ABSTRACT
BACKGROUND: Since the introduction of recombinant tissue plasminogen activator (rt-PA) for acute ischemic stroke, rt-PA rate and number of stroke centers have increased. Despite this, studies have shown racial and ethnic disparities in stroke care especially in Black and Hispanic populations. What factors are related to the administration of rt-PA within the Hispanic population has to date been unclear. METHODS: We performed a retrospective review of IRB approved, prospectively collected data from the UC San Diego Stroke Registry from 7/2004-7/2016. Patients were included based on the primary diagnosis of Transient Ischemic Attack or Ischemic Stroke. Hispanic vs non-Hispanic patients were compared to assess for overall rt-PA treatment rates and process of care intervals. For the Hispanic cohort itself, demographics and NIHSS scores were assessed to determine why some Hispanics received rt-PA while others were not. RESULTS: Overall, 1489 patients (300 Hispanic vs. 1189 non-Hispanic) were included. Comparing Hispanics to non-Hispanics, there was no difference in rt-PA rate (35.3% vs. 33.1%; p=0.49). In rt-PA treated patients, "onset to arrival" interval was higher in Hispanics (1.03 vs. 0.88 hours; p=0.04), while the "arrival to treatment" interval was not different (1.13 vs. 1.02 hours; p=0.07). When looking at Hispanic patients only, there was no difference in baseline characteristics except for initial NIHSS in treated vs. non-treated patients (13.27 vs. 7.24; p<.001). CONCLUSION: Our analyses sought to determine the factors important to administration of rt-PA to Hispanic patients. These findings highlight the need for strategies to improve recognition and presentation pathways for Hispanics.
ABSTRACT
BACKGROUND: Vascular cognitive impairment (VCI) is a heterogeneous entity with multiple aetiologies, all linked to underlying vascular disease. Among these, VCI related to subcortical small vessel disease (SSVD) is emerging as a major homogeneous subtype. Its progressive course raises the need for biomarker identification and/or development for adequate therapeutic interventions to be tested. In order to shed light in the current status on biochemical markers for VCI-SSVD, experts in field reviewed the recent evidence and literature data. METHOD: The group conducted a comprehensive search on Medline, PubMed and Embase databases for studies published until 15.01.2017. The proposal on current status of biochemical markers in VCI-SSVD was reviewed by all co-authors and the draft was repeatedly circulated and discussed before it was finalized. RESULTS: This review identifies a large number of biochemical markers derived from CSF and blood. There is a considerable overlap of VCI-SSVD clinical symptoms with those of Alzheimer's disease (AD). Although most of the published studies are small and their findings remain to be replicated in larger cohorts, several biomarkers have shown promise in separating VCI-SSVD from AD. These promising biomarkers are closely linked to underlying SSVD pathophysiology, namely disruption of blood-CSF and blood-brain barriers (BCB-BBB) and breakdown of white matter myelinated fibres and extracellular matrix, as well as blood and brain inflammation. The leading biomarker candidates are: elevated CSF/blood albumin ratio, which reflects BCB/BBB disruption; altered CSF matrix metalloproteinases, reflecting extracellular matrix breakdown; CSF neurofilment as a marker of axonal damage, and possibly blood inflammatory cytokines and adhesion molecules. The suggested SSVD biomarker deviations contrasts the characteristic CSF profile in AD, i.e. depletion of amyloid beta peptide and increased phosphorylated and total tau. CONCLUSIONS: Combining SSVD and AD biomarkers may provide a powerful tool to identify with greater precision appropriate patients for clinical trials of more homogeneous dementia populations. Thereby, biomarkers might promote therapeutic progress not only in VCI-SSVD, but also in AD.
