Correlation of ultra-high-frequency ultrasound measures with biochemical markers.

<p><b>(Fig 3A–</b>Association of serum phosphate with common carotid artery (CCA) medial thickness (MT), <b>Fig 3B–</b>Association of serum parathyroid hormone level (log transformed) with CCA MT, <b>Fig 3C–</b>Association of mean arterial pressure standard deviation score (SDS) with CCA MT, <b>Fig 3D–</b>Association of diastolic BP SDS with dorsal pedal artery MT).</p

Bland Altman plot comparing the composite measure of intima thickness and medial thickness (IT + MT) by ultra-high-frequency ultrasound with conventional cIMT.

<p>Bland Altman plot comparing the composite measure of intima thickness and medial thickness (IT + MT) by ultra-high-frequency ultrasound with conventional cIMT.</p

Changes in ultra-high-frequency ultrasound measures at one year follow-up.

<p><b>(Fig 4A</b>—Comparison of baseline and 1-year follow-up measures of common carotid artery (CCA) medial thickness (MT) in transplanted children, <b>Fig 4B</b>—Comparison of baseline and 1-year follow-up measures of dorsal pedal artery intimal thickness (IT) in transplanted children).</p

Ultra-high-frequency ultrasound images of carotid and dorsal pedal arteries, and comparison with images obtained by conventional ultrasound.

<p><b>Fig 1A</b>—Carotid artery scanned with 12 MHz (left) and 55 MHz (right) ultrasound. Outtake shows magnification of intima-media complex from 55 MHz image with outline of intima and media thickness. <b>Fig 1B</b>—Dorsal pedal artery of control child (left) and child on hemodialysis (right) scanned with 70 MHz probe).</p

Ultra-high-frequency ultrasound measurements of intima thickness (IT), medial thickness (MT) and the composite measure of IMT in carotid (Fig 2A) and dorsal pedal (Fig 2B) arteries in healthy controls and children with CKD4-5 and on dialysis (CKD4-5D) and transplanted patients.

<p>CCA–common carotid artery.</p

Association between carotid atherosclerosis and brain activation patterns during the Stroop task in older adults: An fNIRS investigation

There is an increasing body of evidence suggesting that vascular disease could contribute to cognitive decline and overt dementia. Of particular interest is atherosclerosis, as it is not only associated with dementia, but could be a potential mechanism through which cardiovascular disease directly impacts brain health. In this work, we evaluated the differences in functional near infrared spectroscopy (fNIRS)-based measures of brain activation, task performance, and the change in central hemodynamics (mean arterial pressure (MAP) and heart rate (HR)) during a Stroop color-word task in individuals with atherosclerosis, defined as bilateral carotid plaques (n = 33) and healthy age-matched controls (n = 33). In the healthy control group, the left prefrontal cortex (LPFC) was the only region showing evidence of activation when comparing the incongruous with the nominal Stroop test. A smaller extent of brain activation was observed in the Plaque group compared with the healthy controls (1) globally, as measured by oxygenated hemoglobin (p = 0.036) and (2) in the LPFC (p = 0.02) and left sensorimotor cortices (LMC)(p = 0.008) as measured by deoxygenated hemoglobin. There were no significant differences in HR, MAP, or task performance (both in terms of the time required to complete the task and number of errors made) between Plaque and control groups. These results suggest that carotid atherosclerosis is associated with altered functional brain activation patterns despite no evidence of impaired performance of the Stroop task or central hemodynamic changes.</p

Study protocol: MyoFit46—the cardiac sub-study of the MRC National Survey of Health and Development

Background: The life course accumulation of overt and subclinical myocardial dysfunction contributes to older age mortality, frailty, disability and loss of independence. The Medical Research Council National Survey of Health and Development (NSHD) is the world’s longest running continued surveillance birth cohort providing a unique opportunity to understand life course determinants of myocardial dysfunction as part of MyoFit46–the cardiac sub-study of the NSHD.  Methods: We aim to recruit 550 NSHD participants of approximately 75 years+ to undertake high-density surface electrocardiographic imaging (ECGI) and stress perfusion cardiovascular magnetic resonance (CMR). Through comprehensive myocardial tissue characterization and 4-dimensional flow we hope to better understand the burden of clinical and subclinical cardiovascular disease. Supercomputers will be used to combine the multi-scale ECGI and CMR datasets per participant. Rarely available, prospectively collected whole-of-life data on exposures, traditional risk factors and multimorbidity will be studied to identify risk trajectories, critical change periods, mediators and cumulative impacts on the myocardium.  Discussion: By combining well curated, prospectively acquired longitudinal data of the NSHD with novel CMR–ECGI data and sharing these results and associated pipelines with the CMR community, MyoFit46 seeks to transform our understanding of how early, mid and later-life risk factor trajectories interact to determine the state of cardiovascular health in older age.  Trial registration: Prospectively registered on ClinicalTrials.gov with trial ID: 19/LO/1774 Multimorbidity Life-Course Approach to Myocardial Health- A Cardiac Sub-Study of the MCRC National Survey of Health and Development (NSHD).</p