Influenza-Like Illness is Associated with Increased Short-Term Risk of Cervical Artery Dissection.

INTRODUCTION: Non-traumatic Cervical Artery Dissection (CeAD) is a leading cause of ischemic stroke in the young. Influenza-like illnesses (ILI) trigger ischemic strokes. We hypothesized that influenza and ILI are associated with CeAD. METHODS: In a case-crossover study within the New York State (NYS) Department of Health Statewide Planning and Research Cooperative System (2006-2014), we used ICD-9 codes to exclude major trauma and to define CeAD, influenza, and the Centers for Disease Control defined ILI. We estimated the association of ILI and influenza with CeAD by comparing their prevalence in intervals immediately prior (0-30,0-90,0-180, and 0-365 days) to CeAD (case period) to their prevalence exactly one and two years earlier (control periods). Conditional logistic regression models generated odds ratios and 95% confidence intervals (OR, 95% CI). Models were adjusted for NYS estimates of influenza prevalence rates. RESULTS: Our sample included 3,610 cases of CeAD (mean age 52±16 years, 54.7% male, 6.2% Hispanic, 9.9% Black, 68.7% White). During case periods, 7.3% had one or more ILI. ILI was more likely within 90 days of CeAD compared to the same time interval one and two years before (0-15 days: adjusted OR 1.88, 95%CI 1.20-2.94; 0-30 days: adjusted OR 1.74, 95%CI 1.22-2.46; 0-90 days: adjusted OR 1.35, 95%CI 1.00-1.81). Influenza trended with CeAD (adjusted OR 1.86, 95%CI 0.37-9.24), but these results were not statistically significant, due to limited instances of confirmed influenza. CONCLUSIONS: ILI may increase risk of CeAD for 15 days, and possibly up to three months.

Clinical risk factors for acute ischaemic and haemorrhagic stroke in patients with infective endocarditis.

BACKGROUND: Stroke as a complication of infective endocarditis portends a poor prognosis, yet risk factors for stroke subtypes have not been well defined. AIM: To identify risk factors associated with ischaemic and haemorrhagic strokes. METHODS: A retrospective patient chart review was performed at a single US academic centre to identify risk factors and imaging for patients who were 18 years or older with infectious endocarditis (IE) and stroke diagnoses. Differences in patient characteristics by stroke status were assessed using univariate analysis, χ2 or student's t-test as well as logistic regression models for multivariable analyses and correlation matrices to identify possible collinearity between variables and to obtain odds ratios (OR) and their 95% confidence intervals. RESULTS: A final sample of 1157 participants was used for this analysis. The total number of non-surgical strokes was 178, with a prevalence of 15.4% (78% ischaemic, 10% parenchymal haemorrhages, 8% subarachnoid haemorrhages and 4% mixed ischaemic/haemorrhagic). Multivariate risk factors for ischaemic stroke included prior stroke (OR 2.0, 1.3-3.1), Staphylococcus infection (OR 2.0, 1.3-3.0), mitral vegetations (OR 2.2, 1.4-3.3) and valvular abscess (OR 2.7, 1.7-4.3). Risk factors for haemorrhagic stroke included fungal infection (OR 6.4, 1.2-34.0), male gender (OR 3.5, 1.4-8.3) and rheumatic heart disease (OR 3.3, 1.1-10.4). CONCLUSION: Among patients with IE, there exist characteristics that relate differentially to ischaemic and haemorrhagic stroke risk.

Geographic Analysis of Mobile Stroke Unit Treatment in a Dense Urban Area: The New York City METRONOME Registry.

Background Mobile stroke units (MSUs) reduce time to intravenous thrombolysis in acute ischemic stroke. Whether this advantage exists in densely populated urban areas with many proximate hospitals is unclear. Methods and Results We evaluated patients from the METRONOME (Metropolitan New York Mobile Stroke) registry with suspected acute ischemic stroke who were transported by a bi-institutional MSU operating in Manhattan, New York, from October 2016 to September 2017. The comparison group included patients transported to our hospitals via conventional ambulance for acute ischemic stroke during the same hours of MSU operation (Monday to Friday, 9 am to 5 pm). Our exposure was MSU care, and our primary outcome was dispatch-to-thrombolysis time. We estimated mean differences in the primary outcome between both groups, adjusting for clinical, demographic, and geographic factors, including numbers of nearby designated stroke centers and population density. We identified 66 patients treated or transported by MSU and 19 patients transported by conventional ambulance. Patients receiving MSU care had significantly shorter dispatch-to-thrombolysis time than patients receiving conventional care (mean: 61.2 versus 91.6 minutes; P=0.001). Compared with patients receiving conventional care, patients receiving MSU care were significantly more likely to be picked up closer to a higher mean number of designated stroke centers in a 2.0-mile radius (4.8 versus 2.7, P=0.002). In multivariable analysis, MSU care was associated with a mean decrease in dispatch-to-thrombolysis time of 29.7 minutes (95% CI, 6.9-52.5) compared with conventional care. Conclusions In a densely populated urban area with a high number of intermediary stroke centers, MSU care was associated with substantially quicker time to thrombolysis compared with conventional ambulance care.

Electrocardiographic left atrial abnormality and silent vascular brain injury: The Northern Manhattan Study.

HYPOTHESIS: We hypothesized that P wave terminal Force in the V1 lead (PTFV1) would be associated with leukoaraiosis and subclinical infarcts, especially cortical infarcts, in a population-based, multi-ethnic cohort. METHODS: PTFV1 was collected manually from baseline electrocardiograms of clinically stroke-free Northern Manhattan Study participants. Investigators read brain MRIs for superficial infarcts, deep infarcts, and white matter hyperintensity volume (WMHV). WMHV was adjusted for head size and log transformed, achieving a normal distribution. Logistic regression models investigated the association of PTFV1 with cortical and with all subclinical infarcts. Linear regression models examined logWMHV. Models were adjusted for demographics and risk factors. RESULTS: Among 1174 participants with PTFV1 measurements, the mean age at MRI was 70 ± 9 years. Participants were 14.4% white, 17.6% black, and 65.8% Hispanic. Mean PTFV1 was 3587.35 ± 2315.62 µV-ms. Of the 170 subclinical infarcts, 40 were cortical. PTFV1 ≥ 5000 µV-ms was associated with WMHV in a fully adjusted model (mean difference in logWMHV 0.15, 95% confidence interval 0.01-0.28). PTFV1 exhibited a trend toward an association with cortical infarcts (unadjusted OR per SD change logPTFV1 1.30, 95% CI 0.94-1.81), but not with all subclinical infarcts. CONCLUSION: Electrocardiographic evidence of left atrial abnormality was associated with leukoaraiosis.

Brain vascular intima vulnerability among HIV-positive and negative individuals.

OBJECTIVE: To test whether HIV is associated with brain large artery vulnerable intima. DESIGN: Cross-sectional study of autopsied HIV-positive (HIV+) cases sex and age-matched to HIV-negative (HIV-) controls. METHODS: Brain large arteries from 302 autopsied cases (50% HIV+) were evaluated morphometrically for the presence of atherosclerosis, size of necrotic core, and fibrous cap thickness. Intima vulnerability was measured as intima elastolytic score [0-5, based on intimal metalloproteinases (MMP)-2, MMP-3, and MMP-9, and tissue inhibitor for MMP-1 and MMP-2 staining], intima inflammatory score (0-3, based on intimal presence of CD3 and CD68 cells and TNF-α staining), neoangiogenesis (factor VIII staining), and apoptosis (caspase 3 staining). Hierarchical generalized linear models were used to obtain the beta estimates and their 95% confidence intervals, adjusting for demographics and vascular risk factors. RESULTS: The prevalence of atherosclerosis did not differ by HIV status. Necrotic cores filled larger proportions of the intima in HIV+ individuals with CD4 cell count above 200 cells/µl at death compared to HIV- controls (adjusted B = 11.6%, P = 0.04). HIV+ individuals had greater elastolytic scores (adjusted B = 0.34, P = 0.02), especially those with less than 200 CD4 cells/µl at death (adjusted B = 0.41, P = 0.01). Intima inflammation, neoangiogenesis, and apoptosis were not different among HIV+ cases versus HIV- controls. CONCLUSION: Individuals with HIV and CD4 cell count at least 200 cells/µl at death had relatively larger necrotic cores, whereas those with HIV and CD4 cell count below 200 cells/µl at death had evidence of increased connective tissue remodeling in the intima. These findings suggest an increased potential for endothelial erosion, thrombosis, and plaque rupture that may relate to higher risk for vascular events.