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In 1924, the founders of the American Heart Association (AHA) envisioned an international society focused on the heart and aimed at facilitating research, disseminating information, increasing public awareness, and developing public health policy related to heart disease. This presidential advisory provides a comprehensive review of the past century of cardiovascular and stroke science, with a focus on the AHA’s contributions, as well as informed speculation about the future of cardiovascular science into the next century of the organization’s history. The AHA is a leader in fundamental, translational, clinical, and population science, and it promotes the concept of the “learning health system,” in which a continuous cycle of evidence-based practice leads to practice-based evidence, permitting an iterative refinement in clinical evidence and care. This advisory presents the AHA’s journey over the past century from instituting professional membership to establishing extraordinary research funding programs; translating evidence to practice through clinical practice guidelines; affecting systems of care through quality programs, certification, and implementation; leading important advocacy efforts at the federal, state and local levels; and building global coalitions around cardiovascular and stroke science and public health. Recognizing an exciting potential future for science and medicine, the advisory offers a vision for even greater impact for the AHA’s second century in its continued mission to be a relentless force for longer, healthier lives. [ABSTRACT FROM AUTHOR]

This article discusses the potential benefits of influenza vaccination in reducing the risk of stroke. While previous recommendations have focused on the use of influenza vaccination to prevent cardiovascular events in patients with coronary artery disease, there has been limited attention given to its role in preventing recurrent stroke. However, recent studies have suggested that seasonal influenza may increase the risk of ischemic stroke, and vaccination against influenza could potentially reduce this risk. A meta-analysis of trials and observational studies found that influenza vaccination was associated with a 20% reduction in stroke risk. Concerns about the potential short-term increase in inflammation after vaccination were addressed by a study conducted in Alberta, Canada, which found that influenza vaccination did not increase the risk of stroke in the short term. The results of these studies provide evidence that influenza vaccination may have a direct effect on reducing stroke risk, and further research, including randomized clinical trials, is needed to confirm these findings. The article also highlights the low overall vaccination rates and emphasizes the importance of encouraging clinicians to recommend influenza vaccination to high-risk populations. [Extracted from the article]

The past 30 years have witnessed great advances in understanding the pathophysiology and treatment of stroke in adult patients, but paediatric stroke remains relatively understudied. This is the largest comparison of motor outcomes in children with stroke to those without stroke to date, and it indicates the large burden of motor disability after paediatric stroke. Similarly, age at stroke onset is associated with differing outcomes, which may be related to the varying prevalence of risk factors by age group.2,7 Given the low number of paediatric stroke patients, it has been difficult to study them in large cohorts. [Extracted from the article]

In 2010, the American Heart Association published a statement concluding that the existing scientific evidence was consistent with a causal relationship between exposure to fine particulate matter and cardiovascular morbidity and mortality, and that fine particulate matter exposure is a modifiable cardiovascular risk factor. Since the publication of that statement, evidence linking air pollution exposure to cardiovascular health has continued to accumulate and the biological processes underlying these effects have become better understood. This increasingly persuasive evidence necessitates policies to reduce harmful exposures and the need to act even as the scientific evidence base continues to evolve. Policy options to mitigate the adverse health impacts of air pollutants must include the reduction of emissions through action on air quality, vehicle emissions, and renewable portfolio standards, taking into account racial, ethnic, and economic inequality in air pollutant exposure. Policy interventions to improve air quality can also be in alignment with policies that benefit community and transportation infrastructure, sustainable food systems, reduction in climate forcing agents, and reduction in wildfires. The health care sector has a leadership role in adopting policies to contribute to improved environmental air quality as well. There is also potentially significant private sector leadership and industry innovation occurring in the absence of and in addition to public policy action, demonstrating the important role of public-private partnerships. In addition to supporting education and research in this area, the American Heart Association has an important leadership role to encourage and support public policies, private sector innovation, and public-private partnerships to reduce the adverse impact of air pollution on current and future cardiovascular health in the United States. [ABSTRACT FROM AUTHOR]

Similar to pandemic influenza in the past century, COVID-19 may also lead to lingering aftereffects, the so-called long-haul COVID syndrome, which remains poorly understood. SARS-CoV-2 is only one of a family of coronaviruses, including Middle East Respiratory Syndrome (MERS) virus found in camels, that causes seasonal outbreaks of even more COVID-19 at 1 Year American Heart Association Presidents Reflect on the Pandemic AHA UPDATE Elkind et al COVID-19 at 1 Year Circulation. Racial and ethnic differences in presentation and outcomes for patients hospitalized with COVID-19: findings from the American Heart Association's COVID-19 Cardiovascular Disease Registry [published online November 17, 2020]. [Extracted from the article]

The article offers information on the placental abruption and neurological disorders in children. Topics discussed include placenta is considered a treasure trove that stores a wealth of information on the woman, her fetus, and the pregnancy; mentions there is a growing evidence for shared risk factors for abruption and neurodevelopmental disorders; and also mentions inflammation and infection are also implicated in preterm delivery.

Background: Epidemiological studies demonstrate that childhood infections, including varicella zoster virus, are associated with an increased risk of arterial ischemic stroke (AIS). Other herpesviruses have been linked to childhood AIS in case reports. We sought to determine whether herpesvirus infections, which are potentially treatable, increase the risk of childhood AIS. Methods and Results: We enrolled 326 centrally confirmed cases of AIS and 115 stroke-free controls with trauma (29 days to 18 years of age) with acute blood samples (≤3 weeks after stroke/trauma); cases had convalescent samples (7-28 days later) when feasible. Samples were tested by commercial enzyme-linked immunosorbent assay kits for immunoglobulin M/immunoglobulin G antibodies to herpes simplex virus 1 and 2, cytomegalovirus, Epstein-Barr virus, and varicella zoster virus. An algorithm developed a priori classified serological evidence of past and acute herpesvirus infection as dichotomous variables. The median (quartiles) age was 7.7 (3.1-14.3) years for cases and 10.7 (6.9-13.2) years for controls (P=0.03). Serological evidence of past infection did not differ between cases and controls. However, serological evidence of acute herpesvirus infection doubled the odds of childhood AIS, even after adjusting for age, race, and socioeconomic status (odds ratio, 2.2; 95% confidence interval, 1.2-4.0; P=0.007). Among 187 cases with acute and convalescent blood samples, 85 (45%) showed evidence of acute herpesvirus infection; herpes simplex virus 1 was found most often. Most infections were asymptomatic. Conclusions: Herpesviruses may act as a trigger for childhood AIS, even if the infection is subclinical. Antivirals like acyclovir might have a role in the prevention of recurrent stroke if further studies confirm a causal relationship. [ABSTRACT FROM AUTHOR]

Background The natural history of intracranial large artery atherosclerosis has been mainly described from lumen-based imaging studies, and much of what is reported to be known about atherosclerosis is derived from non-cerebral arteries. Aims To test the hypothesis that atherosclerosis is only partially represented by stenosis and that advanced atherosclerosis is more common that severe stenosis in noncardioembolic infarcts. Methods Cerebral large arteries from 196 autopsy cases were studied. The revised American Heart Association classification for atherosclerosis was used to determine the phenotype in each available artery. Cross-sectional lumen stenosis was obtained as defined by the Glagov's method. Results As age of cases increased, there was a progressive increment in the frequency of atherosclerotic lesions, rising from 5% of all arteries at age 20-40, to more than 40% at age 60 or older. Stenosis also increased with age: less than 3% of the arteries in those ≤50 years had >40% stenosis, while one out of five arteries in those >80 years had >40% stenosis. In most cases (80%), atherosclerosis and stenosis were directly related. However, one out of five cases with advanced atherosclerosis had <30% stenosis. In arteries supplying brain areas with noncardioembolic infarcts, the majority of segments exhibiting advanced atherosclerosis had lumen stenosis of <40%. Conclusion Although intracranial atherosclerosis is typically associated with stenosis, a substantial minority of cases shows advanced atherosclerosis in the absence of stenosis >40%. Definitions based solely on stenosis may underestimate the extent and role of intracranial large artery atherosclerosis. [ABSTRACT FROM AUTHOR]

Background There is a scarcity of data supporting the association between atherosclerosis and dolichoectasia in unbiased samples. Aims To test the hypothesis that the association between dolichoectasia and extracranial carotid atherosclerosis depends on the degree of collateral circulation. Methods The Northern Manhattan Study magnetic resonance imaging substudy consists of 1290 participants who remained stroke-free at the time of magnetic resonance imaging. Arterial diameters were collected in all participants with available magnetic resonance angiography. Dolichoectasia was defined as a head-size adjusted diameter >2 standard deviation for each artery. Carotid Doppler was used to evaluate for carotid atherosclerosis (carotid plaque, maximum plaque thickness and carotid intima media thickness). Results We included 994 participants with available Doppler and magnetic resonance angiography data (mean age 63 years, 60% female). Any dolichoectasia was reported in 16% of participants, 54% had at least one carotid plaque and the mean carotid intima media thickness was 0·92 ± 0·09 mm. After adjusting for demographic and clinical characteristics, there was no association between markers of carotid atherosclerosis and dolichoectasia. However, stratifying by collaterals, it was observed that dolichoectasia was more likely in the anterior and posterior circulations when collaterals were available among participants with carotid atherosclerosis. These associations were confirmed by noting an increment in arterial diameters in the corresponding arteries ipsilateral and contralateral to each carotid as well as in the posterior circulation. Conclusions We did not find an association of extracranial carotid atherosclerosis with dolichoectasia. However, we found that dolichoectasia is more frequent when intracranial collaterals are available suggesting a compensatory process that needs further investigation. [ABSTRACT FROM AUTHOR]

Pathological arterial wall changes have been cited as potential mechanisms of cerebrovascular disease in the HIV population. We hypothesize that dilatation would be present in arterial walls of patients with HIV compared to controls. Fifty-one intracranial arteries, obtained from autopsies of five individuals with HIV infection and 13 without, were fixed, embedded, stained, and digitally photographed. Cross-sectional areas of intima, media, adventitia and lumen were measured by preset color thresholding. A measure of arterial remodeling was obtained by calculating the ratio between the lumen diameter and the thickness of the arterial wall. Higher numbers indicate arterial dilatation, while lower numbers indicate arterial narrowing. HIV-infected brain donors were more frequently black (80% vs. 15%, P = 0.02) compared with uninfected donors. Inter and intra-reader agreement measures were excellent. The continuous measure of vascular remodeling was significantly higher in the arteries from HIV donors (β = 2.8, P = 0.02). Adjustments for demographics and clinical covariates strengthen this association (β = 9.3, P = 0.01). We found an association of HIV infection with outward brain arterial remodeling. This association might be mediated by a thinner media layer. The reproduction of these results and the implications of this proposed pathophysiology merits further study. [ABSTRACT FROM AUTHOR]

Understanding the vascular injury pathway is crucial to developing rational strategies for secondary stroke prevention in children. The multicenter Vascular Effects of Infection in Pediatric Stroke (VIPS) cohort study will test the hypotheses that (1) infection can lead to childhood arterial ischemic stroke by causing vascular injury and (2) resultant arteriopathy and inflammatory markers predict recurrent stroke. The authors are prospectively enrolling 480 children (aged 1 month through 18 years) with arterial ischemic stroke and collecting extensive infectious histories, blood and serum samples (and cerebrospinal fluid, when clinically obtained), and standardized brain and cerebrovascular imaging studies. Laboratory assays include serologies (acute and convalescent) and molecular assays for herpesviruses and levels of inflammatory markers. Participants are followed prospectively for recurrent ischemic events (minimum of 1 year). The analyses will measure association between markers of infection and cerebral arteriopathy and will assess whether cerebral arteriopathy and inflammatory markers predict recurrent stroke. [ABSTRACT FROM AUTHOR]

Innate inflammation plays an important role in the pathogenesis and progression of atherosclerosis, plaque rupture, thrombosis, and stroke. Inflammatory biomarkers related to innate inflammation, including acute phase proteins, may predict first stroke. The utility of high-sensitivity C-reactive protein and other related markers may diminish among populations with established vascular risk. Other biomarkers, including lipoprotein-associated phospholipase A2, may provide complementary information about prognosis after stroke or subclinical vascular disease. The innate immune system originally evolved to provide protection against bacterial infections. Moreover, infections may also contribute to stroke risk. Summary measures representing multiple chronic infections have been associated with risk of stroke and atherosclerosis. Acute infections, particularly respiratory infections, have also been found to serve as precipitants of stroke in recent epidemiological studies. These findings could have clinical implications. Further studies are needed to determine the role of innate inflammation and infection in stroke pathogenesis and prevention. [ABSTRACT FROM AUTHOR]

Phase I clinical studies are experiments in which a new drug is administered to humans to determine the maximum dose that causes toxicity with a target probability. Phase I dose-finding is often formulated as a quantile estimation problem. For studies with a biological endpoint, it is common to define toxicity by dichotomizing the continuous biomarker expression. In this article, we propose a novel variant of the Robbins–Monro stochastic approximation that utilizes the continuous measurements for quantile estimation. The Robbins–Monro method has seldom seen clinical applications, because it does not perform well for quantile estimation with binary data and it works with a continuum of doses that are generally not available in practice. To address these issues, we formulate the dose-finding problem as root-finding for the mean of a continuous variable, for which the stochastic approximation procedure is efficient. To accommodate the use of discrete doses, we introduce the idea of virtual observation that is defined on a continuous dosage range. Our proposed method inherits the convergence properties of the stochastic approximation algorithm and its computational simplicity. Simulations based on real trial data show that our proposed method improves accuracy compared with the continual re-assessment method and produces results robust to model misspecification. [ABSTRACT FROM PUBLISHER]

Background: Hydroxymethylglutaryl coenzyme A reductase inhibitors (‘statins’) reduce the neuronal injury in dose-dependent fashion in rodent stroke models. We sought to determine whether lovastatin at doses above those currently approved can be administered safely within 24 h after an acute ischemic stroke. Methods: We conducted a phase 1B dose-finding study using an adaptive design novel to stroke trials, the continual reassessment method, to find the highest tolerated dose of lovastatin. Planned doses were 1, 3, 6, 8 and 10 mg/kg/day for 3 days. The primary safety outcomes were myotoxicity and hepatotoxicity. The model was calibrated to select a dose causing 7–13% toxicity. Results: We enrolled 33 patients (16 men/17 women, age range 23–82 years). Three patients were treated at 1 mg/kg, 10 at 3 mg/kg, 12 at 6 mg/kg, and 8 at 8 mg/kg. Thirty of the 33 patients (90.9%) completed at least 11 of 12 doses. Two patients at the 6-mg/kg dose level experienced transient mild elevations in transaminases without clinical sequelae. After an initial dose reduction, the dose was re-escalated to 8 mg/kg, and no further patients reached safety outcomes. No clinical liver disease, myopathy, or creatine phosphokinase elevations occurred. The final model-based toxicity at 8 mg/kg was 13%; no patient was treated at 10 mg/kg. Conclusions: Lovastatin at doses above those currently approved by the Food and Drug Administration is feasible for 3 days after an acute ischemic stroke and the maximum tolerated dose is estimated to be 8 mg/kg/day. Further randomized studies are warranted to confirm its safety and to demonstrate its efficacy in improving functional outcomes after stroke. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Mass levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), a leukocyte-derived enzyme involved in the metabolism of low-density lipoprotein to pro-inflammatory mediators, are associated with prognosis after stroke. Lp-PLA2 mass correlates only moderately with levels of Lp-PLA2 activity. The relationship of Lp-PLA2 activity to risk of stroke recurrence is unknown. We hypothesized that Lp-PLA2 activity levels would predict risk of recurrence. Methods: In the population-based Northern Manhattan Stroke Study, first ischemic stroke patients ≥40 years were followed for recurrent stroke. Levels of Lp-PLA2 activity were assessed in 467 patients, and categorized by quartile. Cox proportional hazard models were used to calculate hazard ratios (HR) and 95% confidence intervals (95% CI) for risk of recurrent stroke associated with marker quartiles after adjusting for demographics, vascular risk factors, and high-sensitivity C-reactive protein (hsCRP). Results: Mean age was 68.9 ± 12.7 years; 54.6% were women; 53.3% Hispanic, 27.2% black, and 17.8% white. Median follow-up was 4.0 years, and there were 80 recurrent strokes. Compared to the lowest quartile of Lp-PLA2 activity, those in the highest had an increased risk of recurrent stroke (adjusted HR 2.54, 95% CI 1.01–6.39). Conclusion: Stroke patients withLp-PLA2 activity levels in the highest quartile, compared to those in the lowest quartile, had an increased risk of recurrence after first ischemic stroke. Further studies are warranted to determine whether this biomarker has clinical utility in determining high-risk populations of stroke survivors, and whether anti-inflammatory strategies that reduce levels of activity of Lp-PLA2 reduce the risk of stroke recurrence. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

There is growing experimental and clinical evidence that by reducing downstream products of the mevalonate pathway other than cholesterol, HMG-CoA reductase inhibitors (‘statins’) have beneficial effects on endothelial function, coronary and cerebral blood flow, inflammation, and hemostasis. Statins have been shown in rodent models of acute ischemic stroke to reduce neuronal injury and infarct size in a dose-dependent fashion. The objective of this early phase trial will be to determine the maximal-tolerated dose of lovastatin for short-term acute stroke therapy. In this multicenter phase 1B dose-escalation and dose-finding study, 33 patients with acute ischemic stroke will be administered lovastatin in increasing doses from one to 10 mg/kg daily for 3 days beginning within 24 hours after symptom onset. The primary safety outcome will be occurrence of myotoxicity or hepatotoxicity, defined by clinical and laboratory criteria, and the study is designed to determine the highest dose of lovastatin that can be administered with <10% risk of myotoxicity or hepatotoxicity. The statistical design of the study utilizes an adaptive design, the Continual Reassessment Method, which is novel to stroke trials, to find the optimal dosage. The dose–toxicity model is calibrated such that the method will eventually select a dose that causes 7–13% dose-limiting toxicity (within 3% of target). A sample size of 33 will ensure that estimates of any binary variables will have a 95% confidence interval of width ≤0·34, and enable us to detect any unexpected toxicity that occurs at 5% rate (in a non-dose-dependent fashion) with probability 0·82. The probability of choosing a dose for further trials with 25% or higher likelihood of toxicity is no more than 23%. The presently described trial represents a new approach for treatment of acute ischemic stroke, as well as a novel way of conducting a phase I trial, evaluating safety and determining an optimal dose of a potential neuroprotectant drug. [ABSTRACT FROM AUTHOR]

The article discusses a study investigating the relationship of inflammatory markers C-reactive protein (CRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) with ischemic stroke. The results showed that high-sensitivity CRP, but not Lp-PLA2, was associated with stroke severity. After adjusting for confounding factors, CRP was found to be associated with risk of death but not risk of recurrent stroke or myocardial infarction.

Background: Inflammation and inflammatory biomarkers play an important role in atherosclerosis and cardiovascular disease. Little information is available, however, on time course of serum markers of inflammation after stroke. Methods: First ischemic stroke patients ≥40 years old had levels of high-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), and fibrinogen measured in plasma samples drawn at 1, 2, 3, 7, 14, 21 and 28 days after stroke. Levels were log-transformed as needed, and parametric and non-parametric statistical tests were used to test for evidence of a trend in levels over time. Levels of hsCRP and SAA were also compared with levels in a comparable population of stroke-free participants. Results: Mean age of participants with repeated measures (n = 21) was 65.6 ± 11.6 years, and 13 (61.9%) were men, and 15 (71.4%) were Hispanic. Approximately 75% of patients (n = 15) had mild strokes (NIH Stroke Scale score 0-5). There was no evidence of a time trend in levels of hsCRP, SAA, or fibrinogen for any of the markers during the 28 days of follow-up. Mean log(hsCRP) was 1.67 ± 1.07 mg/L (median hsCRP 6.48 mg/L) among stroke participants and 1.00 ± 1.18 mg/L (median 2.82 mg/L) in a group of 1176 randomly selected stroke-free participants from the same community (p = 0.0252). Conclusion: Levels of hsCRP are higher in stroke patients than in stroke-free subjects. Levels of inflammatory biomarkers associated with atherosclerosis, including hsCRP, appear to be stable for at least 28 days after first ischemic stroke. [ABSTRACT FROM AUTHOR]

Focuses on stroke in the elderly. Definitions and subtypes; Risk factors and prevention; Information on the treatment.

Fibrinolytic agents catalyze the conversion of the inactive proenzyme plasminogen into the active protease plasmin, degrading fibrin within the thrombus and recanalizing occluded vessels. The history of these medications dates to the discovery of the first fibrinolytic compound, streptokinase, from bacterial cultures in 1933. Over time, researchers identified two other plasminogen activators in human samples, namely urokinase and tissue plasminogen activator (tPA). Subsequently, tPA was cloned using recombinant DNA methods to produce alteplase. Several additional derivatives of tPA, such as tenecteplase and reteplase, were developed to extend the plasma half-life of tPA. Over the past decades, fibrinolytic medications have been widely used to manage patients with venous and arterial thromboembolic events. Currently, alteplase is approved by the U.S. Food and Drug Administration (FDA) for use in patients with pulmonary embolism with hemodynamic compromise, ST-segment elevation myocardial infarction (STEMI), acute ischemic stroke, and central venous access device occlusion. Reteplase and tenecteplase have also received FDA approval for treating patients with STEMI. This review provides an overview of the historical background related to fibrinolytic agents and briefly summarizes their approved indications across various thromboembolic diseases. [ABSTRACT FROM AUTHOR]

Objective Methods Results Interpretation Approximately half of ischemic strokes (IS) in cancer patients are cryptogenic, with many presumed cardioembolic. We evaluated whether there were specific miRNA and mRNA transcriptome architectures in peripheral blood of IS patients with and without comorbid cancer, and between cardioembolic versus noncardioembolic IS etiologies in comorbid cancer.We studied patients with cancer and IS (CS; n = 42), stroke only (SO; n = 41), and cancer only (n = 28), and vascular risk factor‐matched controls (n = 30). mRNA‐Seq and miRNA‐Seq data, analyzed with linear regression models, identified differentially expressed genes in CS versus SO and in cardioembolic versus noncardioembolic CS, and miRNA‐mRNA regulatory pairs. Network‐level analyses identified stroke etiology‐specific responses in CS.A total of 2,085 mRNAs and 31 miRNAs were differentially expressed between CS and SO. In CS, 122 and 35 miRNA‐mRNA regulatory pairs, and 5 and 3 coexpressed gene modules, were associated with cardioembolic and noncardioembolic CS, respectively. Complement, growth factor, and immune/inflammatory pathways showed differences between IS etiologies in CS. A 15‐gene biomarker panel assembled from a derivation cohort (n = 50) correctly classified 81% of CS and 71% of SO participants in a validation cohort (n = 33). Another 15‐gene panel correctly identified etiologies for 13 of 13 CS‐cardioembolic and 11 of 11 CS‐noncardioembolic participants upon cross‐validation; 11 of 16 CS‐cryptogenic participants were predicted cardioembolic.We discovered unique mRNA and miRNA transcriptome architecture in CS and SO, and in CS with different IS etiologies. Cardioembolic and noncardioembolic etiologies in CS showed unique coexpression networks and potential master regulators. These may help distinguish CS from SO and identify IS etiology in cryptogenic CS patients. ANN NEUROL 2024 [ABSTRACT FROM AUTHOR]

Strategies to prevent or delay Alzheimer's disease and related dementias (AD/ADRD) are urgently needed, and blood pressure (BP) management is a promising strategy. Yet the effects of different BP control strategies across the life course on AD/ADRD are unknown. Randomized trials may be infeasible due to prolonged follow-up and large sample sizes. Simulation analysis is a practical approach to estimating these effects using the best available existing data. However, existing simulation frameworks cannot estimate the effects of BP control on both dementia and cardiovascular disease. This manuscript describes the design principles, implementation details, and population-level validation of a novel population-health microsimulation framework, the MIchigan ChROnic Disease SIMulation (MICROSIM), for The Effect of Lower Blood Pressure over the Life Course on Late-life Cognition in Blacks, Hispanics, and Whites (BP-COG) study of the effect of BP levels over the life course on dementia and cardiovascular disease. MICROSIM is an agent-based Monte Carlo simulation designed using computer programming best practices. MICROSIM estimates annual vascular risk factor levels and transition probabilities in all-cause dementia, stroke, myocardial infarction, and mortality in a nationally representative sample of US adults 18+ using the National Health and Nutrition Examination Survey (NHANES). MICROSIM models changes in risk factors over time, cognition and dementia using changes from a pooled dataset of individual participant data from 6 US prospective cardiovascular cohort studies. Cardiovascular risks were estimated using a widely used risk model and BP treatment effects were derived from meta-analyses of randomized trials. MICROSIM is an extensible, open-source framework designed to estimate the population-level impact of different BP management strategies and reproduces US population-level estimates of BP and other vascular risk factors levels, their change over time, and incident all-cause dementia, stroke, myocardial infarction, and mortality. [ABSTRACT FROM AUTHOR]

The article emphasizes on the care for stroke and compares care taken by the hospitals in the U.S. for stroke patients. It mentions that the restructuring of health insurance in the U.S. has stimulated efforts to provide valid measures of health care quality. It informs about a prognostic model developed by the researchers to evaluate the influence of stroke severity. It states that the model consisted of information on age, sex, prior stroke and a large number of comorbid conditions and was compared with a model which already had additionally included information on stroke severity. It also highlights the importance of incorporating information on stroke severity.

Unhealthy diets are a major impediment to achieving a healthier population in the United States. Although there is a relatively clear sense of what constitutes a healthy diet, most of the US population does not eat healthy food at rates consistent with the recommended clinical guidelines. An abundance of barriers, including food and nutrition insecurity, how food is marketed and advertised, access to and affordability of healthy foods, and behavioral challenges such as a focus on immediate versus delayed gratification, stand in the way of healthier dietary patterns for many Americans. Food Is Medicine may be defined as the provision of healthy food resources to prevent, manage, or treat specific clinical conditions in coordination with the health care sector. Although the field has promise, relatively few studies have been conducted with designs that provide strong evidence of associations between Food Is Medicine interventions and health outcomes or health costs. Much work needs to be done to create a stronger body of evidence that convincingly demonstrates the effectiveness and cost-effectiveness of different types of Food Is Medicine interventions. An estimated 90% of the $4.3 trillion annual cost of health care in the United States is spent on medical care for chronic disease. For many of these diseases, diet is a major risk factor, so even modest improvements in diet could have a significant impact. This presidential advisory offers an overview of the state of the field of Food Is Medicine and a road map for a new research initiative that strategically approaches the outstanding questions in the field while prioritizing a human-centered design approach to achieve high rates of patient engagement and sustained behavior change. This will ideally happen in the context of broader efforts to use a health equity-centered approach to enhance the ways in which our food system and related policies support improvements in health. [ABSTRACT FROM AUTHOR]

This commentary is on the original article by Steinlin et al. on pages 713–718 of this issue. [ABSTRACT FROM AUTHOR]

The article discusses the effects of prestroke statin treatment on the functional recovery of a patient after acute ischemic stroke. Preclinical data suggests that statins could help in promoting angiogenesis and neurogenesis, improve blood flow, and modify inflammatory and coagulation pathways. An investigation was conducted on 893 patients who arrived at an institution within 24 hours of the onset of acute ischemic stroke symptoms, as well as a meta-analysis of previously published studies.

The article discusses the benefits of statins as treatment for acute stroke. A Study by the Stroke Prevention by Aggressive Reduction in Cholesterol Levels confirmed that statins reduce the risk of recurrent stroke and transient ischaemic attack. The effects of statins have been investigated in pre-clinical studies. The benefits of thrombolytic therapy may also be augmented by statin therapy. There are evidence on the benefit of statins on functional outcomes.

The pathogenesis of increased stroke risk in human immunodeficiency virus (HIV) remains unclear. Our study investigated the relationship between adventitial and intimal CD3+ T cells and brain arterial remodeling that potentially contributes to HIV-related vasculopathy and stroke. Large brain arteries from 84 HIV+ cases and 78 HIV- cases were analyzed to determine interadventitial and luminal diameters, intimal and wall thickness, percent stenosis, and the presence of atherosclerosis. Immunohistochemical analysis was performed to detect and visually score CD3, a pan-T-cell marker, in the intima and adventitia. Our study showed that numbers of adventitial CD3+ T cells are lower among persons with HIV than among those without HIV, especially if CD4 counts are <200, though intimal CD3+ T cell numbers did not differ by HIV status. Among those with HIV but CD4 counts of <200 at the time of death, intimal CD3+ T cells were associated with hypertrophic outward remodeling, while among those with HIV and CD4 of >200 or HIV- controls, intimal CD3+ T cells were associated with hypertrophic inward remodeling. We conclude that intimal lymphocytic inflammation is involved in brain arterial remodeling that may contribute to HIV-related cerebrovascular pathology. IMPORTANCE Although mortality from human immunodeficiency virus (HIV) has decreased with the use of combination antiretroviral therapies, there is now an increased risk of cardiovascular and cerebrovascular disease associated with HIV. Thus, there is a need to understand the pathogenesis of stroke in HIV infection. Our study examines how lymphocytic inflammation in brain arteries may contribute to increased cerebral vasculopathy. With this understanding, our study can potentially help direct future therapies to target and prevent brain arterial remodeling processes associated with HIV. [ABSTRACT FROM AUTHOR]

The article presents a letter to the editor discussing research results in the article "Incidence and prognosis of transient neurological attacks," published in a previous issue.

Background and Purpose: In patients with dolichoectasia, it is uncertain how dilatation and/or elongation relate to each other. We aimed to examine the correlation between arterial diameter and length within arteries and across the circle of Willis (COW). Methods: We included stroke‐free participants in the Northern Manhattan Study who underwent magnetic resonance angiography. Intracranial artery diameters and lengths were obtained with semiautomated commercial software and were adjusted for head size. We first investigated the correlation between diameters and length using Pearson's correlation coefficient. We then built generalized linear models adjusted for demographics and risk factors. Results: Among 1210 participants included in the analysis (mean age 71 ± 9 years, 59% women, 65% Hispanic), a larger basilar artery (BA) diameter correlated with greater BA length (r =.3), and left and right middle cerebral artery (MCA) diameters correlated with one another (r =.4). Across the COW, BA diameter correlated with MCA diameters (r =.3 for both). In adjusted analyses, MCA diameters were associated with larger posterior circulation diameters (β = 0.07), MCA and BA lengths (β = 0.003 and β = 0.002, respectively), presence of fetal posterior cerebral artery (PCA), (β = 0.11), and a complete COW (β = –0.02). Similarly, BA length was associated with a fetal PCA (β = 1.1), and BA diameter was associated with anterior circulation diameters (β = 0.15) and presence of fetal PCA (β = –0.4). Conclusions: COW configuration should be considered when using arterial diameter cutoffs to define dolichoectasia. Further studies are needed to discern whether arterial diameter or length best identify individuals at risk of vascular events attributable to dolichoectasia. [ABSTRACT FROM AUTHOR]

Background--Psychological stress is a proposed risk factor for cardiovascular disease (CVD), and posttraumatic stress disorder (PTSD), the sentinel stress-related mental disorder, occurs twice as frequently in women as men. However, whether PTSD contributes to CVD risk in women is not established. Methods and Results--We examined trauma exposure and PTSD symptoms in relation to incident CVD over a 20-year period in 49 978 women in the Nurses' Health Study II. Proportional hazards models estimated hazard ratios and 95% confidence intervals for CVD events confirmed by additional information or medical record review (n=548, including myocardial infarction [n=277] and stroke [n=271]). Trauma exposure and PTSD symptoms were assessed by using the Brief Trauma Questionnaire and a PTSD screen. In comparison with no trauma exposure, endorsing =4 PTSD symptoms was associated with increased CVD risk after adjusting for age, family history, and childhood factors (hazard ratio,1.60; 95% confidence interval, 1.20-2.13). Being trauma-exposed and endorsing no PTSD symptoms was associated with elevated CVD risk (hazard ratio, 1.45; 95% confidence interval, 1.15-1.83), although being trauma-exposed and endorsing 1 to 3 PTSD symptoms was not. After adjusting for adult health behaviors and medical risk factors, this pattern of findings was maintained. Health behaviors and medical risk factors accounted for 14% of the trauma/no symptoms-CVD association and 47% of the trauma/4+ symptoms-CVD association. Conclusion--Trauma exposure and elevated PTSD symptoms may increase the risk of CVD in this population of women. These findings suggest that screening for CVD risk and reducing health risk behaviors in trauma-exposed women may be promising avenues for prevention and intervention. [ABSTRACT FROM AUTHOR]

Background: Hypertension is the most important modifiable risk factor for recurrent stroke, and blood pressure (BP) reduction is associated with decreased risk of stroke recurrence. However, hypertension remains poorly controlled in many stroke survivors. Black and Hispanic patients have a higher prevalence of uncontrolled BP and higher rates of stroke. Limited access to care contributes to challenges in post-stroke care. Telehealth After Stroke Care (TASC) is a telehealth intervention that integrates remote BP monitoring (RBPM) including nursing telephone support, tailored BP infographics and telehealth video visits with a multidisciplinary team approach including pharmacy to improve post-stroke care and reduce stroke disparities. Methods: In this pilot trial, 50 acute stroke patients with hypertension will be screened for inclusion prior to hospital discharge and randomized to usual care or TASC. Usual care patients will be seen by a primary care nurse practitioner at 1–2 weeks and a stroke neurologist at 1 and 3 months. In addition to these usual care visits, TASC intervention patients will see a pharmacist at 4 and 8 weeks and will be enrolled in RBPM consisting of home BP monitoring with interval calls by a centralized team of telehealth nurses. As part of RBPM, TASC patients will be provided with a home BP monitoring device and electronic tablet that wirelessly transmits home BP data to the electronic health record. They will also receive tailored BP infographics that help explain their BP readings. The primary outcome will be feasibility including recruitment, adherence to at least one video visit and retention rates. The clinical outcome for consideration in a subsequent trial will be within-patient change in BP from baseline to 3 months after discharge. Secondary outcomes will be medication adherence self-efficacy and satisfaction with post-stroke telehealth, both measured at 3 months. Additional patient reported outcomes will include depression, cognitive function, and socioeconomic determinants. Multidisciplinary team competency and fidelity measures will also be assessed. Conclusions: Integrated team-based interventions may improve BP control and reduce racial/ethnic disparities in post-stroke care. TASC is a post-acute stroke care model that is novel in providing RBPM with tailored infographics, and a multidisciplinary team approach including pharmacy. Our pilot will determine if such an approach is feasible and effective in enhancing post-stroke BP control and promoting self-efficacy. Trial registration: ClinicalTrials.gov NCT04640519 [ABSTRACT FROM AUTHOR]

Background: The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, diet, and weight) and health factors (cholesterol, blood pressure, and glucose control) that contribute to cardiovascular health. The Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, congenital heart disease, rhythm disorders, subclinical atherosclerosis, coronary heart disease, heart failure, valvular disease, venous disease, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs).Methods: The American Heart Association, through its Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current information available in the annual Statistical Update. The 2022 Statistical Update is the product of a full year's worth of effort by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. This year's edition includes data on the monitoring and benefits of cardiovascular health in the population and an enhanced focus on social determinants of health, adverse pregnancy outcomes, vascular contributions to brain health, and the global burden of cardiovascular disease and healthy life expectancy.Results: Each of the chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics.Conclusions: The Statistical Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions. [ABSTRACT FROM AUTHOR]

Recent evidence indicates that our understanding of the relationship between cardiac function and ischemic stroke remains incomplete. The Cardiovascular Health Study enrolled community-dwelling adults ≥ 65 years old. We included participants with speckle-tracking data from digitized baseline study echocardiograms. Exposures were left atrial reservoir strain (primary), left ventricular longitudinal strain, left ventricular early diastolic strain rate, septal e' velocity, and lateral e' velocity. The primary outcome was incident ischemic stroke. Cox proportional hazards models were adjusted for demographics, image quality, and risk factors including left ventricular ejection fraction and incident atrial fibrillation. Among 4,000 participants in our analysis, lower (worse) left atrial reservoir strain was associated with incident ischemic stroke (HR per SD absolute decrease, 1.14; 95% CI 1.04–25). All secondary exposure variables were significantly associated with the outcome. Left atrial reservoir strain was associated with cardioembolic stroke (HR per SD absolute decrease, 1.42; 95% CI 1.21–1.67) and cardioembolic stroke related to incident atrial fibrillation (HR per SD absolute decrease, 1.60; 1.32–1.95). Myocardial dysfunction that can ultimately lead to stroke may be identifiable at an early stage. This highlights opportunities to identify cerebrovascular risk earlier and improve stroke prevention via therapies for early myocardial dysfunction. [ABSTRACT FROM AUTHOR]

Background: The coronavirus disease 2019 (COVID-19) pandemic has exposed longstanding racial and ethnic inequities in health risks and outcomes in the United States. We aimed to identify racial and ethnic differences in presentation and outcomes for patients hospitalized with COVID-19.Methods: The American Heart Association COVID-19 Cardiovascular Disease Registry is a retrospective observational registry capturing consecutive patients hospitalized with COVID-19. We present data on the first 7868 patients by race/ethnicity treated at 88 hospitals across the United States between January 17, 2020, and July 22, 2020. The primary outcome was in-hospital mortality. Secondary outcomes included major adverse cardiovascular events (death, myocardial infarction, stroke, heart failure) and COVID-19 cardiorespiratory ordinal severity score (worst to best: death, cardiac arrest, mechanical ventilation with mechanical circulatory support, mechanical ventilation with vasopressors/inotrope support, mechanical ventilation without hemodynamic support, and hospitalization alone. Multivariable logistic regression analyses were performed to assess the relationship between race/ethnicity and each outcome adjusting for differences in sociodemographic, clinical, and presentation features, and accounting for clustering by hospital.Results: Among 7868 patients hospitalized with COVID-19, 33.0% were Hispanic, 25.5% were non-Hispanic Black, 6.3% were Asian, and 35.2% were non-Hispanic White. Hispanic and Black patients were younger than non-Hispanic White and Asian patients and were more likely to be uninsured. Black patients had the highest prevalence of obesity, hypertension, and diabetes. Black patients also had the highest rates of mechanical ventilation (23.2%) and renal replacement therapy (6.6%) but the lowest rates of remdesivir use (6.1%). Overall mortality was 18.4% with 53% of all deaths occurring in Black and Hispanic patients. The adjusted odds ratios for mortality were 0.93 (95% CI, 0.76-1.14) for Black patients, 0.90 (95% CI, 0.73-1.11) for Hispanic patients, and 1.31 (95% CI, 0.96-1.80) for Asian patients compared with non-Hispanic White patients. The median odds ratio across hospitals was 1.99 (95% CI, 1.74-2.48). Results were similar for major adverse cardiovascular events. Asian patients had the highest COVID-19 cardiorespiratory severity at presentation (adjusted odds ratio, 1.48 [95% CI, 1.16-1.90]).Conclusions: Although in-hospital mortality and major adverse cardiovascular events did not differ by race/ethnicity after adjustment, Black and Hispanic patients bore a greater burden of mortality and morbidity because of their disproportionate representation among COVID-19 hospitalizations. [ABSTRACT FROM AUTHOR]

Background: Influenza may be associated with increased stroke and myocardial infarction (MI) risk. We hypothesized that risk of stroke and MI after influenza-like illness (ILI) would be higher in patients in New York State. We additionally assessed whether this relationship differed across a series of sociodemographic factors.Methods: A case-crossover analysis of the 2012-2014 New York Statewide Planning and Research Cooperative System (SPARCS) was used to estimate odds of ischemic stroke and MI after ILI. Each patient's case window (the time period preceding event) was compared to their control windows (same dates from the previous 2 years) in conditional logistic regression models used to estimate odds ratios and 95% confidence intervals (OR, 95% CI). We varied the case windows from 15 to 365 days preceding event as compared to control windows constructed using the same dates from the previous 2 years. Analyses were stratified by sex, race, and urban-rural status based on residential zip code.Results: A total of 33,742 patients were identified as having ischemic stroke and 53,094 had MI. ILI events in the 15 days prior were associated with a 39% increase in odds of ischemic stroke (95% CI 1.09-1.77), increasing to an almost 70% increase in odds when looking at ILI events over the last year (95% CI 1.56, 1.83). In contrast, the effect of ILI hospitalization on MI was strongest in the 15 days prior (OR = 1.24, 95% CI 1.06-1.44). The risk of ischemic stroke after ILI was higher among individuals living in rural areas in the 90 days prior to stroke and among men in the year prior to event. In contrast, the association between ILI and MI varied only across race with whites having significantly higher ILI associated MI.Conclusion: This study highlights risk period differences for acute cardiovascular events after ILI, indicating possible differences in mechanism behind the risk of stroke after ILI compared to the risk of MI. High risk populations for stroke after ILI include men and people living in rural areas, while whites are at high risk for MI after ILI. Future studies are needed to identify ways to mitigate these risks. [ABSTRACT FROM AUTHOR]

Background: The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, diet, and weight) and health factors (cholesterol, blood pressure, and glucose control) that contribute to cardiovascular health. The Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, congenital heart disease, rhythm disorders, subclinical atherosclerosis, coronary heart disease, heart failure, valvular disease, venous disease, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs).Methods: The American Heart Association, through its Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current information available in the annual Statistical Update. The 2021 Statistical Update is the product of a full year's worth of effort by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. This year's edition includes data on the monitoring and benefits of cardiovascular health in the population, an enhanced focus on social determinants of health, adverse pregnancy outcomes, vascular contributions to brain health, the global burden of cardiovascular disease, and further evidence-based approaches to changing behaviors related to cardiovascular disease.Results: Each of the 27 chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics.Conclusions: The Statistical Update represents a critical resource for the lay public, policy makers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions. [ABSTRACT FROM AUTHOR]

Background: Infection and venous thromboembolism (VTE) are associated with worse outcomes after intracerebral hemorrhage (ICH). The relationship between infection and VTE in ICH patients is unclear. We hypothesized that infection would be associated with subsequent VTE after ICH. Methods: We retrospectively studied consecutively admitted spontaneous primary ICH patients from 2009 to 2018 surviving beyond 24 h. The primary predictor variable was infection, diagnosed prior to VTE. The primary outcome was VTE. We used multivariable logistic regression models to estimate the odds ratios and 95% confidence intervals (OR, 95% CI) for VTE risk after infection of any type, after adjusting for ICH score, length of stay and days to deep venous thrombosis (DVT) prophylaxis. Similar analysis was done to estimate the association of infection subtypes, including respiratory and urinary and blood stream infections (BSI) with VTE. Results: There were 414 patients (mean age 65 years, 47% female) that met were analyzed. Infection was diagnosed in 181 (44%) patients. Incident VTE was diagnosed in 36 (9%) patients, largely comprised of DVT (n = 32; 89%). Infection overall was associated with increased risk of subsequent VTE (adjusted OR 4.5, 95% CI 1.6–12.6). Respiratory (adjusted OR 5.7, 95% CI 2.8–11.7) and BSI (adjusted OR 4.0, 95% CI 1.3–11.0) were associated with future VTE. Urinary and other infections were not associated with subsequent VTE. Conclusions: Infections are associated with subsequent risk of VTE among patients with ICH. Further investigation is required to elucidate mechanisms behind this association and to improve VTE prevention after ICH. [ABSTRACT FROM AUTHOR]

Background: The incidence and prevalence of stroke among the young are increasing in the US. Data on healthcare utilization prior to stroke is limited. We hypothesized those < 45 years were less likely than those 45-65 years old to utilize healthcare in the 1 year prior to stroke.Methods: Patients 18-65 years old who had a stroke between 2008 and 2013 in MarketScan Commercial Claims and Encounters Databases were included. We used descriptive statistics and logistic regression to examine healthcare utilization and risk factors between age groups 18-44 and 45-65 years. Healthcare utilization was categorized by visit type (no visits, inpatient visits only, emergency department visits only, outpatient patient visits only, or a combination of inpatient, outpatient or emergency department visits) during the year prior to stroke hospitalization.Results: Of those 18-44 years old, 14.1% had no visits in the year prior to stroke compared to 11.2% of individuals aged 45-65 [OR = 1.30 (95% CI 1.25,1.35)]. Patients 18-44 years old had higher odds of having preventive care procedures associated with an outpatient visit and lower odds of having cardiovascular procedures compared to patients aged 45-65 years. Of stroke patients aged 18-45 and 45-65 years, 16.8 and 13.2% respectively had no known risk for stroke.Conclusions: Patients aged 45-65 were less commonly seeking preventive care and appeared to be seeking care to manage existing conditions more than patients aged 18-44 years. However, as greater than 10% of both age groups had no prior risk, further exploration of potential risk factors is needed. [ABSTRACT FROM AUTHOR]

Objective: Cognitive decline is a major concern for older adults with epilepsy. Whether and how much faster older adults with epilepsy experience cognitive decline beyond expected age‐related cognitive change remain unclear. We sought to estimate and compare rates of cognitive decline in older adults with and without epilepsy. Methods: The Cardiovascular Health Study is a population‐based longitudinal cohort study of 5888 US adults aged 65+. Cognitive function was assessed annually with Modified Mini‐Mental State Exam (3MS) and Digit Symbol Substitution Test (DSST). We used linear mixed models to estimate average rates of decline in 3MS and DSST scores by epilepsy status (prevalent, incident, or no epilepsy), adjusted for risk factors associated with cognitive decline. Results: The rate of decline in 3MS was significantly faster in prevalent epilepsy (P <.001) and after incident epilepsy (P =.002) compared with no epilepsy. Prevalent epilepsy and apolipoprotein E gene (APOE) ε4 (ApoE4) had a synergistic interaction, whereby prevalent epilepsy and ApoE4 together were associated with 1.51 points faster annual decline in 3MS than would be expected if prevalent epilepsy and ApoE4 did not interact (P <.001). Older adults with prevalent epilepsy had a significantly lower initial DSST score and faster rate of decline compared to those with no epilepsy (P <.001). Significance: Faster decline in global cognitive ability seen in this study validates concerns of patients. ApoE4 allele status was an effect modifier of the relationship between cognitive decline and prevalent epilepsy. Further research is warranted to explore biological mechanisms and possible interventions to mitigate cognitive decline. [ABSTRACT FROM AUTHOR]

Background: Accurate identification of acute ischemic stroke (AIS) patient cohorts is essential for a wide range of clinical investigations. Automated phenotyping methods that leverage electronic health records (EHRs) represent a fundamentally new approach cohort identification without current laborious and ungeneralizable generation of phenotyping algorithms. We systematically compared and evaluated the ability of machine learning algorithms and case-control combinations to phenotype acute ischemic stroke patients using data from an EHR. Materials and methods: Using structured patient data from the EHR at a tertiary-care hospital system, we built and evaluated machine learning models to identify patients with AIS based on 75 different case-control and classifier combinations. We then estimated the prevalence of AIS patients across the EHR. Finally, we externally validated the ability of the models to detect AIS patients without AIS diagnosis codes using the UK Biobank. Results: Across all models, we found that the mean AUROC for detecting AIS was 0.963 ± 0.0520 and average precision score 0.790 ± 0.196 with minimal feature processing. Classifiers trained with cases with AIS diagnosis codes and controls with no cerebrovascular disease codes had the best average F1 score (0.832 ± 0.0383). In the external validation, we found that the top probabilities from a model-predicted AIS cohort were significantly enriched for AIS patients without AIS diagnosis codes (60–150 fold over expected). Conclusions: Our findings support machine learning algorithms as a generalizable way to accurately identify AIS patients without using process-intensive manual feature curation. When a set of AIS patients is unavailable, diagnosis codes may be used to train classifier models. [ABSTRACT FROM AUTHOR]

Background: How cerebrovascular disease and neurodegeneration affect each other to impact cognition is not yet known. We aimed to test whether Alzheimer's disease-signature (AD) cortical thickness mediates the association between cholinergic white matter lesion load and change in domain-specific cognition.Methods: Clinically stroke-free participants from the Northern Manhattan Study with both regional white matter hyperintensity volume (WMHV) and gray matter measurements were included (N = 894). Tract-specific WMHVs were quantified through FSL using the Johns Hopkins University white matter tract atlas. We used Freesurfer 5.1 to estimate regional cortical thickness. We fit structural equation models, including multiple indicator latent change score models, to examine associations between white matter hyperintensity volume (WMHV) in cholinergic tracts, AD-signature region cortical thickness (CT), and domain-specific cognition.Results: Our sample (N = 894) had a mean (SD) age = 70 (9) years, years of education = 10 (5), 63% women, and 67% Hispanics/Latinos. Greater cholinergic WMHV was significantly related to worse processing speed at baseline (standardized β = -0.17, SE = 0.05, p = .001) and over time (standardized β = -0.28, SE = 0.09, p = .003), with a significant indirect effect of AD-signature region CT (baseline: standardized β = -0.02, SE = 0.01, p = .023; change: standardized β = -0.03, SE = 0.02, p = .040).Conclusions: Cholinergic tract WMHV is associated with worse processing speed, both directly and indirectly through its effect on AD-signature region CT. [ABSTRACT FROM AUTHOR]

Background: Key dimensions of cardiac arrest-induced posttraumatic stress disorder (PTSD) symptoms include reexperiencing, avoidance, numbing, and hyperarousal. It remains unknown which dimensions are most predictive of outcome.Purpose: To determine which dimensions of cardiac arrest-induced PTSD are predictive of clinical outcome within 13 months posthospital discharge.Methods: PTSD symptoms were assessed in survivors of cardiac arrest who were able to complete psychological screening measures at hospital discharge via the PTSD Checklist-Specific scale, which queries for 17 symptoms using five levels of severity. Responses on items for each symptom dimension of the four-factor numbing model (reexperiencing, avoidance, numbing, and hyperarousal) were converted to Z-scores and treated as continuous predictors. The combined primary endpoint was all-cause mortality (ACM) or major adverse cardiovascular events (MACE; hospitalization for myocardial infarction, unstable angina, heart failure, emergency coronary revascularization, or urgent defibrillator/pacemaker placements) within 13 months postdischarge. Four bivariate Cox proportional hazards survival models evaluated associations between individual symptom dimensions and ACM/MACE. A multivariable model then evaluated whether significant bivariate predictors remained independent predictors of the primary outcome after adjusting for age, sex, comorbidities, premorbid psychiatric diagnoses, and initial cardiac rhythm.Results: A total of 114 patients (59.6% men, 52.6% white, mean age: 54.6 ± 13 years) were included. In bivariate analyses, only hyperarousal was significantly associated with ACM/MACE. In a fully adjusted model, 1 standard deviation increase in hyperarousal symptoms corresponded to a two-times increased risk of experiencing ACM/MACE.Conclusions: Greater level of hyperarousal symptoms was associated with a higher risk of ACM/MACE within 13 months postcardiac arrest. This initial evidence should be further investigated in a larger sample. [ABSTRACT FROM AUTHOR]

Background: Estimated glomerular filtration rate (eGFR) is routinely utilized as a measure of renal function. While creatinine-based eGFR (eGFRcr) is widely used in clinical practice, the use of cystatin-C to estimate GFR (eGFRcys) has demonstrated superior risk prediction in various populations. Prior studies that derived eGFR formulas have infrequently included high proportions of elderly, African-Americans, and Hispanics. Objective: Our objective as to compare mortality risk prediction using eGFRcr and eGFRcys in an elderly, race/ethnically diverse population. Design: The Northern Manhattan Study (NOMAS) is a multiethnic prospective cohort of elderly stroke-free individuals consisting of a total of 3,298 participants recruited between 1993 and 2001, with a median follow-up of 18 years. Participants: We included all Northern Manhattan Study (NOMAS) participants with concurrent measured creatinine and cystatin-C. Main measures: The eGFRcr was calculated using the CKD-EPI 2009 equation. eGFRcys was calculated using the CKD-EPI 2012 equations. The performance of each eGFR formula in predicting mortality risk was tested using receiver-operating characteristics, calibration and reclassification. Net reclassification improvement (NRI) was calculated based on the Reynolds 10 year risk score from adjusted Cox models with mortality as an outcome. The primary hypothesis was that eGFRcys would better predict mortality than eGFRcr. Results: Participants (n = 2988) had a mean age of 69±10.2 years and were predominantly Hispanic (53%), overweight (69%), and current or former smokers (53% combined). The mean eGFRcr (74.68±18.8 ml/min/1.73m2) was higher than eGFRcys (51.72±17.2 ml/min/1.73m2). During a mean of 13.0±5.6 years of follow-up, 53% of the cohort had died. The AUC of eGFRcys (0.73) was greater than for eGFRcr (0.67, p for difference<0.0001). The proportions of correct reclassification (NRI) based on 10 year mortality for the model with eGFRcys compared to the model with eGFRcr were 4.2% (p = 0.002). Conclusions: In an elderly, race/ethnically diverse cohort low eGFR is associated with risk of all-cause mortality. Estimated GFR based on serum cystatin-C, in comparison to serum creatinine, was a better predictor of all-cause mortality. [ABSTRACT FROM AUTHOR]

Background: Lobar intracerebral hemorrhage (ICH) is known to have better clinical outcomes and preliminary evidence of less hematoma expansion compared to deep ICH. No functional coagulation differences between lobar and deep ICH have been identified using traditional plasma-based coagulation tests. We investigated for coagulation differences between lobar and deep ICH using whole-blood coagulation testing (Rotational Thromboelastometry: [ROTEM]).Methods: Clinical, radiographic, and laboratory data were prospectively collected for primary ICH patients enrolled in a single-center ICH study. Patients with preceding anticoagulant use or admission coagulopathy on traditional laboratory testing were excluded. Lobar and deep ICH patients receiving admission ROTEM were analyzed. Linear regression was used to assess the association of ICH location with coagulation test results after adjusting for potential confounders.Results: There were 12 lobar and 19 deep ICH patients meeting inclusion criteria. Lobar ICH patients were significantly older and predominantly female. Lobar ICH had faster intrinsic pathway coagulation times (139.8 vs 203.2 s; 95% CI - 179.91 to - 45.96; p = 0.002) on ROTEM testing compared to deep ICH after adjusting for age, sex, and hematoma volume. This revealed functional coagulation differences, specifically quicker clot formation in lobar compared to deep ICH. No differences were noted using traditional coagulation testing (prothrombin time/partial thromboplastin time/platelet count).Conclusions: Our pilot data may suggest that there are functional coagulation differences between lobar and deep ICH identified using ROTEM. Whole-blood coagulation testing may be useful in assessing coagulopathy in ICH patients and in determining reversal treatment paradigms, though further work is needed. [ABSTRACT FROM AUTHOR]

Background: Hematoma expansion (HE) after intracerebral hemorrhage (ICH) is associated with worse outcome. Lobar ICHs are known to have better outcomes compared to deep ICH; however, it is unclear whether there are HE differences between these locations. We sought to investigate the hypothesis that lobar ICH has less HE compared to deep ICH.Methods: Primary ICH patients admitted between 2009 and 2016 were included in a prospective single-center ICH cohort study. Patients with preceding anticoagulant use, coagulopathy on admission labs, or presenting after 24 h from symptom onset were excluded. Lobar and deep ICH patients with baseline and follow-up computed tomography (CT) (within 24 h of admission CT) were evaluated. HE was defined primarily as relative growth > 33% given expected baseline hematoma volume differences between locations. Other commonly utilized definitions of HE: > 6 mL, and > 33% or > 6 mL, were additionally assessed. Multivariable logistic regression was used to assess the association of ICH location with HE while adjusting for previously identified covariates of HE.Results: There were 59 lobar and 143 deep ICH patients analyzed. Lobar ICH patients had significantly larger baseline hematoma volumes, lower admission systolic blood pressure, and longer times to admission CT compared to deep ICH. Multivariable logistic regression revealed an association of lobar ICH with lower odds of HE (> 33%) [odds ratio (OR) 0.32; 95% confidence interval (CI) 0.11-0.93; p = 0.04] compared to deep ICH after adjusting for baseline ICH volume, blood pressure, and time to CT. Secondary analysis did not identify an association of lobar ICH with HE defined as > 6 mL (adjusted OR 1.44; 95% CI 0.59-3.50; p = 0.41) or > 33% or > 6 mL (adjusted OR 0.71; 95% CI 0.29-1.70; p = 0.44).Conclusion: We identified less HE in lobar compared to deep ICH. The use of absolute growth thresholds in defining HE may be limited when assessing groups with largely different baseline hematoma sizes. Further study is required to replicate our findings and investigate mechanisms for HE differences between lobar and deep ICH locations. [ABSTRACT FROM AUTHOR]