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The origin of the directional sensitivity (DS) of dynamic cerebral autoregulation (dCA) is not known. In 140 healthy participants (67 male, 27.5 ± 6.1 yr old), middle cerebral artery velocity (MCAv, transcranial Doppler), arterial blood pressure (ABP, Finometer), and end-tidal CO2 (EtCO2, capnography) were recorded at rest. Critical closing pressure (CrCP) and resistance-area product (RAP) were obtained for each cardiac cycle, as well as mean MCAv and ABP (MAP). The integrated positive and negative derivatives of MAP (MAP+D and MAP−D, respectively) were used as simultaneous inputs to an autoregressive moving average model to generate two distinct MCAv step responses. Similar models allowed the estimation of corresponding MAP-CrCP and MAP-RAP responses to step changes in MAP+D and MAP−D. The strength of DS (ΔDS) was expressed by the difference in mean values of the step responses for the time interval 12–18 s. ΔDS was significant for MCAv (8.5 ± 46.9% vs. 26.7 ± 42.0%, P < 0.001) and RAP (−93.9 ± 48.1 vs. −74.5 ± 43.0%, P < 0.001), respectively, for MAP+D and MAP−D inputs, but not for CrCP (2.2 ± 48.1% vs. 0.72 ± 42.9%, P = 0.76). Compared with males, female participants had higher MCAv (63.9 ± 15.6 cm/s vs. 55.4 ± 12.9 cm/s, P < 0.001) but lower EtCO2 (P < 0.001) and RAP (P = 0.015). Sex did not influence ΔDS for any of the three-step responses. The presence of directional sensitivity in the RAP, but not in the CrCP transfer function, suggests that the origin could be solely myogenic, without metabolic involvement. NEW & NOTEWORTHY: The directional sensitivity of the cerebral blood velocity response to a sudden change in mean arterial blood pressure (MAP) is mediated by the resistance-area product, without involvement from the cerebral critical closing pressure. The reduced amplitude of MAP spontaneous fluctuations at rest suggests that it is less likely that directional sensitivity has origins in the sympathetic control of cerebral blood vessels, thus generating the need to consider other alternatives. [ABSTRACT FROM AUTHOR]

Background: Cerebral small vessel disease (CSVD) causes between 25% and 30% of all ischemic strokes. In acute lacunar ischemic stroke, despite often mild initial symptoms, early neurological deterioration (END) occurs in approximately 15–20% of patients and is associated with poor functional outcome, yet its mechanisms are not well understood. Aims: In this review, we systematically evaluated data on: (1) definitions and incidence of END, (2) mechanisms of small vessel occlusion, (3) predictors and mechanisms of END, and (4) prospects for the prevention or treatment of patients with END. Summary of review: We identified 67 reports (including 13,407 participants) describing the incidence of END in acute lacunar ischemic stroke. The specified timescale for END varied from <24 h to 3 weeks. The rate of END ranged between 2.3% and 47.5% with a pooled incidence of 23.54% (95% confidence interval (CI) = 21.02–26.05) but heterogeneity was high (I 2 = 90.29%). The rates of END defined by National Institutes of Health Stroke Scale (NIHSS) decreases of ⩾1, ⩾2, ⩾3, and 4 points were as follows: 24.17 (21.19–27.16)%, 22.98 (20.48–25.30)%, 23.33 (16.23–30.42)%, and 10.79 (2.09–23.13)%, respectively, with lowest heterogeneity and greatest precision for a cutoff of ⩾2 points. Of the 20/67 studies (30%) reporting associations of END with clinical outcome, 19/20 (95%) reported worse outcomes (usually measured using the modified Rankin score at 90 days or at hospital discharge) in patients with END. In a meta-regression analysis, female sex, hypertension, diabetes, and smoking were associated with END. Conclusions: END occurs in more than 20% of patients with acute lacunar ischemic stroke and might provide a novel target for clinical trials. A definition of an NIHSS ⩾2 decrease is most used and provides the best between-study homogeneity. END is consistently associated with poor functional outcome. Further research is needed to better identify patients at risk of END, to understand the underlying mechanisms, and to carry out new trials to test potential interventions. [ABSTRACT FROM AUTHOR]

Introduction: People with HIV (PWH) are at an increased risk of developing cardiovascular disease (CVD) compared to HIV‐negative individuals. We sought to evaluate the adherence to medications for CVD in PWH and identify factors associated with non‐adherence to these medications. Methods: We conducted a cross‐sectional study at the University Hospitals of Leicester NHS Trust between 16 April 2019 and 8 November 2022. We recruited consecutive PWH, who were attending a routine follow‐up outpatient appointment and were prescribed at least one medication for CVD. In addition, we included urinary adherence results of patients with samples collected as part of routine clinical care. We used liquid chromatography–tandem mass spectrometry (LC–MS/MS) to assess if their prescribed medications (antihypertensives, diuretics, beta‐blockers, lipid‐lowering agents, antiplatelets, anticoagulants, antidiabetic medications) were present in the participant's urine sample. Multivariable models were used to identify demographic or clinical features that were associated with non‐adherence. Results: A total of 162 PWH were included in the analysis. Median age was 55 [interquartile range (IQR): 50–61] years, 63% were male, average time living with HIV was 15 years (IQR: 11–19) and the majority (98%) had an undetectable HIV viral load. In approximately one‐third of patients (59/162), at least one prescribed medication of interest was not detected in urine. Non‐adherence to lipid‐lowering agents was common (35/88, 40%). On multivariable logistic regression, the number of prescribed cardiovascular medications, was associated with medication non‐adherence [medication non‐adherence, per one medication increase: adjusted odds ratio (95% confidence interval) = 1.78 (1.34–2.36); p < 0.001]. Conclusion: We found sub‐optimal adherence to medications for CVD in PWH. In order to maximize the clinical benefit of statin therapy in PWH, factors requiring consideration include: improved medication adherence, awareness of polypharmacy, educational interventions and quantitative assessment of sub‐optimal adherence through chemical adherence testing. [ABSTRACT FROM AUTHOR]

Arterial carbon dioxide ( Pa CO 2 ) and posture influence the middle (MCAv) and posterior (PCAv) cerebral artery blood velocities, but there is paucity of data about their interaction and need for an integrated model of their effects, including dynamic cerebral autoregulation (dCA). In 22 participants (11 males, age 30.2 ± 14.3 yr), blood pressure (BP, Finometer), dominant MCAv and nondominant PCAv (transcranial Doppler ultrasound), end-tidal CO2 (EtCO2, capnography), and heart rate (HR, ECG) were recorded continuously. Two recordings (R) were taken when the participant was supine (R1, R2), two taken when the participant was sitting (R3, R4), and two taken when the participant was standing (R5, R6). R1, R3, and R5 consisted of 3 min of 5% CO2 through a mask and R2, R4, and R6 consisted of 3 min of paced hyperventilation. The effects of Pa CO 2 were expressed with a logistic curve model (LCM) for each parameter. dCA was expressed by the autoregulation index (ARI), derived by transfer function analysis. Standing shifted LCM to the left for MCAv (P < 0.001), PCAv (P < 0.001), BP (P = 0.03), and ARI (P = 0.001); downward for MCAv and PCAv (both P < 0.001), and upward for HR (P < 0.001). For BP, LCM was shifted downward by sitting and standing (P = 0.024). For ARI, the hypercapnic range of LCM was shifted upward during standing (P < 0.001). A more complete mapping of the combined effects of posture and arterial CO2 on the cerebral circulation and peripheral variables can be obtained with the LCM over a broad physiological range of EtCO2 values. NEW & NOTEWORTHY: Data from supine, sitting, and standing postures were measured. Modeling the data with logistic curves to express the effects of CO2 reactivity on middle cerebral artery blood velocity (MCAv), posterior cerebral artery blood velocity (PCAv), heart rate, blood pressure (BP), and the autoregulation index (ARI), provided a more comprehensive approach to study the interaction of arterial CO2 with posture than in previous studies. Above all, shifts of the logistic curve model with changes in posture have shown interactions with Pa CO 2 that have not been previously demonstrated. [ABSTRACT FROM AUTHOR]

Previous studies report contradicting age‐related neurovascular coupling (NVC). Few studies assess postural effects, but less investigate relationships between age and NVC within different postures. Therefore, this study investigated the effect of age on NVC in different postures with varying cognitive stimuli. Beat‐to‐beat blood pressure, heart rate and end‐tidal carbon dioxide were assessed alongside middle and posterior cerebral artery velocities (MCAv and PCAv, respectively) using transcranial Doppler ultrasonography in 78 participants (31 young‐, 23 middle‐ and 24 older‐aged) with visuospatial (VST) and attention tasks (AT) in various postures at two timepoints (T2 and T3). Between‐group significance testing utilized one‐way analysis‐of‐variance (ANOVA) (Tukey post‐hoc). Mixed three‐way/one‐way ANOVAs explored task, posture, and age interactions. Significant effects of posture on NVC were driven by a 3.8% increase from seated to supine. For AT, mean supine %MCAv increase was greatest in younger (5.44%) versus middle (0.12%) and older‐age (0.09%) at T3 (p = 0.005). For VST, mean supine %PCAv increase was greatest at T2 and T3 in middle (10.99%/10.12%) and older‐age (17.36%/17.26%) versus younger (9.44%/8.89%) (p = 0.004/p = 0.002). We identified significant age‐related NVC effects with VST‐induced hyperactivation. This may reflect age‐related compensatory processes in supine. Further work is required, using complex stimuli while standing/walking, examining NVC, aging and falls. [ABSTRACT FROM AUTHOR]

The article discusses the importance of cerebrovascular reactivity (CVR) in regulating cerebral blood flow (CBF) and its implications for cognitive processes and brain homeostasis. Various methods, such as transcranial Doppler ultrasound and functional magnetic resonance imaging, are used to measure CVR, with a focus on assessing intracranial and extracranial artery dilation in response to vasodilatory stimuli. Studies have shown that impaired CVR is associated with increased mortality risk and can serve as a prognostic indicator for conditions like small vessel disease and stroke. However, the lack of standardized protocols and diverse research approaches make it challenging to draw definitive conclusions from existing studies, highlighting the need for more consistent methodologies and further research in this area. [Extracted from the article]

Prior studies have identified variable effects of aging on neurovascular coupling (NVC). Carbon dioxide (CO2) affects both cerebral blood velocity (CBv) and NVC, but the effects of age on NVC under different CO2 conditions are unknown. Therefore, we investigated the effects of aging on NVC in different CO2 states during cognitive paradigms. Seventy-eight participants (18–78 yr), with well-controlled comorbidities, underwent continuous recordings of CBv by bilateral insonation of middle (MCA) and posterior (PCA) cerebral arteries (transcranial Doppler), blood pressure, end-tidal CO2, and heart rate during poikilocapnia, hypercapnia (5% CO2 inhalation), and hypocapnia (paced hyperventilation). Neuroactivation via visuospatial (VS) and attention tasks (AT) was used to stimulate NVC. Peak percentage and absolute change in MCAv/PCAv, were compared between CO2 conditions and age groups (≤30, 31–60, and >60 yr). For the VS task, in poikilocapnia, younger adults had a lower NVC response compared with older adults [mean difference (MD): −7.92% (standard deviation (SD): 2.37), P = 0.004], but comparable between younger and middle-aged groups. In hypercapnia, both younger [MD: −4.75% (SD: 1.56), P = 0.009] and middle [MD: −4.58% (SD: 1.69), P = 0.023] age groups had lower NVC responses compared with older adults. Finally, in hypocapnia, both older [MD: 5.92% (SD: 2.21), P = 0.025] and middle [MD: 5.44% (SD: 2.27), P = 0.049] age groups had greater NVC responses, compared with younger adults. In conclusion, the magnitude of NVC response suppression from baseline during hyper- and hypocapnia, did not differ significantly between age groups. However, the middle age group demonstrated a different NVC response while under hypercapnic conditions, compared with hypocapnia. NEW & NOTEWORTHY: This study describes the effects of age on neurovascular coupling under altered CO2 conditions. We demonstrated that both hypercapnia and hypocapnia suppress neurovascular coupling (NVC) responses. Furthermore, that middle age exhibits an NVC response comparable with younger adults under hypercapnia, and older adults under hypocapnia. [ABSTRACT FROM AUTHOR]