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We aim to describe the burden, characteristics, and cognitive associations of cerebral small vessel disease in a Canadian sample living with multimorbidity in precarious housing.

Participants received T1, T2-fluid-attenuated inversion recovery, and susceptibility-weighted imaging 3T magnetic resonance imaging sequences and comprehensive clinical, laboratory, and cognitive assessments. Cerebral small vessel disease burden was characterized using a modified Small Vessel Disease (mSVD) score. One point each was given for moderate-severe white matter hyperintensities, ≥1 cerebral microbleeds, and ≥1 lacune. Multivariable regression explored associations between mSVD score, risk factors, and cognitive performance.

Median age of the 228 participants (77% male) was 44.7 years (range, 23.3-63.2). In n=188 participants with consistent good quality magnetic resonance imaging sequences, mSVD scores were 0 (n=127, 68%), 1 (n=50, 27%), and 2 (n=11, 6%). Overall, one-third had an mSVD ≥1 n=61 (32%); this proportion wage and was associated with poorer cognitive performance.

Swallowing difficulties are common poststroke. National clinical guidelines recommend feeding by percutaneous endoscopic gastrostomy (PEG) when oral nutrition cannot be maintained although survival benefit might be short term. It is unknown whether a decade of general care improvements have impacted upon PEG provision and outcomes. This retrospective cohort study examined PEG placement and mortality poststroke in England.

National Health Service Hospital Episode Statistics and Office for National Statistics mortality data between April 2007 and March 2018 were linked to identify all admissions in England with stroke-related

codes (I61, I63, and I64)±PEG insertion and deaths at 3, 6, and 12 months. Linear and logistic regression examined trends over time and mortality.

Patients (923 236) with stroke underwent 17 532 PEG procedures (mean rate 1.9%), with an average reduction of -27 procedures/year ([95% CI, -56 to 1.4];

=0.06) despite an average increase of 1804 stroke admissions/year. Mortality decr have decreased in the context of general mortality reductions after hospitalization for stroke, but survival at 6 and 12 months remains significantly worse for patients with PEG placement.

Inflammation has emerged as a key component of the pathophysiology of intracranial aneurysms. Mast cells have been detected in human intracranial aneurysm tissues, and their presence was associated with intramural microhemorrhage and wall degeneration. We hypothesized that mast cells play a critical role in the development of aneurysmal rupture, and that mast cells can be used as a therapeutic target for the prevention of aneurysm rupture.

Intracranial aneurysms were induced in adult mice using a combination of induced systemic hypertension and a single injection of elastase into the cerebrospinal fluid. Aneurysm formation and rupture were assessed over 3 weeks. Roles of mast cells were assessed using a mast cell stabilizer (cromolyn), a mast cell activator (C48/80), and mice that are genetically lacking mature mast cells (Kit

mice).

Pharmacological stabilization of mast cells with cromolyn markedly decreased the rupture rate of aneurysms (80% versus 19%, n=10 versus n =16) without affecting the aneurysm formation. The activation of mast cells with C48/80 significantly increased the rupture rate of aneurysms (25% versus 100%, n=4 versus n=5) without affecting the overall rate of aneurysm formation. Furthermore, the genetic deficiency of mast cells significantly prevented aneurysm rupture (80% versus 25%, n=10 versus n=8, wild-type versus Kit

mice).

These results suggest that mast cells play a key role in promoting aneurysm rupture but not formation. Stabilizers of mast cells may have a potential therapeutic value in preventing intracranial aneurysm rupture in patients.

These results suggest that mast cells play a key role in promoting aneurysm rupture but not formation. Stabilizers of mast cells may have a potential therapeutic value in preventing intracranial aneurysm rupture in patients.

Diabetic retinopathy (DR) is a common microvascular complication of diabetes, which causes damage to the retina and may lead to rapid vision loss. Previous research has shown that the macrovascular complications of diabetes, including stroke, are often comorbid with DR. We sought to explore the association between DR and subsequent stroke events.

This is a secondary analysis of patients enrolled in the ACCORD Eye study (Action to Control Cardiovascular Risk in Diabetes). The primary outcome was stroke during follow-up. The exposure was presence of DR at study baseline. We fit adjusted Cox proportional hazards models to provide hazard ratios for stroke and included interaction terms with the ACCORD randomization arms.

We included 2828 patients, in whom the primary outcome of stroke was met by 117 (4.1%) patients during a mean (SD) of 5.4 (1.8) years of follow-up. DR was present in 874 of 2828 (30.9%) patients at baseline and was more common in patients with than without incident stroke (41.0% versus 30.5%;

=0.016). In an adjusted Cox regression model, DR was independently associated with incident stroke (hazard ratio, 1.52 [95% CI, 1.05-2.20];

=0.026). This association was not affected by randomization arm in the ACCORD glucose (

=0.300), lipid (

=0.660), or blood pressure interventions (

=0.469).

DR is associated with an increased risk of stroke, which suggests that the microvascular pathology inherent to DR has larger cerebrovascular implications. This association appears not to be mediated by serum glucose, lipid, and blood pressure interventions.

DR is associated with an increased risk of stroke, which suggests that the microvascular pathology inherent to DR has larger cerebrovascular implications. This association appears not to be mediated by serum glucose, lipid, and blood pressure interventions.

Enlarged perivascular spaces (EPVS) are considered subclinical markers of small vessel disease, associated with increased risk of stroke and dementia. Glesatinib Increasing evidence links chronic kidney disease (CKD) to small vessel disease. We explored the relationship between CKD and EPVS burden and the influence of racial group in this relation.

Consecutive patients with stroke who underwent brain magnetic resonance imaging were included (n=894). Racial group was categorized as White, Black, or other (other racial groups). CKD was defined by glomerular filtration rate <60 mL/minute per 1.73 m

for >3 months. EPVS were rated following a standardized method, dichotomized for analyses (mild [<20] versus severe [≥20]), and stratified by brain region (basal ganglia and centrum semiovale).

In multivariable-adjusted analysis, the association of CKD with severe EPVS varied across racial groups. Comparing patients with and without CKD within racial groups, we found that Whites with CKD had higher odds of severe centrum semiovale EPVS (odds ratio [OR], 2.