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INTRODUCTION AND OBJECTIVES: The association between non-alcoholic fatty liver disease and cerebral hemodynamics arises from cardiovascular damage mechanisms such as endothelial dysfunction, arterial wall increased stiffness, high thickness of the intimate index of the internal carotid artery, left ventricular hypertrophy, left diastolic dysfunction, calcification coronary arteries and increased epicardial fat. The multidirectional relationship between systemic inflammation and lipid metabolism constitutes a common and simultaneous mechanism that causes vascular damage. This study aims to provide insight into the relationship between non-alcoholic fatty liver disease and the function of systemic circulation and cerebral circulation using Doppler ultrasound. PATIENTS AND METHODS: Is an observational, cross-sectional, prospective, comparative study conducted at Medica Sur Hospital. Thirty-five patients were selected consecutively. The patients consulted neurological service for various symptoms without severity criteria, such as vertigo, primary headache and balance disturbances. RESULTS: There is a difference in the variables mean of the right MCA PI (p = 0.023), left MCA PI" (p = 0.004), and left VA PI (p = 0.036) between the control and NAFLD groups. The correlation analysis between these variables and the CAP showed a positive correlation of the three variables with the CAP, "right MCA PI" (r = 0.384), left MCA PI "(r = 0.509) and" left VA PI " (r = 0.551). CONCLUSIONS: This study demonstrates a subclinical process of the middle cerebral artery in subjects with NAFLD, which suggests it may be involved in the disease development and points the need to make decisions for this liver manifestation prevention and treatment.

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BACKGROUND: Impairment of vasodilatory capacity reflecting reduced cerebrovascular reserve was previously shown in adults with sickle cell disease (SCD) and might play a role in the pathophysiology of stroke in such patients. We examined the hypothesis that children with SCD would also have a higher frequency of impaired cerebral vasoreactivity when compared with healthy age- and gender-matched controls. METHODS: Patients were recruited from our hematology outpatient clinic. All SCD patients aged 10-18 years without a history of symptomatic stroke as well as age- and gender-matched healthy children were evaluated with transcranial Doppler (TCD) ultrasonography, with breath-holding maneuver. Breath-holding index (BHI) was calculated by dividing the percentage increase in mean flow velocity occurring during breath holding by the length of time subjects hold their breath after a normal inspiration. BHI was considered abnormal if less than .69. RESULTS: TCD was performed in 42 patients (mean age 12.7 ± 2.2 years) and 20 controls (mean age 13.90 ± 3.04 years). Blood flow velocities were higher in patients with SCD than in controls in all arteries evaluated (P < .001). BHI values in patients with SCD were significantly lower than in control subjects (1.27 ± .65 versus 1.74 ± .15, P = .013 on the left and 1.16 ± .45 versus 1.61 ± .11, P = .002 on the right). BHI was abnormal in 19% of the patients and in none of the controls, P = .036. CONCLUSIONS: Children with SCD may have impaired cerebral vasoreactivity, with low BHI values suggesting a reduced autoregulation capacity.

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This study investigated the association of nutritional and haematological variables with maximum time-averaged mean velocity (TAMV) measured by transcranial Doppler (TCD) velocity and the agreement of classification between two protocols. TCD categories included: normal (<170 cm/s), conditional (170-199 cm/s) and abnormal (≥200 cm/s) based on TAMV in distal internal carotid artery (dICA), middle cerebral artery (MCA), internal carotid bifurcation, anterior and posterior cerebral arteries. Of 358 children with sickle cell anaemia (SCA) examined, the mean age (±standard deviation) was 7·4 ± 2·7 years; 13·1% and 6·7% had conditional and abnormal velocities, respectively. Children with abnormal TCD velocities had higher prevalence of prior stroke (P = 0·006). Increased TAMV was associated with younger age (P = 0·001), lower weight (P = 0·001), height (P = 0·007) and oxygen saturation (P = 0·005). There was no association of TAMV with height-age or body mass index (BMI) z-scores. Adjusting for gender, BMI z-score, age, previous stroke and oxygen saturation, mean corpuscular volume (P = 0·005) and reticulocyte count (P = 0·013) were positively associated with TAMV, while haemoglobin concentration (P = 0·009) was negatively associated. There was good agreement [99%; weighted Kappa 0·98 (95% confidence interval 0·89-1), P = 0·0001] in TCD classification using data from five vessels versus two vessels (dICA and MCA). Haematological variables, rather than nutritional status, may be useful markers that identify high-risk children with SCA.

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This study aimed to investigate the protective effect of salvinorin A on the cerebral pial artery after forebrain ischemia and explore related mechanisms. Thirty Sprague-Dawley rats received forebrain ischemia for 10 min. The dilation responses of the cerebral pial artery to hypercapnia and hypotension were assessed in rats before and 1 h after ischemia. The ischemia reperfusion (IR) control group received DMSO (1 µL/kg) immediately after ischemia. Two different doses of salvinorin A (10 and 20 µg/kg) were administered following the onset of reperfusion. The 5th, 6th, and 7th groups received salvinorin A (20 µg/kg) and LY294002 (10 µM), L-NAME (10 µM), or norbinaltorphimine (norBIN, 1 µM) after ischemia. The levels of cGMP in the cerebrospinal fluid (CSF) were also measured. The phosphorylation of AKT (p-AKT) was measured in the cerebral cortex by western blot at 24 h post-ischemia. Cell necrosis and apoptosis were examined by hematoxylin-eosin staining (HE) and TUNEL staining, respectively. The motor function of the rats was evaluated at 1, 2, and 5 days post-ischemia. The dilation responses of the cerebral pial artery were significantly impaired after ischemia and were preserved by salvinorin A treatment. In addition, salvinorin A significantly increased the levels of cGMP and p-AKT, suppressed cell necrosis and apoptosis of the cerebral cortex and improved the motor function of the rats. These effects were abolished by LY294002, L-NAME, and norBIN. Salvinorin A preserved cerebral pial artery autoregulation in response to hypercapnia and hypotension via the PI3K/AKT/cGMP pathway.

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This study aimed to investigate the protective effect of salvinorin A on the cerebral pial artery after forebrain ischemia and explore related mechanisms. Thirty Sprague-Dawley rats received forebrain ischemia for 10 min. The dilation responses of the cerebral pial artery to hypercapnia and hypotension were assessed in rats before and 1 h after ischemia. The ischemia reperfusion (IR) control group received DMSO (1 µL/kg) immediately after ischemia. Two different doses of salvinorin A (10 and 20 µg/kg) were administered following the onset of reperfusion. The 5th, 6th, and 7th groups received salvinorin A (20 µg/kg) and LY294002 (10 µM), L-NAME (10 μM), or norbinaltorphimine (norBIN, 1 μM) after ischemia. The levels of cGMP in the cerebrospinal fluid (CSF) were also measured. The phosphorylation of AKT (p-AKT) was measured in the cerebral cortex by western blot at 24 h post-ischemia. Cell necrosis and apoptosis were examined by hematoxylin-eosin staining (HE) and TUNEL staining, respectively. The motor function of the rats was evaluated at 1, 2, and 5 days post-ischemia. The dilation responses of the cerebral pial artery were significantly impaired after ischemia and were preserved by salvinorin A treatment. In addition, salvinorin A significantly increased the levels of cGMP and p-AKT, suppressed cell necrosis and apoptosis of the cerebral cortex and improved the motor function of the rats. These effects were abolished by LY294002, L-NAME, and norBIN. Salvinorin A preserved cerebral pial artery autoregulation in response to hypercapnia and hypotension via the PI3K/AKT/cGMP pathway.

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RATIONALE: The role of hypertension in cerebral small vessel disease is poorly understood. At the base of the brain (the 'vascular centrencephalon'), short straight arteries transmit blood pressure directly to small resistance vessels; the cerebral convexity is supplied by long arteries with many branches, resulting in a drop in blood pressure. Hypertensive small vessel disease (lipohyalinosis) causes the classically described lacunar infarctions at the base of the brain; however, periventricular white matter intensities (WMIs) seen on MRI and WMI in subcortical areas over the convexity, which are often also called 'lacunes', probably have different aetiologies. OBJECTIVES: We studied pressure gradients from proximal to distal regions of the cerebral vasculature by mathematical modelling. METHODS AND RESULTS: Blood flow/pressure equations were solved in an Anatomically Detailed Arterial Network (ADAN) model, considering a normotensive and a hypertensive case. Model parameters were suitably modified to account for structural changes in arterial vessels in the hypertensive scenario. Computations predict a marked drop in blood pressure from large and medium-sized cerebral vessels to cerebral peripheral beds. When blood pressure in the brachial artery is 192/113 mm Hg, the pressure in the small arterioles of the posterior parietal artery bed would be only 117/68 mm Hg. In the normotensive case, with blood pressure in the brachial artery of 117/75 mm Hg, the pressure in small parietal arterioles would be only 59/38 mm Hg. CONCLUSION: These findings have important implications for understanding small vessel disease. The marked pressure gradient across cerebral arteries should be taken into account when evaluating the pathogenesis of small WMIs on MRI. Hypertensive small vessel disease, affecting the arterioles at the base of the brain should be distinguished from small vessel disease in subcortical regions of the convexity and venous disease in the periventricular white matter.

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Fluid-structure interaction simulations of three patient-specific models of cerebral aneurysms were carried out with the objective of quantifying the effects of non-Newtonian blood flow and the vessel mechanical behavior on the time-dependent fluid shear and normal stresses, and structural stress and stretch. The average wall shear stress at peak systole was found to be approximately one order of magnitude smaller than the shear stresses in the proximal communicating arteries, regardless of the shape or size of the aneurysms. Spatial distributions of oscillatory shear index were consistent with the reciprocal of wall shear stress distributions at peak systole for all aneurysm geometries, demonstrating that oscillatory shear index correlates inversely with wall shear at this time point in the cardiac cycle. An aneurysm wall modeled with an isotropic material resulted in an underestimation of both the maximum principal stress and stretch, compared to the anisotropic material model. For the three aneurysm geometries, anisotropic peak wall stresses were approximately 50% higher than for an isotropic material. Regardless of the constitutive material, the maximum stresses were consistently located at the aneurysm neck; stresses in the dome were 30% of those in the neck.

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Assessment of the fetal cerebral circulation provides important information on the hemodynamic changes associated with chronic hypoxia and intrauterine growth restriction. Despite the incorporation of new US parameters, the landmark for the fetal brain hemodynamic evaluation is still the middle cerebral artery. However, new vascular territories, such as the anterior and posterior cerebral arteries, might provide additional information on the onset of the brain sparing effect. The fractional moving blood volume estimation and three-dimensional power Doppler ultrasound indices are new techniques that seem to be promising in identifying cases at earlier stages of vascular deterioration; still, they are not available for clinical application and more information is needed on the reproducibility and advantages of three-dimensional power Doppler ultrasound blood flow indices. In the past, the brain sparing effect was considered as a protective mechanism; however, recent information challenges this concept. There is growing evidence of an association between brain sparing effect and increased risk of abnormal neurodevelopment after birth. Even in mild late-onset intrauterine growth restriction affected fetuses with normal umbilical artery blood flow, increased cerebral blood perfusion can be associated with a substantial risk of abnormal neuroadaptation and neurodevelopment during childhood.

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OBJECTIVE: To evaluate cerebral blood flow abnormalities in primary antiphospholipid syndrome (PAPS) patients without ongoing neurological manifestations. PATIENTS AND METHODS: We included 28 PAPS patients and 28 healthy controls. Carotid Doppler ultrasound, and echocardiographic evaluation were done. Transcranial Doppler ultrasonography measured mean flow velocity (MFV) in the carotid siphon, middle, anterior, posterior, intracranial vertebral arteries, and basilar artery (11 cerebral arteries). Results were considered abnormal when the MFV was out of the normal range according to age and/or flow asymmetry and/or more than four arterial segments affected. RESULTS: The mean age of patients was 41.4 ± 11.2 and 39.3 ± 8.6 years in controls. Disease duration was 11 ± 2.7 years. A significant increase in MFV in 7/11 cerebral arteries in PAPS patients, mainly in the middle and anterior cerebral arteries was found compared with controls. A significant association between lupus anticoagulant, history of stroke and obesity with a greater number of affected arteries was found. We did not find an association between MFV and abnormal echocardiography, arterial hypertension and carotid intima-media thickness. CONCLUSIONS: Asymptomatic patients with PAPS can have significantly increased MFVs. These alterations may be the consequence of accelerated atherosclerosis, PAPS vasculopathy or both. Whatever the cause, these findings can represent a risk for stroke in PAPS patients that needs the trial of other therapeutic options.

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Objective: To evaluate longitudinal changes in the cardiac function parameters in relation to the hemodynamic worsening in growth restricted (IUGR) fetuses. Methods: The cardiac function was serially studied in a cohort of 46 IUGR fetuses below 32 weeks of gestation by 2-D and Doppler ultrasound parameters. IUGR was defined as an estimated fetal weight below the 10th percentile with a Doppler pulsatility index (PI) in the umbilical artery (UA) above 2 standard deviations of the mean. Longitudinal changes, perinatal deaths and survivors were evaluated. Results: All cardiac parameters were significantly different in IUGR fetuses. Aortic isthmus blood flow index (IFI) and Modified myocardial performance index (Mod-MPI) showed the clearest longitudinal changes and temporal deterioration. Conclusions: IFI and Mod-MPI showed consistent longitudinal changes in IUGR fetuses. These 2 markers could be added to the DV to evaluate the fetal deterioration and indicate the optimal time of delivery.

Objetivo: Evaluar cambios longitudinales de los parámetros de función cardíaca en relación al agravamiento hemodinámico en fetos con restricción del crecimiento intrauterino (RCIU). Métodos: La función cardíaca fue estudiada en una cohorte de 46 fetos RCIU con menos de 32 semanas de gestación con parámetros 2-D y ultrasonografía Doppler. Se definió RCIU como un peso fetal estimado bajo el percentil 10 asociado a un índice de pulsatilidad (IP) al Doppler de la arteria umbilical (AU) por debajo de dos desviaciones estándar del promedio. Se evaluaron cambios longitudinales, mortalidad y sobrevida perinatal. Resultados: Todos los parámetros tuvieron diferencias estadísticamente significativas en fetos RCIU. El índice de velocidad de flujo del istmo aórtico (IFI) y el índice de función miocárdico modificado (IFM-mod) mostraron los más evidentes cambios longitudinales y deterioro en el tiempo. Conclusiones: El IFI y el IFM-mod mostraron consistentes cambios longitudinales en fetos RCIU. Estos dos marcadores podrían ser usados junto a la medición del ductus venoso para evaluar el deterioro fetal y la indicación óptima del momento del parto.

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