Purpose Immediately following reactive hyperemia, the arteries in some individuals constrict before they begin to dilate. We have defined this physiological response high flow-mediated constriction (H-FMC). The aim of this study was to describe the frequency of the H-FMC during reactive hyperemia in children and adolescents throughout a range of body mass index (BMI) values and investigate differences in flow-mediated dilation (FMD), cardiovascular, and anthropometric measures between those subjects who experience this phenomenon and those who do not. Methods FMD was assessed in 136 children and adolescents (61 male, 75 female; 13±3 years) by ultrasound imaging the brachial artery. H-FMC was characterized as the lowest point from the baseline brachial artery diameter immediately following reactive hyperemia cuff release. Independent t-tests were used to compare differences between subjects who demonstrated an H-FMC vs. Non-H-FMC. Results H-FMC was observed in 91 of the 136 participants (66.9%). No significant difference was found between H-FMC vs. Non-H-FMC subjects for age (P=0.602), gender (P=0.767), height (P=0.227) or weight (P=0.171). BMI percentile was trending toward significance in H-FMC vs. Non-H-FMC individuals (91.8th±14.9thvs.84.6th±22.8th percentile, P=0.057). FMD was significantly lower in H-FMC vs. Non-H-FMC subjects (5.43±3.41vs.8.05±3.97%, P<0.001). If the H-FMC was added to the FMD there was no significant difference in dilation between H-FMC and Non-H-FMC individuals (8.03±3.27%vs.8.05±3.97%, P=0.977). Conclusion Approximately 67% of participants demonstrated the high flow-mediated constriction during reactive hyperemia with BMI percentile being higher and FMD lower in children and adolescents who displayed this phenomenon.
Summary Hypercapnia has been utilized as a stimulus to elicit changes in cerebral blood flow (CBF). However, in many instances it has been delivered in a non-controlled method that is often difficult to reproduce. The purpose of this study was to examine the within- and between-visit reproducibility of blood oxygen level-dependent (BOLD) signal changes to an iso-oxic square wave alteration in end-tidal carbon dioxide partial pressure (PetCO2). Two 3-Tesla (3T) MRI scans were performed on the same visit, with two square wave alterations administered per scan. The protocol was repeated on a separate visit with minimum of 3 days between scanning sessions. PetCO2 was altered to stimulate changes in cerebral vascular reactivity (CVR), while PetO2 was held constant. Eleven subjects (six females; mean age 26·5 ± 5·7 years) completed the full testing protocol. Excellent within-visit square wave reproducibility (ICC > 0·75) was observed. Similarly, square waves were reproducible between scanning sessions (ICC > 0·7). This study demonstrates BOLD signal changes in response to alterations in PetCO2 are reproducible both within- and between-visit MRI scans.
Flow-mediated dilation (FMD) relies on reactive hyperemia to stimulate the endothelium to release nitric oxide, causing smooth muscle relaxation. Hypercapnia also produces vasodilation, which is thought to be nitric oxide-independent. The purpose of this study was to compare and contrast the effects of hypercapnia and reactive hyperemia as stimuli for brachial artery dilation. On separate days, twenty-five participants underwent vasodilation studies via reactive hyperemia or hypercapnia (i.e. 10 mmHg increase in end-tidal carbon dioxide [PetCO2)]). During both studies changes in brachial artery diameter were recorded using continuous ultrasound imaging. Heart rate (HR) was measured throughout both tests. Resting HR (63 ± 11 versus 68 ± 14 beats min(-1), p = 0.0027) and baseline brachial artery diameter measurements (4.57 ± 1.51 versus 5.28 ± 1.86 mm, p = 0.022) were significantly different between reactive hyperemia and hypercapnia, respectively. HR at peak dilation (65 ± 11 versus 76 ± 14 beats min(-1), p < 0.0001), peak vessel dilation (8.68 ± 4.50 versus 5.28 ± 1.86%, p = 0.002), and time to peak dilation (90.8 ± 120.1 versus 658.3 ± 226.6 s, p < 0.0001) were also significantly different between reactive hyperemia and hypercapnia. The dynamics by which reactive hyperemia and hypercapnia stimulate vasodilation appear to differ. Hypercapnia produces a smaller and slower vasodilatory effect than reactive hyperemia. Further research is necessary to better understand the mechanisms of vasodilation under hypercapnic conditions.
Background: Cardiovascular disease frequently causes morbidity and mortality in mucopolysaccharidoses (MPS); however, cardiovascular anatomy and dysfunction in MPS IVA (Morquio A disease) is not well described. Consequently, the study aimed to compare carotid artery structure and elasticity of MPS IVA patients with other MPS patients and healthy control subjects, and quantitate frequency of MPS IVA cardiac structural and functional abnormalities. Methods: Prospective, multi-center echocardiogram and carotid ultrasound evaluations of 12 Morquio A patients were compared with other MPS and healthy control subjects. Average differences between groups were adjusted for age, sex, and height with robust variance estimation for confidence intervals and P-values. Results: Morquio A patients demonstrated significantly higher (P < 0.001) adjusted carotid intima-media thickness (cIMT), mean (SD) of 0.56 mm (0.03) compared to control subjects, 0.44 mm (0.04). The Morquio A cohort had significantly greater adjusted carotid elasticity (carotid cross-sectional compliance + 43%, P < 0.001; carotid incremental elastic modulus − 33%, P = 0.003) than control subjects and other MPS patients. Aortic root dilatation was noted in 56% of the Morquio A cohort, which also had highly prevalent mitral (73%) and aortic (82%) valve thickening, though hemodynamically significant valve dysfunction was less frequent (9%). Conclusions: Increased carotid elasticity in Morquio A patients is an unexpected contrast to the reduced elasticity observed in other MPS. These Morquio A cIMT findings corroborate MPS IVA arterial post-mortem reports and are consistent with cIMT of other MPS. Aortic root dilatation in Morquio A indicates arterial elastin dysfunction, but their carotid hyperelasticity indicates other vascular intima/media components, such as proteoglycans, may also influence artery function. Studying MPS I and IVA model systems may uniquely illuminate the function of glycosaminoglycanbearing proteoglycans in arterial health.
Though individual differences in arterial carbon dioxide and oxygen levels inherently exist, the degree of their influence on cerebral vascular reactivity (CVR) is less clear. We examined the reproducibility of BOLD signal changes to an iso‐oxic ramping PetCO2 protocol. CVR changes were induced by altering PetCO2 while holding PetO2 constant using a computer‐controlled sequential gas delivery (SGD) device. Two MRI scans, each including a linear change in PetCO2, were performed using a 3‐Tesla (3T) scanner. This ramp sequence consisted of 1 min at 30 mmHg followed by 4 min period during where PetCO2 was linearly increased from 30 to 50 mmHg, 1 min at 51 mmHg, and concluded with 4 min at baseline. The protocol was repeated at a separate visit with 3 days between visits (minimum). Intraclass correlation coefficients (ICC) and coefficients of variation (CV) were used to verify reproducibility. Eleven subjects (6 females; mean age 26.5 ± 5.7 years) completed the full testing protocol. Good reproducibility was observed for the within‐visit ramp sequence (Visit 1: ICC = 0.82, CV = 6.5%; Visit 2: ICC = 0.74, CV = 6.4%). Similarly, ramp sequence were reproducible between visits (Scan 1: ICC = 0.74, CV = 6.5%; Scan 2: ICC = 0.66, CV = 6.1%). Establishing reproducible methodologies for measuring BOLD signal changes in response to PetCO2 alterations using a ramp protocol will allow researchers to study CVR functionality. Finally, adding a ramping protocol to CVR studies could provide information about changes in CVR over a broad range of PetCO2.
Background Circulating endothelial cells (CECs) reflect early changes in endothelial health; however, the degree to which CEC number and activation is related to adiposity and cardiovascular risk factors in youth is not well described. Methods and Results Youth in this study (N=271; aged 8–20 years) were classified into normal weight (body mass index [BMI] percentage <85th; n=114), obesity (BMI percentage ≥95th to <120% of the 95th; n=63), and severe obesity (BMI percentage ≥120% of the 95th; n=94) catagories. CEC enumeration was determined using immunohistochemical examination of buffy coat smears and activated CEC (percentage of vascular cell adhesion molecule‐1 expression) was assessed using immunofluorescent staining. Cardiovascular risk factors included measures of body composition, blood pressure, glucose, insulin, lipid profile, C‐reactive protein, leptin, adiponectin, oxidized low‐density lipoprotein cholesterol, carotid artery intima–media thickness, and pulse wave velocity. Linear regression models examined associations between CEC number and activation with BMI and cardiovascular risk factors. CEC number did not differ among BMI classes ( P >0.05). Youth with severe obesity had a higher degree of CEC activation compared with normal weight youth (8.3%; 95% CI, 1.1–15.6 [ P =0.024]). Higher CEC number was associated with greater body fat percentage (0.02 per percentage; 95% CI, 0.00–0.03 [ P =0.020]) and systolic blood pressure percentile (0.01 per percentage; 95% CI, 0.00–0.01 [ P =0.035]). Higher degree of CEC activation was associated with greater visceral adipose tissue (5.7% per kg; 95% CI, 0.4–10.9 [ P =0.034]) and non–high‐density lipoprotein cholesterol (0.11% per mg/dL; 95% CI, 0.01–0.21 [ P =0.039]). Conclusions Methods of CEC quantification are associated with adiposity and cardiometabolic risk factors and may potentially reflect accelerated atherosclerosis as early as childhood.
INTRODUCTION-Subclinical cardiovascular risks of secondhand smoke (SHS) exposure among children and adolescents remains insufficiently described.METHODS-This was a cross-sectional study of 298 children and adolescents (48.0% male, body mass index: 27.0±8.9kg/m 2 ), including 49 self-reported cases with SHS. Arterial elasticity and stiffness (distensibility, compliance, incremental elastic modulus [IEM]) were obtained via ultrasound imaging in the abdominal aorta, brachial, and carotid arteries. A one-way analysis of variance compared differences between groups, and multiple linear regression adjusted for covariates.RESULTS-SHS was associated with lower abdominal aorta diameter distensibility (aDD) (13.4±3.6% vs. 16.0±5.2%, p=0.009), and abdominal aorta cross-sectional distensibility (aCSD) (28.8±8.3% vs. 35.1±12.2% p=0.009), as well as higher abdominal aorta IEM (aIEM) (1241±794mmHg vs. 935±388mmHg, p=0.001). After adjustment for covariates, aDD (p=0.047), aCSD (p=0.040), and aIEM (p=0.017) remained significant; this significance persisted with the additional adjustment of percent body fat. Measures of brachial and carotid compliance and distensibility were not associated with SHS.CONCLUSIONS-SHS was associated with abdominal aorta stiffness; the majority of vascular measures within the brachial and carotid artery remained unaffected following adjustment for Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:
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