Flow Mediated Dilatation as a Biomarker in Vascular Surgery Research.
Ontology highlight
ABSTRACT:
SUBMITTER: Bellamkonda K
PROVIDER: S-EPMC5556184 | biostudies-other | 2017 Aug
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Key pointsThe endothelium plays a pivotal role in the vascular response to chemical and mechanical stimuli. The endothelium is exquisitely sensitive to ACh, although the physiological significance of ACh-induced activation of the endothelium is unknown. In the present study, we investigated the mechanisms of flow-mediated endothelial calcium signalling. Our data establish that flow-mediated endothelial calcium responses arise from the autocrine action of non-neuronal ACh released by the endothelium.AbstractCirculating blood generates frictional forces (shear stress) on the walls of blood vessels. These frictional forces critically regulate vascular function. The endothelium senses these frictional forces and, in response, releases various vasodilators that relax smooth muscle cells in a process termed flow-mediated dilatation. Although some elements of the signalling mechanisms have been identified, precisely how flow is sensed and transduced to cause the release of relaxing factors is poorly understood. By imaging signalling in large areas of the endothelium of intact arteries, we show that the endothelium responds to flow by releasing ACh. Once liberated, ACh acts to trigger calcium release from the internal store in endothelial cells, nitric oxide production and artery relaxation. Flow-activated release of ACh from the endothelium is non-vesicular and occurs via organic cation transporters. ACh is generated following mitochondrial production of acetylCoA. Thus, we show ACh is an autocrine signalling molecule released from endothelial cells, and identify a new role for the classical neurotransmitter in endothelial mechanotransduction.
| S-EPMC5157078 | biostudies-literature
Project description:BackgroundAcute ischaemic stroke is associated with alteration in systemic markers of vascular function. We measured forearm vascular function (using forearm flow mediated dilatation) to clarify whether recent acute ischaemic stroke/TIA is associated with impaired systemic vascular function.MethodsProspective case control study enrolling 17 patients with recent acute ischaemic stroke/TIA and 17 sex matched controls with stroke more than two years previously. Forearm vascular function was measured using flow medicated dilatation (FMD).ResultsFlow mediated dilatation was 6.0 ± 1.1% in acute stroke/TIA patients and 4.7 ± 1.0% among control subjects (p = 0.18). The mean paired difference in FMD between subjects with recent acute stroke and controls was 1.25% (95% CI -0.65, 3.14; p = 0.18). Endothelium independent dilatation was measured in six pairs of participants and was similar in acute stroke/TIA patients (22.6 ± 4.3%) and control subjects (19.1 ± 2.6%; p = 0.43).ConclusionsDespite the small size of this study, these data indicate that recent acute stroke is not necessarily associated with a clinically important reduction in FMD.
| S-EPMC2970588 | biostudies-literature
Project description:Biomarker(s) for prediction of the future progression rate of abdominal aortic aneurysms (AAA) may be useful to stratify the management of individual patients. AAAs are associated with features of systemic inflammation and endothelial dysfunction. Flow mediated dilatation (FMD) of the brachial artery is a recognised non-invasive measurement for endothelial function. We hypothesised that FMD is a potential biomarker of AAA progression and reflects the temporal changes of endothelial function during AAA progression.In a prospectively recruited cohort of patients with AAAs (Oxford Abdominal Aortic Aneurysm Study), AAA size was recorded by antero-posterior diameter (APD) (outer to outer) on ultrasound. Annual AAA progression was calculated by (?APD/APD at baseline)/(number of days lapsed/365 days). FMD was assessed at the same time as AAA size measurement. Analyses of data were performed in the overall cohort, and further in subgroups of AAA by size (small: 30-39 mm; moderate: 40-55 mm; large: > 55 mm).FMD is inversely correlated with the diameter of AAAs in all patients (n=162, Spearman's r=-.28, p<.001). FMD is inversely correlated with AAA diameter progression in the future 12 months (Spearman's r=-.35, p=.001), particularly in the moderate size group. Furthermore, FMD deteriorates during the course of AAA surveillance (from a median of 2.0% at baseline to 1.2% at follow-up; p=.004), while surgical repair of AAAs (n=50 [open repair n=22, endovascular repair n=28)] leads to an improvement in FMD (from 1.1% pre-operatively to 3.8% post-operatively; p<.001), irrespective of the type of surgery.FMD is inversely correlated with future AAA progression in humans. FMD deteriorates during the natural history of AAA, and is improved by surgery. The utility of FMD as a potential biomarker in the context of AAA warrants further investigation.
| S-EPMC5496669 | biostudies-other
Project description:ObjectiveTo investigate the association between sympathetic activity, reactive hyperemia and brachial artery flow-mediated dilation (FMD).BackgroundIt is claimed that major surgery has an impact on endothelial function, as observed by post-operative reduced brachial artery FMD response. However, another explanation for the observed reduced FMD response post-operatively may be sympathetic stress-induced reduction in blood flow.MethodsSeventeen healthy volunteers with a median age (25th-75th percentiles) of 23.5 (23-24.8) years were recruited. Participants' brachial blood flow and FMD response were measured (i) during normal non-stress conditions (Normal1); (ii) during exposure to ice water; and (iii) afterwards, under normal non-stress conditions (Normal2). We continuously measured arterial blood pressure (Finometer), heart rate (ECG), skin blood flow of the index finger (laser Doppler), and brachial artery blood flow and diameter (Ultrasound Doppler). Measurements were taken at baseline; before a 5-min suprasystolic forearm occlusion; and following a 3-min post-occlusion, to measure reactive hyperemia and FMD.ResultsMedian (25th-75th percentiles) FMD response after exposure to ice water was reduced compared to non-stress conditions [4.9 (2.9-8.4) % during ice water vs. 9.7 (7.6-12.2) % Normal1 and 9.7 (6.4-10.3) % Normal2, P < 0.001]. Blood flow 60 s after cuff-deflation during ice water exposure was significantly reduced to 328 (289-421) mL compared to non-stress conditions (both P < 0.05). No differences were observed between Normal1 [446 (359-506) mL] and Normal2 [455 (365-515) mL] (both P > 0.05). Heart rate significantly increased during ice water exposure [67 (59-69) beats/min)] compared to 55 (49-60) beats/min during Normal1 and 54 (47-60) beats/min during Normal2 (both P < 0.05). MAP did not change during Normal1 [72 (64-84)] or during Normal2 [71 (65-81) mm Hg] (both P > 0.05), but increased to 86 (75-98) mm Hg during ice water exposure (P < 0.05).ConclusionsIncreased sympathetic activity resulted in decreased blood flow and brachial artery FMD response in healthy volunteers, independent of endothelial dysfunction. Future studies should adjust for blood flow when interpreting the FMD response.
| S-EPMC6743752 | biostudies-literature
Project description:A direct comparison of the effects of febuxostat and allopurinol on flow-mediated dilatation (FMD) will help to clarify which agent provides a better reduction of cardiovascular risk in hypertensive patients. Hypertensive patients with hyperuricemia were randomized into a febuxostat (10-40 mg, n = 33) or allopurinol (100-200 mg, n = 31) group and followed up for 6 months. Both the febuxostat (7.9 ± 1.3 mg/dL vs 5.6 ± 1.0 mg/dL, P < .001) and allopurinol (8.2 ± 1.3 mg/dL vs 6.1 ± 1.0 mg/dL, P < .001) groups exhibited significant reductions in uric acid after treatment. There was no significant difference in the change in FMD between the two treatment groups (0.6 ± 2.6% vs 0.2 ± 2.3%, P = .504). However, stratified analysis showed that febuxostat achieved a significantly greater change in FMD compared to allopurinol in the elderly group (1.3 ± 2.9% vs -0.7%±1.8%, P = .047). There was no difference in the improvement of FMD between febuxostat and allopurinol, but febuxostat may provide an improvement of FMD in elderly people.
| S-EPMC8029901 | biostudies-literature
Project description:BACKGROUND Endothelial dysfunction, which can be measured by flow-mediated dilatation (FMD), is an early clinical marker of atherosclerosis, which is considered to be the main cause of the observed cardiovascular complications in obstructive sleep apnea (OSA) patients. The association between OSA and endothelial dysfunction has been reported in a number of studies; however, the findings are not entirely consistent. Our aim was to meta-analytically synthesize the existing evidence to explore the association between OSA and endothelial dysfunction. MATERIAL AND METHODS Data from PubMed, EMBASE, the Cochrane library, and Google Scholar for all trials that investigated the relationship between endothelial dysfunction and OSA were systematically reviewed. The minimum inclusion criteria for the studies were reporting of the Apnea-Hypopnea Index (AHI) and FMD measurements (as an indicator of endothelial dysfunction) for both OSA and control groups. Data from case-control studies that met the inclusion criteria were extracted. RESULTS Twenty-eight studies comprising a total of 1496 OSA patients and 1135 controls were included in the meta-analysis. A random-effects model was used. The weighted mean difference in the FMD measurements was -3.07 and the 95% confidence interval was -3.71 to -2.43 (P<0.01). Meta-regression analysis showed that age, sex, body mass index (BMI), blood pressure, glucose, high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) cholesterol did not explain the heterogeneity. CONCLUSIONS This meta-analysis showed that patients with OSA have decreased FMD, which may contribute to the development of atherosclerosis.
| S-EPMC5341907 | biostudies-other
Project description:Changes in shear and medial wall stress induced by blood flow contribute to vascular remodeling, but details of these relations remain undefined. We hypothesized that remodeling has a strong genetic component and that phenotypic responses to hemodynamic stress will differ among rat strains. Here, we characterized phenotypic traits related to carotid remodeling in the 2 rat strains that we previously showed the greatest difference in shear stress regulation: Genetically Hypertensive (GH) and Brown Norway (BN) rat strains.Left internal and external carotid arteries were ligated and blood flow was reduced in the left common (LCA) by 90% and increased in the right common carotid artery (RCA) by 60%. Rats were studied for up to 28 days after flow modification and carotid outer diameters were measured in vivo, and wall and luminal components by histomorphometry, to obtain indices of remodeling. Blood flow and pressure measurements were made at corresponding time points.By day 28, remodeling in the GH was greater in response to high flow than in BN, and shear stress was normalized. In contrast, remodeling in the BN was greater in the low flow LCA than in GH. Media stress was greater in GH than BN for any value of carotid shear stress and remained relatively unchanged in low flow, but markedly increased in high flow remodeling. Importantly, pressure was not a major determinant of flow remodeling in these conditions.There are key differences in the ability of carotids in GH and BN rats to adhere to hemodynamic laws during vascular remodeling. GH rats exhibit intact regulatory mechanisms for increased, but not reduced, shear stress. Moreover, the ability to maintain physiological shear and media stresses during vascular remodeling in response to modified flow appears to be intrinsically "genetically" determined.
| S-EPMC2758035 | biostudies-literature
Project description:More than 80% of patients entering cardiac rehabilitation are overweight, with a high prevalence of associated insulin resistance, diabetes, hypertension, hyperlipidemia, and a prothrombotic state. Because each of these characteristics is associated with abnormalities of endothelial-dependent flow-mediated dilatation (FMD), a predictor of long-term prognosis in patients with coronary heart disease (CHD), we assessed the effect of exercise training and weight reduction on FMD in overweight patients with CHD.All patients (N = 38) participated in behavioral weight loss while taking their usual preventive medications. Subjects were randomized to one of two exercise protocols, which differed by caloric expenditure. The primary outcome was extent (%) of brachial artery FMD measured by ultrasonography before and after the 4-month exercise and weight-loss program.Both study groups experienced an increase in brachial artery FMD after weight loss and exercise. Patients randomized to the higher-caloric exercise condition (longer-distance walking) lost more weight (8.6 ± 4.1 kg vs 2.3 ± 3.3 kg [P < .001]) and experienced a greater percentage increase in brachial artery FMD (3.6% ± 4.1% vs 1.3% ± 2.1%, P < .05) than did subjects in the lower-caloric-expenditure exercise group who lost less weight. Both groups increased peak aerobic capacity similarly. Increased FMD correlated with changes in body weight more than with measures of abdominal fat, glucose disposal, lipid measure, BP, or measures of physical activity or cardiorespiratory fitness.Exercise and weight loss increased FMD in overweight and obese patients with CHD. Greater weight reduction was associated with a greater improvement in FMD; thus, there was a dose effect.ClinicalTrials.gov; No.: NCT00628277; URL: www.clinicaltrials.gov.
| S-EPMC3231959 | biostudies-literature
Project description:PurposeTo examine possible hemodynamic alterations in adolescent to adult Marfan syndrome (MFS) patients with aortic root dilatation.Materials and methodsFour-dimensional flow MRI was performed in 20 MFS patients and 12 age-matched normal subjects with a 3T system. The cross-sectional areas of 10 planes along the aorta were segmented for calculating the axial and circumferential wall shear stress (WSSaxial , WSScirc ), oscillatory shear index (OSIaxial , OSIcirc ), and the nonroundness (NR), presenting the asymmetry of segmental WSS. Pearson's correlation analysis was performed to present the correlations between the quantified indices and the body surface area (BSA), aortic root diameter (ARD), and Z score of the ARD. P < 0.05 indicated statistical significance.ResultsPatients exhibited lower WSSaxial in the aortic root and the WSScirc in the arch (P < 0.05-0.001). MFS patients exhibited higher OSIaxial and OSIcirc in the sinotubular junction and arch, but lower OSIcirc in the descending aorta (all P < 0.05). The NR values were lower in patients (P < 0.05). The WSSaxial or WSScirc exhibited moderate to strong correlations with BSA, ARD, or Z score (R(2) ?=?0.50-0.72) in MFS patients.ConclusionThe significant differences in the quantified indices, which were associated with BSA, ARD, or Z score, in MFS were opposite to previous reports for younger MFS patients, indicating that altered flows in MFS patients may depend on the disease progress. The possible time dependency of hemodynamic alterations in MFS patients strongly suggests that longitudinal follow-up of 4D Flow is needed to comprehend disease progress. J. Magn. Reson. Imaging 2016;44:500-508.
| S-EPMC5132207 | biostudies-literature
Project description: Not available
| S-EPMC7528793 | biostudies-literature