Mechanistic insights on age-related changes in heart-aorta-brain hemodynamic coupling using a pulse wave model of the entire circulatory system.

Age-related changes in aortic biomechanics can impact the brain by reducing blood flow and increasing pulsatile energy transmission. Clinical studies have shown that impaired cardiac function in patients with heart failure is associated with cognitive impairment. Although previous studies have attempted to elucidate the complex relationship between age-associated aortic stiffening and pulsatility transmission to the cerebral network, they have not adequately addressed the effect of interactions between aortic stiffness and left ventricle (LV) contractility (neither on energy transmission nor on brain perfusion). In this study, we use a well-established and validated one-dimensional blood flow and pulse wave computational model of the circulatory system to address how age-related changes in cardiac function and vasculature affect the underlying mechanisms involved in the LV-aorta-brain hemodynamic coupling. Our results reveal how LV contractility affects pulsatile energy transmission to the brain, even with preserved cardiac output. Our model demonstrates the existence of an optimal heart rate (near the normal human heart rate) that minimizes pulsatile energy transmission to the brain at different contractility levels. Our findings further suggest that the reduction in cerebral blood flow at low levels of LV contractility is more prominent in the setting of age-related aortic stiffening. Maintaining optimal blood flow to the brain requires either an increase in contractility or an increase in heart rate. The former consistently leads to higher pulsatile power transmission, and the latter can either increase or decrease subsequent pulsatile power transmission to the brain.NEW & NOTEWORTHY We investigated the impact of major aging mechanisms of the arterial system and cardiac function on brain hemodynamics. Our findings suggest that aging has a significant impact on heart-aorta-brain coupling through changes in both arterial stiffening and left ventricle (LV) contractility. Understanding the underlying physical mechanisms involved here can potentially be a key step for developing more effective therapeutic strategies that can mitigate the contributions of abnormal LV-arterial coupling toward neurodegenerative diseases and dementia.

Vascular risk profile and white matter hyperintensity volume among Mexican Americans and non-Hispanic Whites: The HABLE study.

INTRODUCTION: Among vascular risk factors we hypothesized that an increased prevalence of diabetes in Hispanics would be associated with greater white matter hyperintensity (WMH) volume, which may contribute to cognitive decline. METHODS: A total of 1318 participants (60% female; 49% Hispanic, 51% non-Hispanic White; age 66.2 ± 8.9 years) underwent clinical evaluation and brain magnetic resonance imaging (MRI). WMH volume associations were assessed with age, sex, and ethnicity and then with vascular risk factors in a selective regression model. RESULTS: WMH volume was greater with older age (P < .0001), Hispanic ethnicity (P = .02), and female sex (P = .049). WMH volume was best predicted by age, diastolic blood pressure, hypertension history, hemoglobin A1c (HbA1c), white blood cell count, and hematocrit (P < .01 for all). Elevated HbA1c was associated with greater WMH volume among Hispanics (parameter estimate 0.08 ± 0.02, P < .0001) but not non-Hispanic Whites (parameter estimate 0.02 ± 0.04, P = .5). DISCUSSION: WMH volume was greater in Hispanics, which may be partly explained by increased WMH volume related to elevated HbA1c among Hispanics but not non-Hispanic Whites.

Regional relationships between CSF VEGF levels and Alzheimer's disease brain biomarkers and cognition.

Vascular endothelial growth factor (VEGF) is a complex signaling protein that supports vascular and neuronal function. Alzheimer's disease (AD) -neuropathological hallmarks interfere with VEGF signaling and modify previously detected positive associations between cerebral spinal fluid (CSF) VEGF and cognition and hippocampal volume. However, it remains unknown 1) whether regional relationships between VEGF and glucose metabolism and cortical thinning exist, and 2) whether AD-neuropathological hallmarks (CSF Aß, t-tau, p-tau) also modify these relationships. We addressed this in 310 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants (92 cognitively normal, 149 mild cognitive impairment, 69 AD; 215 CSF Aß+, 95 CSF Aß-) with regional cortical thickness and cognition measurements and 158 participants with FDG-PET. In Aß + participants (CSF Aß42 ≤ 192 pg/mL), higher CSF VEGF levels were associated with greater FDG-PET signal in the inferior parietal, and middle and inferior temporal cortices. Abnormal CSF amyloid and tau levels strengthened the positive association between VEGF and regional FDG-PET indices. VEGF also had both direct associations with semantic memory, as well as indirect associations mediated by regional FDG-PET signal to cognition.

Algorithms for segmenting cerebral time-of-flight magnetic resonance angiograms from volunteers and anemic patients.

Purpose: To evaluate six cerebral arterial segmentation algorithms in a set of patients with a wide range of hemodynamic characteristics to determine real-world performance. Approach: Time-of-flight magnetic resonance angiograms were acquired from 33 subjects: normal controls ( N = 11 ), sickle cell disease ( N = 11 ), and non-sickle anemia ( N = 11 ) using a 3 Tesla Philips Achieva scanner. Six segmentation algorithms were tested: (1) Otsu's method, (2) K-means, (3) region growing, (4) active contours, (5) minimum cost path, and (6) U-net machine learning. Segmentation algorithms were tested with two region-selection methods: global, which selects the entire volume; and local, which iteratively tracks the arteries. Five slices were manually segmented from each patient by two readers. Agreement between manual and automatic segmentation was measured using Matthew's correlation coefficient (MCC). Results: Median algorithm segmentation times ranged from 0.1 to 172.9 s for a single angiogram versus 10 h for manual segmentation. Algorithms had inferior performance to inter-observer vessel-based ( p < 0.0001 , MCC = 0.65 ) and voxel-based ( p < 0.0001 , MCC = 0.73 ) measurements. There were significant differences between algorithms ( p < 0.0001 ) and between patients ( p < 0.0042 ). Post-hoc analyses indicated (1) local minimum cost path performed best with vessel-based ( p = 0.0261 , MCC = 0.50 ) and voxel-based ( p = 0.0131 , MCC = 0.66 ) analyses; and (2) higher vessel-based performance in non-sickle anemia ( p = 0.0002 ) and lower voxel-based performance in sickle cell ( p = 0.0422 ) compared with normal controls. All reported MCCs are medians. Conclusions: The best-performing algorithm (local minimum cost path, voxel-based) had 9.59% worse performance than inter-observer agreement but was 3 orders of magnitude faster. Automatic segmentation was non-inferior in patients with sickle cell disease and superior in non-sickle anemia.

MRI Automated T1 Signal Intensity Detection of Diffuse Brain Manganese Accumulation in Cirrhosis.

BACKGROUND AND PURPOSE: Cirrhosis is associated with diffuse brain manganese deposition, which results in increased signal intensity (SI) in the brain on T1-weighted images, most often visualized in the globus pallidus. The purpose of this study was to determine if automated image intensity measurements can detect SI differences in the basal ganglia and other regions reported to have manganese deposition in patients with cirrhosis compared with controls. METHODS: T1 FSPGR images were acquired on 28 patients with cirrhosis and 28 age-sex-matched controls. FreeSurfer T1 SI values were obtained for the globus pallidus, putamen, cerebral white matter, cerebral cortex, and brainstem. SI ratios were computed for globus pallidus normalized to white matter and brainstem. SI values and SI ratios were compared between groups using t-tests. RESULTS: Among people with cirrhosis, T1 SI was significantly increased in the globus pallidus, putamen, cerebral white matter, cerebral cortex, and brainstem (P< .001), and the globus pallidus to brainstem ratio was significantly increased (P< .001). No significant difference was seen for globus pallidus to cerebral white matter T1 SI ratio (P = .38). CONCLUSIONS: Automatic assessment of T1 SI allows for rapid, objective identification of widespread T1 shortening associated with manganese deposition in cirrhosis, consistent with the global deposition of neurotoxic manganese seen in pathology studies. This automated T1 assessment may have broader utility for other conditions beyond cirrhosis impacting T1 SI.

Brain MR Spectroscopy Markers of Encephalopathy Due to Nonalcoholic Steatohepatitis.

BACKGROUND AND PURPOSE: In hepatic encephalopathy (HE), osmotic stressors promoting brain edema result in a compensatory drop in the astrocyte metabolite myo-inositol (mI). Identifying differences between nonalcoholic steatohepatitis (NASH) with and without HE and healthy controls using proton magnetic resonance spectroscopy (MRS) and evaluating hypoalbuminemia and hyperammonemia as osmotic stressors that predict the reduction of mI allow further understanding of mechanisms that promote brain edema in HE. The aim of this study was to assess brain edema in HE using characteristic MRS markers and serum albumin. METHODS: We evaluated between group differences among 19 NASH cirrhosis without HE (Crhs-HE) (age = 63 ± 8.7), 9 NASH cirrhosis with HE (Crhs+HE) (age = 63 ± 9.2), and 16 controls (age = 57.8 ± 11.7) using 1 H MRS. Glutamine (Gln/tCr) and serum albumin were evaluated as predictors of myo-inositol (mI/tCr) using linear regression. Statistical significance was set at P < .05 with adjustment for multiple comparisons. RESULTS: Brain mI/tCr was decreased, and Gln/tCr increased in Crhs+HE compared to Crhs-HE and controls in both brain regions (P < .001 for all). Evaluated together as joint predictors, serum albumin but not Gln/tCr significantly predicted mI/tCr in GM (P = .02 and P = .2, respectively) and PWM (P = .01 and P = .1, respectively). CONCLUSION: Low mI/tCr and increased Gln/tCr were characteristics of Crhs+HE. Low serum albumin was the strongest predictor of brain osmotic stress indicated by reduced mI/tCr, with no residual independent association seen for brain Gln/tCr concentration. This suggests that hypoalbuminemia in chronic liver disease may promote brain edema in HE.

Dynamic Effects of Aortic Arch Stiffening on Pulsatile Energy Transmission to Cerebral Vasculature as A Determinant of Brain-Heart Coupling.

Aortic stiffness increases with age and is a robust predictor of brain pathology including Alzheimer's and other dementias. Aging causes disproportionate stiffening of the aorta compared with the carotid arteries, reducing protective impedance mismatches at their interface and affecting transmission of destructive pulsatile energy to the cerebral circulation. Recent clinical studies have measured regional stiffness within the aortic arch using pulse wave velocity (PWV) and have found a stronger association with cerebrovascular events than global stiffness measures. However, effects of aortic arch PWV on the transmission of harmful excessive pulsatile energy to the brain is not well-understood. In this study, we use an energy-based analysis of hemodynamic waves to quantify the effect of aortic arch stiffening on transmitted pulsatility to cerebral vasculature, employing a computational approach using a one-dimensional model of the human vascular network. Results show there exists an optimum wave condition-occurring near normal human heart rates-that minimizes pulsatile energy transmission to the brain. This indicates the important role of aortic arch biomechanics on heart-brain coupling. Our results also suggest that energy-based indices of pulsatility combining pressure and flow data are more sensitive to increased stiffness than using flow or pressure pulsatility indices in isolation.

Group delay method for MRI aortic pulse wave velocity measurements in clinical protocols with low temporal resolution: Validation in a heterogeneous cohort.

BACKGROUND: MRI assessment of aortic pulse wave velocity (PWV) helps predict the risk of vascular events, but the recommended phase contrast sampling rate is faster than what is utilized in most clinical sequences. There are many existing MRI databases obtained for assessment of cardiac output using lower temporal frequency sampling where information might be obtained about aortic stiffness (PWV). In this work, we sought to evaluate whether the Group Delay (GD) method can generate a reproducible measure of stiffness and describe expected age-related stiffening of the aortic arch using lower sampling rates in standard clinical sequences. METHODS: Phase contrast (PC) MRI was obtained on the ascending and descending aortic arch in a heterogeneous adult cohort (n = 23; 9 women) spanning over a wide range of ages (ages 24-89, mean 49.4 ± 18.4). Data was collected with standard cardiac MRI protocols for cardiac output evaluation (repetition time = 7.8 ms, views-per-segment = 4, encoding velocity = 200 cm/s). Pulse wave transit times (TT) were computed using the GD method, two other validated automated approaches (cross correlation TT Algorithm by Gaddum and Segment by Medviso), and the manual tangent method. Pressure waveforms from tonometry and flow waveforms from PC MRI were used to assess wave reflections. RESULTS: Group Delay and TT-Algorithm showed significant and high retest reproducibility (r = 0.86 for both) as well as high PWV correlation with age (r = 0.93, P-value < 0.00005 and r = 0.96, P-value < 0.00005 respectively) and with each other (r = 0.94, P-value < 0.00001, RMSE = 0.94 m/s). Arbitrary altering of the image acquisition trigger in the GD method introduced error of 10%-13%, but the TT-algorithm error range was 11%-25%. CONCLUSION: Group Delay enables reproducible assessment of transit time to derive PWV from low temporal resolution clinical cardiac MRI sequences that can also identify age-related stiffening.

White matter hyperintensities and their relationship to cognition: Effects of segmentation algorithm.

White matter hyperintensities (WMHs) are brain white matter lesions that are hyperintense on fluid attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) scans. Larger WMH volumes have been associated with Alzheimer's disease (AD) and with cognitive decline. However, the relationship between WMH volumes and cross-sectional cognitive measures has been inconsistent. We hypothesize that this inconsistency may arise from 1) the presence of AD-specific neuropathology that may obscure any WMH effects on cognition, and 2) varying criteria for creating a WMH segmentation. Manual and automated programs are typically used to determine segmentation boundaries, but criteria for those boundaries can differ. It remains unclear whether WMH volumes are associated with cognitive deficits, and which segmentation criteria influence the relationships between WMH volumes and clinical outcomes. In a sample of 260 non-demented participants (ages 55-90, 141 males, 119 females) from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we compared the performance of five WMH segmentation methods, by relating the WMH volumes derived using each method to both clinical diagnosis and composite measures of executive function and memory. To separate WMH effects on cognition from effects related to AD-specific processes, we performed analyses separately in people with and without abnormal cerebrospinal fluid amyloid levels. WMH volume estimates that excluded more diffuse, lower-intensity lesions were more strongly correlated with clinical diagnosis and cognitive performance, and only in those without abnormal amyloid levels. These findings may inform best practices for WMH segmentation, and suggest that AD neuropathology may mask WMH effects on clinical diagnosis and cognition.

White matter hypointensities and hyperintensities have equivalent correlations with age and CSF ß-amyloid in the nondemented elderly.

INTRODUCTION: T1- and T2-weighted sequences from MRI often provide useful complementary information about tissue properties. Leukoaraiosis results in signal abnormalities on T1-weighted images, which are automatically quantified by FreeSurfer, but this marker is poorly characterized and is rarely used. We evaluated associations between white matter hyperintensity (WM-hyper) volume from FLAIR and white matter hypointensity (WM-hypo) volume from T1-weighted images and compared their associations with age and cerebrospinal fluid (CSF) ß-amyloid and tau. METHODS: A total of 56 nondemented participants (68-94 years) were recruited and gave informed consent. All participants went through MR imaging on a GE 1.5T scanner and of these 47 underwent lumbar puncture for CSF analysis. WM-hypo was calculated using FreeSurfer analysis of T1 FSPGR 3D, and WM-hyper was calculated with the Lesion Segmentation Toolbox in the SPM software package using T2-FLAIR. RESULTS: WM-hyper and WM-hypo were strongly correlated (r = .81; parameter estimate (p.e.): 1.53 ± 0.15; p < .0001). Age was significantly associated with both WM-hyper (r = .31, p.e. 0.078 ± 0.030, p = .013) and WM-hypo (r = .42, p.e. 0.055 ± 0.015, p < .001). CSF ß-amyloid levels were predicted by WM-hyper (r = .33, p.e. -0.11 ± 0.044, p = .013) and WM-hypo (r = .42, p.e. -0.24 ± 0.073, p = .002). CSF tau levels were not correlated with either WM-hyper (p = .9) or WM-hypo (p = .99). CONCLUSIONS: Strong correlations between WM-hyper and WM-hypo, and similar associations with age, abnormal ß-amyloid, and tau suggest a general equivalence between these two imaging markers. Our work supports the equivalence of white matter hypointensity volumes derived from FreeSurfer for evaluating leukoaraiosis. This may have particular utility when T2-FLAIR is low in quality or absent, enabling analysis of older imaging data sets.

Alpha desynchronization during simple working memory unmasks pathological aging in cognitively healthy individuals.

Our aim is to explore if cognitive challenge combined with objective physiology can reveal abnormal frontal alpha event-related desynchronization (ERD), in early Alzheimer's disease (AD). We used quantitative electroencephalography (qEEG) to investigate brain activities during N-back working memory (WM) processing at two different load conditions (N = 0 or 2) in an aging cohort. We studied 60-100 year old participants, with normal cognition, and who fits one of two subgroups from cerebrospinal fluid (CSF) proteins: cognitively healthy (CH) with normal amyloid/tau ratio (CH-NAT, n = 10) or pathological amyloid/tau ratio (CH-PAT, n = 14). We recorded behavioral performances, and analyzed alpha power and alpha spectral entropy (SE) at three occasions: during the resting state, and at event-related desynchronization (ERD) [250 ~ 750 ms] during 0-back and 2-back. During 0-back WM testing, the behavioral performance was similar between the two groups, however, qEEG notably differentiated CH-PATs from CH-NATs on the simple, 0-back testing: Alpha ERD decreased from baseline only in the parietal region in CH-NATs, while it decreased in all brain regions in CH-PATs. Alpha SE did not change in CH-NATs, but was increased from baseline in the CH-PATs in frontal and left lateral regions (p<0.01), and was higher in the frontal region (p<0.01) of CH-PATs compared to CH-NATs. The alpha ERD and SE analyses suggest there is frontal lobe dysfunction during WM processing in the CH-PAT stage. Additional power and correlations with behavioral performance were also explored. This study provide pilot information to further evaluate whether this biomarker has clinical significance.

Distinguishing Brain Impact of Aging and HIV Severity in Chronic HIV Using Multiparametric MR Imaging and MR Spectroscopy.

BACKGROUND: Combination antiretroviral therapy (cART) has transformed HIV into a manageable but complex chronic disease, in which it is uncertain which brain insults may relate to age vs initial disease severity. We evaluate N-acetyl-aspartate/creatine (NAA/Cr), white matter hyperintensities (WMH), and mean cortical thickness to identify which subclinical markers of brain insult best relate to CD4 nadir and aging. This is a prospective study of the association between brain markers with age and initial infection severity, based on CD4 nadir, in chronic HIV patients. METHODS: Thirty-seven chronic HIV patients (age 25-77 years) with successful viral suppression were scanned on a GE 3T magnetic resonance imaging scanner to obtain NAA/Cr (standardized and averaged over 5 brain regions), log-transformed WMH volume, and mean cortical thickness. The brain measures were fitted with both CD4 nadir and age to evaluate the significance of their relationship. RESULTS: NAA/Cr, WMH, and cortical thickness were all correlated with age and CD4 nadir in unadjusted associations. Stepwise regression models showed that NAA/Cr alone best predicted CD4 nadir (ß = 40.1 ± 13.3; P = .005), whereas WMH (ß = 2.3 ± .9; P = .02) and mean cortical thickness (ß = -2.7 ± 6.6; P < .0001) together produced the best model fit with age. NAA/Cr was higher for HIV stage 1 (CD4 nadir ≥ 500 cells/ µL; n = 15) compared with stage 2 (200 ≥ CD4 nadir < 500; n = 13) and stage 3 (CD4 nadir < 200; n = 9; P < .01 for both). CONCLUSIONS: In patients with effectively suppressed HIV, NAA reflects the subclinical brain impact of initial disease severity related to development of even mild immune compromise, whereas cortical thickness and WMH volume are useful to evaluate age-related changes.

No-reflow phenomenon in the heart and brain.

The no-reflow phenomenon refers to the observation that when an organ is made ischemic by occlusion of a large artery supplying it, restoration of patency in that artery does not restore perfusion to the microvasculature supplying the parenchyma of that organ. This has been observed after prolonged arterial occlusions in the heart (30-90 min), brain, skin, and kidney. In experimental models, zones of no reflow in the heart are characterized by ultrastructural microvascular damage, including focal endothelial swelling obstructing the lumen of small vessels. Blood elements such as neutrophil plugs, platelets, and stacking of erythrocytes have also been implicated. No reflow is associated with poor healing of the myocardial infarction. In patients, no reflow is associated with a poor clinical outcome independent of infarct size, suggesting that therapy for no reflow may be an important approach to improving outcome for ST elevation myocardial infarction. No reflow occurs after reperfusion of experimental cerebral ischemia and may be observed after only 5-min episodes of ischemia. Aggregation of blood elements may play a greater role than in cardiac no reflow. No reflow in the brain may involve cortical spreading depression with disturbed local vascular control and high, vasculotonic levels of extracellular K+ concentration, postischemic swelling in endothelial cells and abutting end feet of pericytes, pericyte contraction and death, interstitial edema with collapse of cerebral capillaries, and inflammatory reaction. New guidelines suggesting that reperfusion for stroke may be considered as late as 24 h after the onset of symptoms suggest that clinicians may be seeing more no reflow in the future.

Detrimental effect of systemic vascular risk factors on brain hemodynamic function assessed with MRI.

Background and purpose Vascular risk factors have been associated with decreased cerebral blood flow (CBF) but this is etiologically nonspecific and may result from vascular insufficiency or a response to decreased brain metabolic activity. We apply new MRI techniques to measure oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen consumption (CMRO2), hypothesizing that decreased CBF related to these vascular risk factors will be associated with increased OEF, confirming a primary vascular insufficiency. Methods 3T MRI was obtained on 70 community-based participants in this IRB-approved study with informed consent, with previous assessment of systolic blood pressure, hypertension medication, elevated serum triglycerides, low serum HDL, and diabetes mellitus. CBF was measured using phase contrast adjusted for brain volume (ml/100 g/min), OEF (%) was obtained from T2-Relaxation-Under-Spin-Tagging (TRUST), and CMRO2 (µmol/100 g/min) was derived using the Fick principle. Stepwise linear regression identified optimal predictors of CBF with age, sex, and hematocrit included for adjustment. This predictive model was then evaluated against OEF and CMRO2. Results Hypertriglyceridemia was associated with low CBF and high OEF. High systolic blood pressure was associated with high CBF and low OEF, which was primarily attributable to those with pressures above 160 mmHg. Neither risk factor was associated with significant differences in cerebral metabolic rate. Conclusion Low CBF related to hypertriglyceridemia was accompanied by high OEF with no significant difference in CMRO2, confirming subclinical vascular insufficiency. High CBF related to high systolic blood pressure likely reflected limitations of autoregulation at higher blood pressures.

Heart Failure-Induced Brain Injury.

Heart failure (HF) is a systemic illness with grave implications for bodily functions. The brain, among other vital organs, often suffers insults as a result of HF, and both anatomic and functional brain abnormalities were found in the HF population. This injury was demonstrated across a wide range of clinical conditions and cardiac functions and was shown to affect patients' outcomes. Although reduced cardiac output and high burden of cardiovascular risk factors are the prevailing explanations for these findings, there are data showing the involvement of neurohormonal, nutritional, and inflammatory mechanisms in this complex process. Here, the authors review the suggested pathophysiology behind brain injury in HF, describe its effect on patients' outcomes, offer a diagnostic approach, and discuss possible therapeutic options.

Ethnic Difference in Proximal Aortic Stiffness: An Observation From the Dallas Heart Study.

OBJECTIVES: This study aims to compare ethnic difference in proximal aortic pulse wave velocity (PWV) and characteristic impedance (Zc). BACKGROUND: Increased aortic stiffness is an independent predictor of target organ damage, incident hypertension, and all-cause mortality. However, previous studies have not directly assessed proximal aortic function in Blacks, the ethnic population with disproportionately high risk for incident hypertension and target organ complications. METHODS: We evaluated the multiethnic, population-based DHS (Dallas Heart Study) participants (N = 2,544, 54.2% women, 49.7% Black) who underwent cardiac magnetic resonance at 1.5-T. Aortic stiffness and Zc were determined from aortic arch PWV and lumen area measurements. Linear regression was used to evaluate ethnic differences in proximal aortic wall stiffness using aortic arch PWV and Zc as dependent variables with and without adjustment for traditional cardiovascular risk factors. Because cardiac output was significantly higher in Blacks compared to Whites and Hispanics, additional comparisons of PWV and Zc were performed after adjustment for cardiac output and peripheral vascular resistance. RESULTS: Compared with Whites, both Blacks and Hispanics had higher levels of aortic arch PWV (4.25, 95% confidence interval [CI]: 4.15 to 4.35 m/s, vs. 4.72, 95% CI: 4.64 to 4.81 m/s, vs. 4.48, 95% CI: 4.33 to 4.63 m/s, respectively, both p < 0.05 vs. White), and Zc (64.9, 95% CI: 63.3 to 66.6 dyne·s/cm5, vs. 75.6, 95% CI: 74.0 to 77.2 dyne·s/cm5, vs. 70.1, 95% CI: 67.6 to 72.8 dyne·s/cm5, respectively, both p < 0.01 vs. White) after adjustment for age, age squared, sex, body mass index, height, mean arterial blood pressure, antihypertensive treatment, heart rate, total cholesterol, diabetes mellitus, and smoking. Compared with Hispanics, Blacks also had higher level of both PWV and Zc (both p < 0.01). Ethnic differences in PWV and Zc persisted after adjustment for cardiac output and peripheral vascular resistance. CONCLUSIONS: In a multiethnic population-based-sample, Blacks and Hispanics had higher proximal aortic stiffness compared with Whites independent of blood pressure and relevant risk factors.

Relationship between leukoaraiosis, carotid intima-media thickness and intima-media thickness variability: Preliminary results.

OBJECTIVE: To assess the relationship between the degree of leukoaraiosis (LA), carotid intima-media thickness (IMT) and intima-media thickness variability (IMTV). MATERIALS AND METHODS: Sixty-one consecutive patients, who underwent a brain MRI examination and a carotid artery ultrasound, were included in this retrospective study, which conformed with the Declaration of Helsinki. Written informed consent was waived. In each patient, right/left carotid arteries and brain hemispheres were assessed using automated software for IMT, IMTV and LA volume. RESULTS: The mean hemispheric LA volume was 2,224 mm3 (SD 2,702 mm3) and there was no statistically significant difference in LA volume between the right and left hemispheres (p value = 0.628). The mean IMT and IMTV values were 0.866 mm (SD 0.170) and 0.143 mm (SD 0.100), respectively, without significant differences between the right and left sides (p values 0.733 and 0.098, respectively). The correlation coefficient between IMTV and LA volume was 0.41 (p value = 0.0001), and 0.246 (p value = 0.074) between IMT and LA volume. CONCLUSIONS: IMTV significantly correlates with LA volume. Further studies are warranted to verify whether this parameter can be used clinically as a marker of cerebrovascular risk. KEY POINTS: • Intima-media thickness variability (IMTV) significantly correlates with leukoaraiosis volume. • IMTV could be used as a marker for cerebrovascular risk. • IMTV seems to be a better predictor of weighted mean difference than IMT.

Predicting Meningioma Consistency on Preoperative Neuroimaging Studies.

This article provides an overview of the neuroimaging literature focused on preoperative prediction of meningioma consistency. A validated, noninvasive neuroimaging method to predict tumor consistency can provide valuable information regarding neurosurgical planning and patient counseling. Most of the neuroimaging literature indicates conventional MRI using T2-weighted imaging may be helpful to predict meningioma consistency; however, further rigorous validation is necessary. Much less is known about advanced MRI techniques, such as diffusion MRI, MR elastography (MRE), and MR spectroscopy. Of these methods, MRE and diffusion tensor imaging appear particularly promising.

Correction and optimization of a T2-based approach to map blood oxygenation in small cerebral veins.

PURPOSE: Cerebral venous blood oxygenation (Yv ) is an important biomarker in brain physiology and function. The present study proposes a procedure to provide a quantitative map of the brain's intravascular Yv. THEORY AND METHODS: The method is based on a pulse sequence, T2 -Relaxation-Under-Phase-Contrast (TRU-PC) MRI, with postprocessing approaches to correct eddy-current effects. A complete scan protocol consists of four TRU-PC scans sensitized to large and small vessels with anterior-posterior and foot-head flow-encoding directions, and the data are analyzed conjunctively. Eddy-current correction was performed by fitting the tissue phase to a hyperplane, and then subtracting the eddy-current phase from the measured vessel phase. The reproducibility of the Yv-maps was examined in five participants. Sensitivity of the Yv map to a caffeine challenge was studied in another five participants. RESULTS: Removal of eddy-current induced artifact allowed for the correction of T2 measurements, as demonstrated in vivo and with simulation. A Yv-map depicting all vessels in the slice can be obtained with the proposed protocol. Test-retest variability of the Yv -map was 3.7 ± 1.2%. Yv reduction can be reliably detected (P < 0.001) following the caffeine ingestion. CONCLUSION: With the proposed TRU-PC protocol and eddy-current correction procedure, an accurate, vessel-specific Yv map of the human brain can be obtained.