.