Our purpose was to evaluate the safety and efficacy of endovascular treatment (EVT) of stroke caused by large vessel occlusions (LVO) performed by general interventional radiologists in cooperation with stroke neurologists and neuroradiologists at a center with a limited annual number of procedures. We aimed to compare our results with those previously reported from larger stroke centers.

Background and Objectives: For using appropriate goal-directed fluid therapy during the surgical conditions of pneumoperitoneum in the reverse Trendelenburg position, we investigated the predictability of various hemodynamic parameters for fluid responsiveness by using a mini-volume challenge test. Materials and Methods: 42 adult patients scheduled for laparoscopic cholecystectomy were enrolled. After general anesthesia was induced, CO2 pneumoperitoneum was applied and the patient was placed in the reverse Trendelenburg position. The mini-volume challenge test was carried out with crystalloid 4 mL/kg over 10 min. Hemodynamic parameters, including stroke volume variation (SVV), cardiac index (CI), stroke volume index (SVI), mean arterial pressure (MAP), and heart rate (HR), were measured before and after the mini-volume challenge test. The positive fluid responsiveness was defined as an increase in stroke volume index ≥10% after the mini-volume challenge. For statistical analysis, a Shapiro-Wilk test was used to test the normality of the data. Continuous variables were compared using an unpaired t-test or the Mann-Whitney rank-sum test. Categorical data were compared using the chi-square test. A receiver operating characteristic curve analysis was used to assess the predictability of fluid responsiveness after the mini-volume challenge. Results: 31 patients were fluid responders. Compared with the MAP and HR, the SVV, CI, and SVI showed good predictability for fluid responsiveness after the mini-volume challenge test (area under the curve was 0.900, 0.833, and 0.909, respectively; all p-values were <0.0001). Conclusions: SVV and SVI effectively predicted fluid responsiveness after the mini-volume challenge test in patients placed under pneumoperitoneum and in the reverse Trendelenburg position.

We know surprisingly little on how heartbeat-evoked responses (HERs) vary with cardiac parameters. Here, we measured both stroke volume, or volume of blood ejected at each heartbeat, with impedance cardiography, and HER amplitude with magneto-encephalography, in 21 male and female participants at rest with eyes open. We observed that HER co-fluctuates with stroke volume on a beat-to-beat basis, but only when no correction for cardiac artifact was performed. This highlights the importance of an ICA correction tailored to the cardiac artifact. We also observed that easy-to-measure cardiac parameters (interbeat intervals, ECG amplitude) are sensitive to stroke volume fluctuations and can be used as proxies when stroke volume measurements are not available. Finally, interindividual differences in stroke volume were reflected in MEG data, but whether this effect is locked to heartbeats is unclear. Altogether, our results question assumptions on the link between stroke volume and HERs.

The insula has been implicated in many sequelae of stroke. It is the area most commonly infarcted in people with post-stroke arrhythmias, loss of thermal sensation, hospital acquired pneumonia, and apraxia of speech. We hypothesized that some of these results reflect the fact that: (1) ischemic strokes that involve the insula are larger than strokes that exclude the insula (and therefore are associated with more common and persistent deficits); and (2) insular involvement is a marker of middle cerebral artery (MCA) occlusion. We analyzed MRI scans of 861 patients with acute ischemic hemispheric strokes unselected for functional deficits, and compared infarcts involving the insula to infarcts not involving the insula using t-tests for continuous variables and chi square tests for dichotomous variables. Mean infarct volume was larger for infarcts including the insula (n = 232) versus excluding the insula (n = 629): 65.8 ± 78.8 versus 10.2 ± 15.9 cm(3) (p < 0.00001). Even when we removed lacunar infarcts, mean volume of non-lacunar infarcts that included insula (n = 775) were larger than non-lacunar infarcts (n = 227) that excluded insula: 67.0 cm(3) ± 79.2 versus 11.5 cm(3) ± 16.7 (p < 0.00001). Of infarcts in the 90th percentile for volume, 87% included the insula (χ(2) = 181.8; p < 0.00001). Furthermore, 79.0% infarcts due to MCA occlusion included the insula; 78.5% of infarcts without MCA occlusion excluded the insula (χ(2) = 93.1; p < 0.0001). The association between insular damage and acute or chronic sequelae likely often reflects the fact that insular infarct is a marker of large infarcts caused by occlusion of the MCA more than a specific role of the insula in a range of functions. Particularly in acute stroke, some deficits may also be due to ischemia of the MCA or ICA territory caused by large vessel occlusion.

Atrial cardiopathy without atrial fibrillation (AF) may be a potential cardiac source of embolic strokes of undetermined source (ESUS). Atrial volume is a feature of atrial cardiopathy, but the relationship between atrial volume and ESUS remains unclear.

Pulse pressure variation (PPV) and stroke volume variation (SVV) are frequently used to assess fluid responsiveness in critically ill patients on mechanical ventilation (MV). There are many factors, in addition to preload that influence the magnitude of these cyclic variations. We sought to investigate the effect of tidal volume (V(T)) on PPV and SVV, and prediction of fluid responsiveness in a model of intra-abdominal hypertension (IAH).

Stroke volume measurement should provide estimates of acute treatment responses. The current pulse contour method estimates left ventricle stroke volume. Heart-lung interactions change right ventricular stroke volume acutely. We investigated the accuracy, precision, and trending abilities of four calibrated stroke volume estimates based on pulmonary artery pulse contour analysis.

Previously, brain volume (BV) and intracranial cerebrospinal fluid volume (CSFV) have been investigated regarding clinical outcomes of subgroups of ischemic stroke patients. This study aimed to examine if the preexisting, preischemic BV and CSFV have an impact on good functional outcome and mortality in acute ischemic stroke (AIS) patients treated with mechanical thrombectomy (MT).

Vertigo is a common presentation of vertebrobasilar stroke. Anecdotal reports have shown that vertigo occurs more often in multiple than in single brainstem or cerebellar infarctions. We examined the relation between the location and volume of infarction and vertigo in patients with vertebrobasilar stroke.

Cardiac output increases during incremental-load exercise to meet metabolic skeletal muscle demand. This response requires a fast adjustment in heart rate and stroke volume. The heart rate is well known to increase linearly with exercise load; however, data for stroke volume during incremental-load exercise are unclear. Our objectives were to (a) review studies that have investigated stroke volume on incremental load exercise and (b) summarize the findings for stroke volume, primarily at maximal-exercise load.

Background: Stroke survivors are at high risk of dementia, associated with increasing age and vascular burden and with pre-existing cognitive impairment, older age. Brain atrophy patterns are recognised as signatures of neurodegenerative conditions, but the natural history of brain atrophy after stroke remains poorly described. We sought to determine whether stroke survivors who were cognitively normal at time of stroke had greater total brain (TBV) and hippocampal volume (HV) loss over 3 years than controls. We examined whether stroke survivors who were cognitively impaired (CI) at 3 months following their stroke had greater brain volume loss than cognitively normal (CN) stroke participants over the next 3 years. Methods: Cognition And Neocortical Volume After Stroke (CANVAS) study is a multi-centre cohort study of first-ever or recurrent adult ischaemic stroke participants compared to age- and sex-matched community controls. Participants were followed with MRI and cognitive assessments over 3 years and were free of a history of cognitive impairment or decline at inclusion. Our primary outcome measure was TBV change between 3 months and 3 years; secondary outcomes were TBV and HV change comparing CI and CN participants. We investigated associations between group status and brain volume change using a baseline-volume adjusted linear regression model with robust standard error. Results: Ninety-three stroke (26 women, 66.7 ± 12 years) and 39 control participants (15 women, 68.7 ± 7 years) were available at 3 years. TBV loss in stroke patients was greater than controls: stroke mean (M) = 20.3 cm3 ± SD 14.8 cm3; controls M = 14.2 cm3 ± SD 13.2 cm3; [adjusted mean difference 7.88 95%CI (2.84, 12.91) p-value = 0.002]. TBV decline was greater in those stroke participants who were cognitively impaired (M = 30.7 cm3; SD = 14.2 cm3) at 3 months (M = 19.6 cm3; SD = 13.8 cm3); [adjusted mean difference 10.42; 95%CI (3.04, 17.80), p-value = 0.006]. No statistically significant differences in HV change were observed. Conclusions: Ischaemic stroke survivors exhibit greater neurodegeneration compared to stroke-free controls. Brain atrophy is greater in stroke participants who were cognitively impaired early after their stroke. Early cognitive impairment was associated greater subsequent atrophy, reflecting the combined impacts of stroke and vascular brain burden. Atrophy rates could serve as a useful biomarker for trials testing interventions to reduce post-stroke secondary neurodegeneration. Clinical Trail Registration: http://www.clinicaltrials.gov, identifier: NCT02205424.

Spleen volume reduction followed by re-expansion has been described in acute ischemic stroke in both animal and human studies. Splenic contraction might be partially due to sympathetic hyperactivity and might be accompanied by release of splenocytes in the peripheral circulation, leading to immunodepression.

Animal studies describe changes in the spleen following a stroke, with an immediate reduction in volume associated with changes in the counts of specific blood white blood cell (WBCs). This brain-spleen cell cycling after stroke affects systemic inflammation and the brain inflammatory milieu and may be a target for emerging therapeutic studies. This study aimed to evaluate features of this brain-spleen model in human patients admitted for acute stroke.

The role of the right hemisphere (RH) in recovery from aphasia is incompletely understood. The present study quantified RH grey matter (GM) volume in individuals with chronic stroke-induced aphasia and cognitively healthy people using voxel-based morphometry. We compared group differences in GM volume in the entire RH and in RH regions-of-interest. Given that lesion site is a critical source of heterogeneity associated with poststroke language ability, we used voxel-based lesion symptom mapping (VLSM) to examine the relation between lesion site and language performance in the aphasic participants. Finally, using results derived from the VLSM as a covariate, we evaluated the relation between GM volume in the RH and language ability across domains, including comprehension and production processes both at the word and sentence levels and across spoken and written modalities. Between-subject comparisons showed that GM volume in the RH SMA was reduced in the aphasic group compared to the healthy controls. We also found that, for the aphasic group, increased RH volume in the MTG and the SMA was associated with better language comprehension and production scores, respectively. These data suggest that the RH may support functions previously performed by LH regions and have important implications for understanding poststroke reorganization.

Lesion volume measurements with magnetic resonance imaging are widely used to assess outcome in rodent models of stroke. In this study, we improved a mathematical framework to correct lesion size for edema which is based on manual delineation of the lesion and hemispheres. Furthermore, a novel MATLAB toolbox to register mouse brain MR images to the Allen brain atlas is presented. Its capability to calculate edema-corrected lesion size was compared to the manual approach. Automated image registration performed equally well in in a mouse middle cerebral artery occlusion model (Pearson r = 0.976, p = 2.265e-11). Information encapsulated in the registration was used to generate maps of edema induced tissue volume changes. These showed discrepancies to simplified tissue models underlying the manual approach. The presented techniques provide biologically more meaningful, voxel-wise biomarkers of vasogenic edema after stroke.

White matter hyperintensities of presumed vascular origin (WMH) are a prevalent form of cerebral small-vessel disease and an important risk factor for post-stroke cognitive dysfunction. Despite this prevalence, it is not well understood how WMH contributes to post-stroke cognitive dysfunction. Preliminary findings suggest that increasing WMH volume is associated with total hippocampal volume in chronic stroke patients. The hippocampus, however, is a complex structure with distinct subfields that have varying roles in the function of the hippocampal circuitry and unique anatomical projections to different brain regions. For these reasons, an investigation into the relationship between WMH and hippocampal subfield volume may further delineate how WMH predispose to post-stroke cognitive dysfunction. In a prospective study of acute ischemic stroke patients with moderate/severe WMH burden, we assessed the relationship between quantitative WMH burden and hippocampal subfield volumes. Patients underwent a 3T MRI brain within 2-5 days of stroke onset. Total WMH volume was calculated in a semi-automated manner. Mean cortical thickness and hippocampal volumes were measured in the contralesional hemisphere. Total and subfield hippocampal volumes were measured using an automated, high-resolution, ex vivo computational atlas. Linear regression analyses were performed for predictors of total and subfield hippocampal volumes. Forty patients with acute ischemic stroke and moderate/severe white matter hyperintensity burden were included in this analysis. Median WMH volume was 9.0 cm3. Adjusting for intracranial volume and stroke laterality, age (β = -3.7, P < 0.001), hypertension (β = -44.7, P = 0.04), WMH volume (β = -0.89, P = 0.049), and mean cortical thickness (β = 286.2, P = 0.006) were associated with total hippocampal volume. In multivariable analysis, age (β = -3.3, P < 0.001) and cortical thickness (β = 205.2, P = 0.028) remained independently associated with total hippocampal volume. In linear regression for predictors of hippocampal subfield volume, increasing WMH volume was associated with decreased hippocampal-amygdala transition area volume (β = -0.04, P = 0.001). These finding suggest that in ischemic stroke patients, increased WMH burden is associated with selective hippocampal subfield degeneration in the hippocampal-amygdala transition area.

The aim of this clinical trial was to investigate changes in stroke volume variability (SVV) and left ventricular end-diastolic volume (LVEDV) after a fluid bolus of crystalloid or colloid using real-time three-dimensional transesophageal echocardiography (3D-TEE) and the Vigileo-FloTrac™ system.

Acute ischemic stroke (AIS) is a common neurological event that causes varying degrees of disability. AIS outcome varies considerably, from complete recovery to complete loss of tissue and function. This diversity is partly explained by the compensatory ability of the collateral circulation and the ensuing cerebral flow grade. The collateral flow to the anterior circulation largely supplies the cortical areas. The deep brain tissue is supplied by penetrating arteries and has little or no collateral supply. Although these brain compartments differ substantially in their collateral supply, there are no published data on the different effects the collateral circulation has on them. In addition, the influence of baseline collateral flow on the final infarct size following endovascular or reperfusion therapies remains unknown. This study was designed to determine the effect of the collateral circulation on cortical infarct volume and deep infarct volume, and to investigate the relation between the collateral grade, response to reperfusion therapy and clinical outcome.

The prediction of infarction volume after stroke onset depends on the shape of the growth dynamics of the infarction. To understand growth patterns that predict lesion volume changes, we studied currently available models described in literature and compared the models with Adaptive Neuro-Fuzzy Inference System [ANFIS], a method previously unused in the prediction of infarction growth and infarction volume (IV). We included 67 patients with malignant middle cerebral artery [MMCA] stroke who underwent decompressive hemicraniectomy. All patients had at least three cranial CT scans prior to the surgery. The rate of growth and volume of infarction measured on the third CT was predicted with ANFIS without statistically significant difference compared to the ground truth [P = 0.489]. This was not possible with linear, logarithmic or exponential methods. ANFIS was able to predict infarction volume [IV3] over a wide range of volume [163.7-600 cm3] and time [22-110 hours]. The cross correlation [CRR] indicated similarity between the ANFIS-predicted IV3 and original data of 82% for ANFIS, followed by logarithmic 70%, exponential 63% and linear 48% respectively. Our study shows that ANFIS is superior to previously defined methods in the prediction of infarction growth rate (IGR) with reasonable accuracy, over wide time and volume range.

There remains a debate whether the ventricular volume within prolapsing mitral valve (MV) leaflets should be included in the left ventricular (LV) end-systolic volume, and therefore factored in LV stroke volume (SV), in cardiac magnetic resonance (CMR) assessments. This study aims to compare LV volumes during end-systolic phases, with and without the inclusion of the volume of blood on the left atrial aspect of the atrioventricular groove but still within the MV prolapsing leaflets, against the reference LV SV by four-dimensional flow (4DF). A total of 15 patients with MV prolapse (MVP) were retrospectively enrolled in this study. We compared LV SV with (LV SVMVP) and without (LV SVstandard) MVP left ventricular doming volume, using 4D flow (LV SV4DF) as the reference value. Significant differences were observed when comparing LV SVstandard and LV SVMVP (p < 0.001), and between LV SVstandard and LV SV4DF (p = 0.02). The Intraclass Correlation Coefficient (ICC) test demonstrated good repeatability between LV SVMVP and LV SV4DF (ICC = 0.86, p < 0.001) but only moderate repeatability between LV SVstandard and LV SV4DF (ICC = 0.75, p < 0.01). Calculating LV SV by including the MVP left ventricular doming volume has a higher consistency with LV SV derived from the 4DF assessment. In conclusion, LV SV short-axis cine assessment incorporating MVP dooming volume can significantly improve the precision of LV SV assessment compared to the reference 4DF method. Hence, in cases with bi-leaflet MVP, we recommend factoring in MVP dooming into the left ventricular end-systolic volume to improve the accuracy and precision of quantifying mitral regurgitation.