Cerebrovascular Disease*

This talk will cover how the evaluation, care and management of young stroke patients has recently evolved, including hyperacute and acute treatment options based on stroke etiologies.

The frequency of cardiomyopathy in patients admitted to the hospital for acute ischemic stroke as well as in-hospital outcome differences in this population has been incompletely characterized. Compared to those with acute ischemic stroke who do not have cardiomyopathy, we explored the overall frequency of concomitant disease and the use of acute stroke therapies, therapeutic cardiac procedures, in-hospital mortality, and disposition differences between the two groups.

Sleep is essential to human survival and overall vascular health. Sleep health encompasses the objective and subjective qualities associated with sleep and wakefulness. Impaired sleep duration and quality can increase stroke risk and mediate the relationship between the physical aspects of the environment and disparities in stroke incidence. Sleep disturbances have been shown to affect poor and minority populations disproportionately, partly related to the influence of the neighborhood environment. Yet, few stroke survivors are evaluated for sleep disorders. Here we review observational studies evaluating the association between sleep health and stroke; the implications of sleep disorders before and after stroke; and the association between sleep environment and neighborhood characteristics with sleep health. Given the regional and racial or ethnic differences in stroke risk, an understanding of novel vascular risk factors, such as the multifaceted role of sleep health, will be critical to develop effective public policies to improve population health.

This lecture will cover evidence for sex and gender differences in stroke outcomes including patient reported outcomes, activity limitations, and death following stroke. The presentation will also cover major contributors to the differences in post stroke outcomes between women and men as well as ideas for moving toward the development of interventions to improve outcomes in women after stroke.

Polymorphonuclear leukocytes (PMN) are among the first leukocytes recruited in ischemic stroke. Although blocking leukocyte transendothelial migration (TEM) reduces infarct size in preclinical studies, clinical trials have been unsuccessful. Understanding PMN recruitment and extravasation patterns may clarify these failures and improve therapies. Circulating PMN were labeled with 5-Ethynyl-2’-deoxyuridine (EdU) to track their recruitment and persistence post-ischemia/reperfusion in stroke. Using the transient middle cerebral artery occlusion model (tMCAO), we simulated large vessel occlusion and reperfusion. The percentage of EdU+ PMNs was compared between circulation and the ischemic hemisphere via flow cytometry. Wide field fluorescence microscopy determined EdU-labeled PMN positions in coronal sections. Our results indicate PMN recruitment and infiltration post-stroke evolve over days, with most PMN recruited within 48 hours and persisting to longer timepoints. Modulating PMN labeling timing can enhance understanding of their spatiotemporal behavior and inform future therapeutic strategies targeting leukocytes.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic angiopathy caused by mutations in the Notch 3 gene and is the most common hereditary stroke disorder. The hallmark of CADASIL is the accumulation of white matter hyperintensities (WMH) on T2-weighted MRI, particularly in the temporal lobes, which radiographically distinguishes it from sporadic cerebral small vessel disease (SCSVD). Both CADASIL and SCSVD can be associated with cognitive decline but are phenotypically different. Disruption of the blood-brain barrier has been implicated in the pathogenesis of SCSVD, however its role in CADASIL remains in dispute. In this study, we investigated the relationship between WMH, BBB disruption, and cognitive performance in a cohort of patients with genetically confirmed CADASIL.