In vivo quantification of hyperoxic arterial blood water T-1

Normocapnic hyperoxic and hypercapnic hyperoxic gas challenges are increasingly being used in cerebrovascular reactivity (CVR) and calibrated functional MRI experiments. The longitudinal arterial blood water relaxation time (T-1a) change with hyperoxia will influence signal quantification through mechanisms relating to elevated partial pressure of plasma-dissolved O-2 (pO(2)) and increased oxygen bound to hemoglobin in arteries (Y-a) and veins (Y-v). The dependence of T-1a on Y-a and Y-v has been elegantly characterized ex vivo; however, the combined influence of pO(2), Y-a and Y-v on T(1a)in vivo under normal ventilation has not been reported. Here, T-1a is calculated during hyperoxia in vivo by a heuristic approach that evaluates T-1-dependent arterial spin labeling (ASL) signal changes to varying gas stimuli. Healthy volunteers (n=14; age, 31.5 +/- 7.2years) were scanned using pseudo-continuous ASL in combination with room air (RA; 21% O-2/79% N-2), hypercapnic normoxic (HN; 5% CO2/21% O-2/74% N-2) and hypercapnic hyperoxic (HH; 5% CO2/95% O-2) gas administration. HH T-1a was calculated by requiring that the HN and HH cerebral blood flow (CBF) change be identical. The HH protocol was then repeated in patients (n=10; age, 61.4 +/- 13.3years) with intracranial stenosis to assess whether an HH T-1a decrease prohibited ASL from being performed in subjects with known delayed blood arrival times. Arterial blood T-1a decreased from 1.65s at baseline to 1.49 +/- 0.07s during HH. In patients, CBF values in the affected flow territory for the HH condition were increased relative to baseline CBF values and were within the physiological range (RA CBF=36.6 +/- 8.2mL/100g/min; HH CBF=45.2 +/- 13.9mL/100g/min). It can be concluded that hyperoxic (95% O-2) 3-T arterial blood T-1aHH=1.49 +/- 0.07s relative to a normoxic T-1a of 1.65s. Copyright (c) 2015 John Wiley & Sons, Ltd

In vivo quantification of hyperoxic arterial blood water T-1

Normocapnic hyperoxic and hypercapnic hyperoxic gas challenges are increasingly being used in cerebrovascular reactivity (CVR) and calibrated functional MRI experiments. The longitudinal arterial blood water relaxation time (T-1a) change with hyperoxia will influence signal quantification through mechanisms relating to elevated partial pressure of plasma-dissolved O-2 (pO(2)) and increased oxygen bound to hemoglobin in arteries (Y-a) and veins (Y-v). The dependence of T-1a on Y-a and Y-v has been elegantly characterized ex vivo; however, the combined influence of pO(2), Y-a and Y-v on T(1a)in vivo under normal ventilation has not been reported. Here, T-1a is calculated during hyperoxia in vivo by a heuristic approach that evaluates T-1-dependent arterial spin labeling (ASL) signal changes to varying gas stimuli. Healthy volunteers (n=14; age, 31.5 +/- 7.2years) were scanned using pseudo-continuous ASL in combination with room air (RA; 21% O-2/79% N-2), hypercapnic normoxic (HN; 5% CO2/21% O-2/74% N-2) and hypercapnic hyperoxic (HH; 5% CO2/95% O-2) gas administration. HH T-1a was calculated by requiring that the HN and HH cerebral blood flow (CBF) change be identical. The HH protocol was then repeated in patients (n=10; age, 61.4 +/- 13.3years) with intracranial stenosis to assess whether an HH T-1a decrease prohibited ASL from being performed in subjects with known delayed blood arrival times. Arterial blood T-1a decreased from 1.65s at baseline to 1.49 +/- 0.07s during HH. In patients, CBF values in the affected flow territory for the HH condition were increased relative to baseline CBF values and were within the physiological range (RA CBF=36.6 +/- 8.2mL/100g/min; HH CBF=45.2 +/- 13.9mL/100g/min). It can be concluded that hyperoxic (95% O-2) 3-T arterial blood T-1aHH=1.49 +/- 0.07s relative to a normoxic T-1a of 1.65s. Copyright (c) 2015 John Wiley & Sons, Ltd

The Cumulative Influence of Hyperoxia and Hypercapnia on Blood Oxygenation and R2

Cerebrovascular reactivity (CVR)-weighted blood-oxygenation-level-dependent magnetic resonance imaging (BOLD-MRI) experiments are frequently used in conjunction with hyperoxia. Owing to complex interactions between hyperoxia and hypercapnia, quantitative effects of these gas mixtures on BOLD responses, blood and tissue R-2*, and blood oxygenation are incompletely understood. Here we performed BOLD imaging (3 T; TE/TR = 35/2,000 ms; spatial resolution = 3 x 3 x 3.5 mm(3)) in healthy volunteers (n = 12; age = 29 +/- 4.1 years) breathing (i) room air (RA), (ii) normocapnic-hyperoxia (95% O-2/5% N-2, HO), (iii) hypercapnic-normoxia (5% CO2/21% O-2/74% N-2, HC-NO), and (iv) hypercapnic-hyperoxia (5% CO2/95% O-2, HC-HO). For HC-HO, experiments were performed with separate RA and HO baselines to control for changes in O2. T-2-relaxation-under-spin-tagging MRI was used to calculate basal venous oxygenation. Signal changes were quantified and established hemodynamic models were applied to quantify vasoactive blood oxygenation, blood-water R-2(*), and tissue-water R-2*. In the cortex, fractional BOLD changes (stimulus/baseline) were HO/RA = 0.011 +/- 0.007; HC-NO/RA = 0.014 +/- 0.004; HC-HO/HO = 0.020 +/- 0.008; and HC-HO/RA = 0.035 +/- 0.010; for the measured basal venous oxygenation level of 0.632, this led to venous blood oxygenation levels of 0.660 (HO), 0.665 (HC-NO), and 0.712 (HC-HO). Interleaving a HC-HO stimulus with HO baseline provided a smaller but significantly elevated BOLD response compared with a HC-NO stimulus. Results provide an outline for how blood oxygenation differs for several gas stimuli and provides quantitative information on how hypercapnic BOLD CVR and R-2(*) are altered during hyperoxia

Language discordance as a marker of disparities in cerebrovascular risk and stroke outcomes: A multi-center Canadian study

Background: Differences in ischemic stroke outcomes occur in those with limited English proficiency. These health disparities might arise when a patient's spoken language is discordant from the primary language utilized by the health system. Language concordance is an understudied concept. We examined whether language concordance is associated with differences in vascular risk or post-stroke functional outcomes, depression, obstructive sleep apnea and cognitive impairment. Methods: This was a multi-center observational cross-sectional cohort study. Patients with ischemic stroke/transient ischemic attack (TIA) were consecutively recruited across eight regional stroke centers in Ontario, Canada (2012 – 2018). Participants were language concordant (LC) if they spoke English as their native language, ESL if they used English as a second language, or language discordant (LD) if non-English speaking and requiring translation. Results: 8156 screened patients. 6,556 met inclusion criteria: 5067 LC, 1207 ESL and 282 LD. Compared to LC patients: (i) ESL had increased odds of diabetes (OR = 1.28, p = 0.002), dyslipidemia (OR = 1.20, p = 0.007), and hypertension (OR = 1.37, p<0.001) (ii) LD speaking patients had an increased odds of having dyslipidemia (OR = 1.35, p = 0.034), hypertension (OR = 1.37, p<0.001), and worse functional outcome (OR = 1.66, p<0.0001). ESL (OR = 1.88, p<0.0001) and LD (OR = 1.71, p<0.0001) patients were more likely to have lower cognitive scores. No associations were noted with obstructive sleep apnea (OSA) or depression. Conclusions: Measuring language concordance in stroke/TIA reveals differences in neurovascular risk and functional outcome among patients with limited proficiency in the primary language of their health system. Lower cognitive scores must be interpreted with caution as they may be influenced by translation and/or greater vascular risk. Language concordance is a simple, readily available marker to identify those at risk of worse functional outcome. Stroke systems and practitioners must now study why these differences exist and devise adaptive care models, treatments and education strategies to mitigate barriers influenced by language discordance