Assessment of arterial pulsatility of cerebral perforating arteries using 7T high-resolution dual-VENC phase-contrast MRI.

PURPOSE: Directly imaging the function of cerebral perforating arteries could provide valuable insight into the pathology of cerebral small vessel diseases (cSVD). Arterial pulsatility has been identified as a useful biomarker for assessing vascular dysfunction. In this study, we investigate the feasibility and reliability of using dual velocity encoding (VENC) phase-contrast MRI (PC-MRI) to measure the pulsatility of cerebral perforating arteries at 7 T. METHODS: Twenty participants, including 12 young volunteers and 8 elder adults, underwent high-resolution 2D PC-MRI scans with VENCs of 20 cm/s and 40 cm/s at 7T. The sensitivity of perforator detection and the reliability of pulsatility measurement of cerebral perforating arteries using dual-VENC PC-MRI were evaluated by comparison with the single-VENC data. The effects of temporal resolution in the PC-MRI acquisition and aging on the pulsatility measurements were investigated. RESULTS: Compared to the single VENCs, dual-VENC PC-MRI provided improved sensitivity of perforator detection and more reliable pulsatility measurements. Temporal resolution impacted the pulsatility measurements, as decreasing temporal resolution led to an underestimation of pulsatility. Elderly adults had elevated pulsatility in cerebral perforating arteries compared to young adults, but there was no difference in the number of detected perforators between the two age groups. CONCLUSION: Dual-VENC PC-MRI is a reliable imaging method for the assessment of pulsatility of cerebral perforating arteries, which could be useful as a potential imaging biomarker of aging and cSVD.

Direct angiographic comparison of different velocity-selective saturation, inversion, and DANTE labeling modules on cerebral arteries.

PURPOSE: This study evaluated the velocity-selective (VS) MRA with different VS labeling modules, including double refocused hyperbolic tangent, eight-segment B1-insensitive rotation, delay alternating with nutation for tailored excitation, Fourier transform-based VS saturation, and Fourier transform-based inversion. METHODS: These five VS labeling modules were evaluated first through Bloch simulations, and then using VSMRA directly on various cerebral arteries of healthy subjects. The relative signal ratios from arterial ROIs and surrounding tissues as well as relative arteria-tissue contrast ratios of different methods were compared. RESULTS: Double refocused hyperbolic tangent and eight-segment B1-insensitive rotation showed very similar labeling effects. Delay alternating with nutation for tailored excitation yielded high arterial signal but with residual tissue signal due to the spatial banding effect. Fourier transform-based VS saturation with half the time of other techniques serves as an efficient nonsubtractive VSMRA method, but the remaining tissue signal still obscured some small distal arteries that were delineated by other subtraction-based VSMRA, allowing more complete cancelation of static tissue. Fourier transform-based inversion produced the highest arterial signal in VSMRA with minimal tissue background. CONCLUSION: This is the first study that angiographically compared five different VS labeling modules. Their labeling characteristics on arteries and tissue and implications for VSMRA and VS arterial spin labeling are discussed.

A comprehensive study on the arterial vasculature of the brain in water buffalo (Bubalus bubalis): Clinical correlates.

The present study was designed to provide a comprehensive analysis of the anatomical aspects of arterial blood vasculature in the water buffalo brains. Fifty cranial cavities of adult water buffaloes were opened via both the dorsal and ventral approaches and the arteries were exposed and photographed. The buffalo rostral epidural rete mirabile generally resembled that of large ruminants. The oculomotor, abducent and trigeminal nerves were intimately associated with the rostral rete. Similar to the majority of ruminants, the arterial circle of the brain was heart-shaped in buffalos and presented all collateral blood vessels as mentioned in the previous literature. The study further revealed that the cranial nerve roots were closely related to the arterial circle of the brain and could be used as indicators for differentiating various branches of the arterial circle of the brain. In addition to the usual variations of the arterial circle of the brain, a bihemispheric rostral cerebral artery along with an aplastic rostral cerebral artery were reported for the first time. The deviant behaviour of the rostral cerebral artery forms a baseline to study various clinical conditions of the blood vasculature in the buffalo brain. The rostral choroidal, middle cerebral and the caudal cerebral arteries constantly were emerged as single vessels without any variations. In conclusion, the anatomy of the arterial vasculature of the buffalo brain observed in the present study provided evidence of its morphological resemblance to other species of the Bovini tribe.

Tissue-growth-based synthetic tree generation and perfusion simulation.

Biological tissues receive oxygen and nutrients from blood vessels by developing an indispensable supply and demand relationship with the blood vessels. We implemented a synthetic tree generation algorithm by considering the interactions between the tissues and blood vessels. We first segment major arteries using medical image data and synthetic trees are generated originating from these segmented arteries. They grow into extensive networks of small vessels to fill the supplied tissues and satisfy the metabolic demand of them. Further, the algorithm is optimized to be executed in parallel without affecting the generated tree volumes. The generated vascular trees are used to simulate blood perfusion in the tissues by performing multiscale blood flow simulations. One-dimensional blood flow equations were used to solve for blood flow and pressure in the generated vascular trees and Darcy flow equations were solved for blood perfusion in the tissues using a porous model assumption. Both equations are coupled at terminal segments explicitly. The proposed methods were applied to idealized models with different tree resolutions and metabolic demands for validation. The methods demonstrated that realistic synthetic trees were generated with significantly less computational expense compared to that of a constrained constructive optimization method. The methods were then applied to cerebrovascular arteries supplying a human brain and coronary arteries supplying the left and right ventricles to demonstrate the capabilities of the proposed methods. The proposed methods can be utilized to quantify tissue perfusion and predict areas prone to ischemia in patient-specific geometries.

Aging-Induced Down-Regulation of PKA/BKCa Pathway in Rat Cerebral Arteries.

The incidence of cerebrovascular diseases increases significantly with aging. This study aimed to test the hypothesis that aging may influence the protein kinase A (PKA)-dependent vasodilation via RyR/BKCa pathway in the middle cerebral arteries (MCA). Male Sprague-Dawley rats were randomly divided into control (4-6 month-old) and aged (24-month-old) groups. The functions of MCA and ion channel activities in smooth muscle cells were examined using myograph system and patch-clamp. Aging decreased the isoproterenol/forskolin-induced relaxation in the MCA. Large-conductance Ca(2+)-activated-K(+) (BKCa) channel inhibitor, iberiotoxin, significantly attenuated the forskolin-induced vasodilatation and hyperpolarization in the young group, but not in the aged group. The amplitude and frequency of spontaneous transient outward currents (STOCs) were significantly decreased in the aged group. Single channel recording revealed that the mean open time of BKCa channels were decreased, while an increased mean closed time of BKCa channels were found in the aged group. The Ca(2+)/voltage sensitivity of the channels was decreased accompanied by reduced BKCa alpha and beta1-subunit, the expression of RyR2, PKA-Calpha and PKA-Cbeta subunits were also declined in the aged group. Aging induced down-regulation of PKA/BKCa pathway in cerebral artery in rats. The results provides new information on further understanding in cerebrovascular diseases resulted from age-related cerebral vascular dysfunction.

Genetic ablation of smooth muscle KIR2.1 is inconsequential to the function of mouse cerebral arteries.

Cerebral blood flow is a finely tuned process dependent on coordinated changes in arterial tone. These changes are strongly tied to smooth muscle membrane potential and inwardly rectifying K+ (KIR) channels are thought to be a key determinant. To elucidate the role of KIR2.1 in cerebral arterial tone development, this study examined the electrical and functional properties of cells, vessels and living tissue from tamoxifen-induced smooth muscle cell (SMC)-specific KIR2.1 knockout mice. Patch-clamp electrophysiology revealed a robust Ba2+-sensitive inwardly rectifying K+ current in cerebral arterial myocytes irrespective of KIR2.1 knockout. Immunolabeling clarified that KIR2.1 expression was low in SMCs while KIR2.2 labeling was remarkably abundant at the membrane. In alignment with these observations, pressure myography revealed that the myogenic response and K+-induced dilation were intact in cerebral arteries post knockout. At the whole organ level, this translated to a maintenance of brain perfusion in SMC KIR2.1-/- mice, as assessed with arterial spin-labeling MRI. We confirmed these findings in superior epigastric arteries and implicated KIR2.2 as more functionally relevant in SMCs. Together, these results suggest that subunits other than KIR2.1 play a significant role in setting native current in SMCs and driving arterial tone.

Changes in cerebral arterial pulsatility and hippocampal volume: a transcranial doppler ultrasonography study.

The physiological mechanisms of age-related cognitive decline remain unclear, in no small part due to the lack of longitudinal studies. Extant longitudinal studies focused on gross neuroanatomy and diffusion properties of the brain. We present herein a longitudinal analysis of changes in arterial pulsatility - a proxy for arterial stiffness - in two major cerebral arteries, middle cerebral and vertebral. We found that pulsatility increased in some participants over a relatively short period and these increases were associated with hippocampal shrinkage. Higher baseline pulsatility was associated with lower scores on a test of fluid intelligence at follow-up. This is the first longitudinal evidence of an association between increase in cerebral arterial stiffness over time and regional shrinkage.

Deep Cerebral Perforators: Anatomical Distribution and Clinical Symptoms: An Overview.

The anatomic distribution of the deep cerebral perforators is considered either a given or subject to enormous variability. Most published overviews on this topic only report findings from a limited number of anatomic dissections, and no attempt has been made to date to provide a comprehensive overview of all published data. A comprehensive literature search was performed on MEDLINE, Embase, and Google Scholar with the help of an information specialist. Three types of studies were included: (1) articles that described the anatomy and distribution territories of perforator groups arising from the arteries of the circle of Willis; (2) studies that evaluated the anatomy of the deep cerebral perforators using imaging techniques; and (3) studies that evaluated either microsurgically or radiologically confirmed perforator occlusion and reported the (magnetic resonance imaging-confirmed) distribution territory of the infarction together with a description of the clinical symptoms associated as a result of the infarction. A total of 2715 articles were screened and 53 were included. Of these, 40 dealt with the anatomic and imaging anatomy of perforator groups (37 reported results of dissections and 3 results of imaging studies), with a total of 2421 hemispheres investigated. Another 13 articles with 680 patients were included that evaluated perforator infarction territories. The deep cerebral perforator distribution shows large variability with poor concordance rates among reported studies, with the exception of the posterior communicating and anterior choroidal artery perforators. Despite the assumption that cerebral perforator anatomy is a given, studies show large variability in the anatomic distribution of various perforator groups. Perforator anatomy and relationships between perforator groups, as well as potential collateral circulation in these territories should be prioritized as a research topic in cerebrovascular disease in the near future.

Effect of menopause on cerebral artery blood flow velocity and cerebrovascular reactivity: Systematic review and meta-analysis.

BACKGROUND: Menopause and its associated decline in oestrogen is linked to chronic conditions like cardiovascular disease and osteoporosis, which may be difficult to disentangle from the effects of ageing. Further, post-menopausal women are at increased risk of cerebrovascular disease, linked to declines in cerebral blood flow (CBF) and cerebrovascular reactivity (CVR), yet the direct understanding of the impact of the menopause on cerebrovascular function is unclear. The aim of this systematic review and meta-analysis was to examine the literature investigating CBF and CVR in pre- compared with post-menopausal women METHODS: Five databases were searched for studies assessing CBF or CVR in pre- and post-menopausal women. Meta-analysis examined the effect of menopausal status on middle cerebral artery velocity (MCAv), and GRADE-assessed evidence certainty RESULTS: Nine studies (n=504) included cerebrovascular outcomes. Six studies (n=239) reported negligible differences in MCAv between pre- and post-menopausal women [2.11cm/s (95% CI: -8.94 to 4.73, p=0.54)], but with a "low" certainty of evidence. MCAv was lower in post-menopausal women in two studies, when MCAv was adjusted for blood pressure. CVR was lower in post- compared with pre-menopausal women in two of three studies, but high-quality evidence is lacking. Across outcomes, study methodology and reporting criteria for menopause were inconsistent CONCLUSIONS: MCAv was similar in post- compared with pre-menopausal women. Methodological differences in characterising menopause and inconsistent reporting of cerebrovascular outcomes make comparisons difficult. Comprehensive assessments of cerebrovascular function of the intra- and extracranial arteries to determine the physiological implications of menopause on CBF with healthy ageing is warranted.

Effect of jump exercise training on long-term head-down bed rest-induced cerebral blood flow responses in arteries and veins.

NEW FINDINGS: What is the central question of this study? What is the effect of an exercise countermeasure on microgravity-induced change in cerebral blood flow? What is the main finding and its importance? Jump exercise training as a countermeasure did not modify the heterogeneous cerebral blood flow response to head-down bed rest, suggesting that this method is effective in preventing cardiovascular system deconditioning but is not good for cerebral haemodynamics. ABSTRACT: This study aimed to examine the effect of an exercise countermeasure on cerebral blood flow (CBF) response to long-term -6° head-down bed rest (HDBR) in all cerebral arteries and veins. Twenty male volunteers were exposed to HDBR for 60 days with (training group, n = 10) or without (control group, n = 10) jump exercise training as a countermeasure to spaceflight. The blood flow in the neck conduit arteries (internal carotid and vertebral artery; ICA and VA) and veins (internal jugular and vertebral veins; IJV and VV) was measured, using ultrasonography before (baseline) HDBR, on the 30th and 57th day of HDBR. Long-term HDBR causes a heterogeneous CBF response between the anterior and the posterior brain or between arteries and veins. Long-term HDBR decreased anterior cerebral arterial and venous blood flow, while posterior cerebral arterial and venous blood flows were well maintained. However, exercise jump training did not change each arterial and venous CBF responses to HDBR (control vs. training; ICA, P = 0.643; VA, P = 0.542; external carotid artery, P = 0.644; IJV, P = 0.980; VV, P = 0.999). These findings suggest that jump exercise training did not modify the heterogeneous CBF response to long-term HDBR.

Cerebral arterial architectonics and CFD simulation in mice with type 1 diabetes mellitus of different duration.

Type 1 diabetes is a chronic autoimmune disease that affects tens of millions of people. Diabetes mellitus is one of the strongest factors in the development of cerebrovascular diseases. In this study we used NOD.CB17 Prkdcscid mice and the pharmacological model of type 1 diabetes mellitus of different duration to study changes in the cerebral vasculature. We used two combined approaches using magnetic resonance angiography both steady and transient CFD blood flow modeling. We identified the influence of type 1 diabetes on the architectonics and hemodynamics of the large blood vessels of the brain as the disease progresses. For the first time, we detected a statistically significant change in angioarchitectonics (the angles between the vessels of the circle of Willis, cross-sections areas of vessels) and hemodynamic (maximum blood flow rate, hydraulic resistance) in animals with diabetes duration of 2 months, that is manifested by the development of asymmetry of cerebral blood flow. The result shows the negative effect of diabetes on cerebral circulation as well as the practicability of CFD modeling. This may be of extensive interest, in pharmacological and preclinical studies.

Characterizing cerebral hemodynamics across the adult lifespan with arterial spin labeling MRI data from the Human Connectome Project-Aging.

Arterial spin labeling (ASL) magnetic resonance imaging (MRI) has become a popular approach for studying cerebral hemodynamics in a range of disorders and has recently been included as part of the Human Connectome Project-Aging (HCP-A). Due to the high spatial resolution and multiple post-labeling delays, ASL data from HCP-A holds promise for localization of hemodynamic signals not only in gray matter but also in white matter. However, gleaning information about white matter hemodynamics with ASL is challenging due in part to longer blood arrival times in white matter compared to gray matter. In this work, we present an analytical approach for deriving measures of cerebral blood flow (CBF) and arterial transit times (ATT) from the ASL data from HCP-A and report on gray and white matter hemodynamics in a large cohort (n = 234) of typically aging adults (age 36-90 years). Pseudo-continuous ASL data were acquired with labeling duration = 1500 ms and five post-labeling delays = 200 ms, 700 ms, 1200, 1700 ms, and 2200 ms. ATT values were first calculated on a voxel-wise basis through normalized cross-correlation analysis of the acquired signal time course in that voxel and an expected time course based on an acquisition-specific Bloch simulation. CBF values were calculated using a two-compartment model and with age-appropriate blood water longitudinal relaxation times. Using this approach, we found that white matter CBF reduces (ρ = 0.39) and white matter ATT elongates (ρ = 0.42) with increasing age (p < 0.001). In addition, CBF is lower and ATTs are longer in white matter compared to gray matter across the adult lifespan (Wilcoxon signed-rank tests; p < 0.001). We also found sex differences with females exhibiting shorter white matter ATTs than males, independently of age (Wilcoxon rank-sum test; p < 0.001). Finally, we have shown that CBF and ATT values are spatially heterogeneous, with significant differences in cortical versus subcortical gray matter and juxtacortical versus periventricular white matter. These results serve as a characterization of normative physiology across the human lifespan against which hemodynamic impairment due to cerebrovascular or neurodegenerative diseases could be compared in future studies.

Cerebral arterial pulsatility is linked to hippocampal microvascular function and episodic memory in healthy older adults.

Microvascular damage in the hippocampus is emerging as a central cause of cognitive decline and dementia in aging. This could be a consequence of age-related decreases in vascular elasticity, exposing hippocampal capillaries to excessive cardiac-related pulsatile flow that disrupts the blood-brain barrier and the neurovascular unit. Previous studies have found altered intracranial hemodynamics in cognitive impairment and dementia, as well as negative associations between pulsatility and hippocampal volume. However, evidence linking features of the cerebral arterial flow waveform to hippocampal function is lacking. We used a high-resolution 4D flow MRI approach to estimate global representations of the time-resolved flow waveform in distal cortical arteries and in proximal arteries feeding the brain in healthy older adults. Waveform-based clustering revealed a group of individuals featuring steep systolic onset and high amplitude that had poorer hippocampus-sensitive episodic memory (p = 0.003), lower whole-brain perfusion (p = 0.001), and weaker microvascular low-frequency oscillations in the hippocampus (p = 0.035) and parahippocampal gyrus (p = 0.005), potentially indicating compromised neurovascular unit integrity. Our findings suggest that aberrant hemodynamic forces contribute to cerebral microvascular and hippocampal dysfunction in aging.

Regional and depth-dependence of cortical blood-flow assessed with high-resolution Arterial Spin Labeling (ASL).

Methods for imaging of cerebral blood flow do not typically resolve the cortex and thus underestimate flow. However, recent work with high-resolution MRI has emphasized the regional and depth-dependent structural, functional and relaxation times variations within the cortex. Using high-resolution Arterial Spin Labeling (ASL) and T1 mapping acquisitions, we sought to probe the effects of spatial resolution and tissue heterogeneity on cortical cerebral blood flow (CBF) measurements with ASL. We acquired high-resolution (1.6mm)3 whole brain ASL data in a cohort of 10 volunteers at 3T, along with T1 and transit-time (ATT) mapping, followed by group cortical surface-based analysis using FreeSurfer of the different measured parameters. Fully resolved regional analysis showed higher than average mid-thickness CBF in primary motor areas (+15%,p<0.002), frontal regions (+17%,p<0.01) and auditory cortex, while occipital regions had lower average CBF (-20%,p<10-5). ASL signal was higher towards the pial surface but correction for the shorter T1 near the white matter surface reverses this gradient, at least when using the low-resolution ATT map. Similar to structural measures, fully-resolved ASL CBF measures show significant differences across cortical regions. Depth-dependent variation of T1 in the cortex complicates interpretation of depth-dependent ASL signal and may have implications for the accurate CBF quantification at lower resolutions.

The Cerebro-Renal System- Anatomical and Physiological Considerations.

The brain and kidney both uniquely are highly susceptible to vascular injury from shared vascular risk factors. However these are not sufficient to explain the complete extent of cerebrovascular disease especially small vessel disease in its myriad presentations that patients with chronic kidney disease manifest. They both require a large amount of blood supply to function optimally. Shared anatomical and physiological factors such as the presence of strain vessels, the local vascular autoregulation that control blood supply possible, results in the vulnerability of these organs to the vascular risk factors. Because it is a bidirectional system where each affects the other, it is best considered as a cerebro-renal unit.

Metoprolol Impairs ß1-Adrenergic Receptor-Mediated Vasodilation in Rat Cerebral Arteries: Implications for ß-Blocker Therapy.

The practice of prescribing ß-blockers to lower blood pressure and mitigate perioperative cardiovascular events has been questioned because of reports of an increased risk of stroke. The benefit of ß-blocker therapy primarily relies on preventing activation of cardiac ß1-adrenergic receptors (ARs). However, we reported that ß1ARs also mediate vasodilator responses of rat cerebral arteries (CAs), implying that ß-blockers may impair cerebral blood flow under some conditions. Here, we defined the impact of metoprolol (MET), a widely prescribed ß1AR-selective antagonist, on adrenergic-elicited diameter responses of rat CAs ex vivo and in vivo. MET (1-10 µmol/l) prevented ß1AR-mediated increases in diameter elicited by dobutamine in cannulated rat CAs. The ß1AR-mediated dilation elicited by the endogenous adrenergic agonist norepinephrine (NE) was reversed to a sustained constriction by MET. Acute oral administration of MET (30 mg/kg) to rats in doses that attenuated resting heart rate and dobutamine-induced tachycardia also blunted ß1AR-mediated dilation of CAs. In the same animals, NE-induced dilation of CAs was reversed to sustained constriction. Administration of MET for 2 weeks in drinking water (2 mg/ml) or subcutaneously (15 mg/kg per day) also resulted in NE-induced constriction of CAs in vivo. Thus, doses of MET that protect the heart from adrenergic stimulation also prevent ß1AR-mediated dilation of CAs and favor anomalous adrenergic constriction. Our findings raise the possibility that the increased risk of ischemic stroke in patients on ß-blockers relates in part to adrenergic dysregulation of cerebrovascular tone. SIGNIFICANCE STATEMENT: ß-Blocker therapy using second-generation, cardioselective ß-blockers is associated with an increased risk of stroke, but the responsible mechanisms are unclear. Here, we report that either acute or chronic systemic administration of a cardioselective ß-blocker, metoprolol, mitigates adrenergic stimulation of the heart as an intended beneficial action. However, metoprolol concomitantly eliminates vasodilator responses to adrenergic stimuli of rat cerebral arteries in vivo as a potential cause of dysregulated cerebral blood flow predisposing to ischemic stroke.

The effect of hypercapnia on regional cerebral blood flow regulation during progressive lower-body negative pressure.

PURPOSE: Previous work indicates that dynamic cerebral blood flow (CBF) regulation is impaired during hypercapnia; however, less is known about the impact of resting hypercapnia on regional CBF regulation during hypovolemia. Furthermore, there is disparity within the literature on whether differences between anterior and posterior CBF regulation exist during physiological stressors. We hypothesized: (a) lower-body negative pressure (LBNP)-induced reductions in cerebral blood velocity (surrogate for CBF) would be more pronounced during hypercapnia, indicating impaired CBF regulation; and (b) the anterior and posterior cerebral circulations will exhibit similar responses to LBNP. METHODS: In 12 healthy participants (6 females), heart rate (electrocardiogram), mean arterial pressure (MAP; finger photoplethosmography), partial pressure of end-tidal carbon dioxide (PETCO2), middle cerebral artery blood velocity (MCAv) and posterior cerebral artery blood velocity (PCAv; transcranial Doppler ultrasound) were measured. Cerebrovascular conductance (CVC) was calculated as MCAv or PCAv indexed to MAP. Two randomized incremental LBNP protocols were conducted (- 20, - 40, - 60 and - 80 mmHg; three-minute stages), during coached normocapnia (i.e., room air), and inspired 5% hypercapnia (~ + 7 mmHg PETCO2 in normoxia). RESULTS: The main findings were: (a) static CBF regulation in the MCA and PCA was similar during normocapnic and hypercapnic LBNP trials, (b) MCA and PCA CBV and CVC responded similarly to LBNP during normocapnia, but (c) PCAv and PCA CVC were reduced to a greater extent at - 60 mmHg LBNP (P = 0.029; P < 0.001) during hypercapnia. CONCLUSION: CBF regulation during hypovolemia was preserved in hypercapnia, and regional differences in cerebrovascular control may exist during superimposed hypovolemia and hypercapnia.

Doppler ultrasound cardiac gating of intracranial flow at 7T.

BACKGROUND: Ultra-high field magnetic resonance imaging (MR) may be used to improve intracranial blood flow measurements. However, standard cardiac synchronization methods tend to fail at ultra-high field MR. Therefore, this study aims to investigate an alternative synchronization technique using Doppler ultrasound. METHODS: Healthy subjects (n = 9) were examined with 7T MR. Flow was measured in the M1-branch of the middle cerebral artery (MCA) and in the cerebral aqueduct (CA) using through-plane phase contrast (2D flow). Flow in the circle of Willis was measured with three-dimensional, three-directional phase contrast (4D flow). Scans were gated with Doppler ultrasound (DUS) and electrocardiogram (ECG), and pulse oximetry data (POX) was collected simultaneously. False negative and false positive trigger events were counted for ECG, DUS and POX, and quantitative flow measures were compared. RESULTS: There were fewer false positive triggers for DUS compared to ECG (5.3 ± 11 vs. 25 ± 31, p = 0.031), while no other measured parameters differed significantly. Net blood flow in M1 was similar between DUS and ECG for 2D flow (1.5 ± 0.39 vs. 1.6 ± 0.41, bias ± 1.96SD: - 0.021 ± 0.36) and 4D flow (1.8 ± 0.48 vs. 9 ± 0.59, bias ± 1.96SD: - 0.086 ± 0.57 ml). Net CSF flow per heart beat in the CA was also similar for DUS and ECG (3.6 ± 2.1 vs. 3.0 ± 5.8, bias ± 1.96SD: 0.61 ± 13.6 µl). CONCLUSION: Gating with DUS produced fewer false trigger events than using ECG, with similar quantitative flow values. DUS gating is a promising technique for cardiac synchronization at 7T.