Central Artery Stiffness in Hypertension and Aging: A Problem With Cause and Consequence.
Ontology highlight
ABSTRACT:
SUBMITTER: Humphrey JD
PROVIDER: S-EPMC4745997 | biostudies-literature | 2016 Feb
REPOSITORIES: biostudies-literature
Publications
Central Artery Stiffness in Hypertension and Aging: A Problem With Cause and Consequence.
Humphrey Jay D JD Harrison David G DG Figueroa C Alberto CA Lacolley Patrick P Laurent Stéphane S
Circulation research 20160201 3
Similar Datasets
Project description:Blood ejected from the left ventricle perfuses the brain via central elastic arteries, which stiffen with advancing age and may elevate the risk of end-organ damage. The purpose of this study was to determine the impact of central arterial aging on cerebral hemodynamics. Eighty-three healthy participants aged 22 to 80 years underwent the measurements of cerebral blood flow (CBF) and CBF velocity (CBFV) using magnetic resonance imaging (MRI) and transcranial Doppler, respectively. The CBF pulsatility was determined by the relative amplitude of CBFV to the mean value (CBFV%). Central arterial stiffness (carotid-femoral pulse wave velocity), wave reflection (carotid augmentation index), and pressure were measured using applanation tonometry. Total volume of white-matter hyperintensity (WMH) was quantified from MR images. Total CBF decreased with age while systolic and pulsatile CBFV% increased and diastolic CBFV% decreased. Women showed greater total CBF and lower cerebrovascular resistance than men. Diastolic CBFV% was lower in women than in men. Age- and sex-related differences in CBF pulsatility were independently associated with carotid pulse pressure and arterial wave reflection. In older participants, higher pulsatility of CBF was associated with the greater total volume of WMH. These findings indicate that central arterial aging has an important role in age-related differences in cerebral hemodynamics.
| S-EPMC4050241 | biostudies-literature
Project description:Pulmonary arterial hypertension (PAH) is a rare, complex, and progressive disease that is characterized by the abnormal remodeling of the pulmonary arteries that leads to right ventricular failure and death. Although our understanding of the causes for abnormal vascular remodeling in PAH is limited, accumulating evidence indicates that endothelial cell (EC) dysfunction is one of the first triggers initiating this process. EC dysfunction leads to the activation of several cellular signalling pathways in the endothelium, resulting in the uncontrolled proliferation of ECs, pulmonary artery smooth muscle cells, and fibroblasts, and eventually leads to vascular remodelling and the occlusion of the pulmonary blood vessels. Other factors that are related to EC dysfunction in PAH are an increase in endothelial to mesenchymal transition, inflammation, apoptosis, and thrombus formation. In this review, we outline the latest advances on the role of EC dysfunction in PAH and other forms of pulmonary hypertension. We also elaborate on the molecular signals that orchestrate EC dysfunction in PAH. Understanding the role and mechanisms of EC dysfunction will unravel the therapeutic potential of targeting this process in PAH.
| S-EPMC7827874 | biostudies-literature
Project description:ObjectivesCOVID-19 viral pneumonia can result in increased arterial stiffness, along with cardiac and systemic inflammatory responses. This study aimed to investigate the association between arterial stiffness, inflammation severity, and all-cause mortality in patients with COVID-19.MethodsIn this study, anthropometric data, pneumonia infection severity, and blood tests were analyzed. Arterial stiffness was assessed using the non-invasive assessment indices, including arterial velocity pulse index (AVI) and central arterial pulse pressure (CAPP). Infection volumes and percentages for the whole lungs, most lobes, and most segments were extracted from CT images using artificial intelligence-based quantitative analysis software. The relationship between arterial stiffness, central hemodynamics, and all-cause mortality was investigated.ResultsIn multivariable Cox regression analysis, high CAPP was significantly associated with all-cause mortality (hazard ratio: 0.263, 95% CI, 0.073-0.945, p = 0.041). Whole lung infection percentages were independently associated with high CAPP, with an area under the curve (AUC) of 0.662 and a specificity of 89.09%.ConclusionsHigh CAPP, but not high AVI, demonstrated independent prognostic value for all-cause mortality in patients due to COVID-19 pneumonia infection. Evaluating this parameter could help in risk assessment and improve diagnostic and therapeutic strategies in viral pneumonia infections.
| S-EPMC11492499 | biostudies-literature
Project description:Large artery stiffness, as measured by pulse wave velocity, is correlated with high blood pressure and may be a causative factor in essential hypertension. The extracellular matrix components, specifically the mix of elastin and collagen in the vessel wall, determine the passive mechanical properties of the large arteries. Elastin is organized into elastic fibers in the wall during arterial development in a complex process that requires spatial and temporal coordination of numerous proteins. The elastic fibers last the lifetime of the organism but are subject to proteolytic degradation and chemical alterations that change their mechanical properties. This review discusses how alterations in the amount, assembly, organization, or chemical properties of the elastic fibers affect arterial stiffness and blood pressure. Strategies for encouraging or reversing alterations to the elastic fibers are addressed. Methods for determining the efficacy of these strategies, by measuring elastin amounts and arterial stiffness, are summarized. Therapies that have a direct effect on arterial stiffness through alterations to the elastic fibers in the wall may be an effective treatment for essential hypertension.
| S-EPMC3383658 | biostudies-literature
Project description:The age-associated increase in arterial stiffness has long been considered to parallel or to cause the age-associated increase in blood pressure (BP). Yet, the rates at which pulse wave velocity (PWV), a measure of arterial stiffness, and BP trajectories change over time within individuals who differ by age and sex have not been assessed and compared. This study determined the evolution of BP and aortic PWV trajectories during a 9.4-year follow-up in >4000 community-dwelling men and women of 20 to 100 years of age at entry into the SardiNIA Study. Linear mixed effects model analyses revealed that PWV accelerates with time during the observation period, at about the same rate over the entire age range in both men and women. In men, the longitudinal rate at which BP changed over time, however, did not generally parallel that of PWV acceleration: at ages>40 years the rates of change in systolic BP (SBP) and pulse pressure (PP) increase plateaued and then declined so that SBP, itself, also declined at older ages, whereas PP plateaued. In women, SBP, diastolic BP, and mean BP increased at constant rates across all ages, producing an increasing rate of increase in PP. Therefore, increased aortic stiffness is implicated in the age-associated increase in SBP and PP. These findings indicate that PWV is not a surrogate for BP and that arterial properties other than arterial wall stiffness that vary by age and sex also modulate the BP trajectories during aging and lead to the dissociation of PWV, PP, and SBP trajectories in men.
| S-EPMC4231012 | biostudies-literature
Project description:Metabolic syndrome is a cluster of conditions that results from the interplay of genetic and environmental factors, which increase the comorbidity risk of obesity, hyperglycemia, dyslipidemia, arterial hypertension, stroke, and cardiovascular disease. In this article, we review various high-impact studies which link epigenetics with metabolic syndrome by comparing each study population, methylation effects, and strengths and weaknesses of each research. We also discuss world statistical data on metabolic syndrome incidence in developing countries where the metabolic syndrome is common condition that has significant public health implications.
| S-EPMC10637881 | biostudies-literature
Project description:Cerebral hypoperfusion elevates the risk of brain white matter (WM) lesions and cognitive impairment. Central artery stiffness impairs baroreflex, which controls systemic arterial perfusion, and may deteriorate neuronal fiber integrity of brain WM. The purpose of this study was to examine the associations among brain WM neuronal fiber integrity, baroreflex sensitivity (BRS), and central artery stiffness in older adults. Fifty-four adults (65 ± 6 years) with normal cognitive function or mild cognitive impairment (MCI) were tested. The neuronal fiber integrity of brain WM was assessed from diffusion metrics acquired by diffusion tensor imaging. BRS was measured in response to acute changes in blood pressure induced by bolus injections of vasoactive drugs. Central artery stiffness was measured by carotid-femoral pulse wave velocity (cfPWV). The WM diffusion metrics including fractional anisotropy (FA) and radial (RD) and axial (AD) diffusivities, BRS, and cfPWV were not different between the control and MCI groups. Thus, the data from both groups were combined for subsequent analyses. Across WM, fiber tracts with decreased FA and increased RD were associated with lower BRS and higher cfPWV, with many of the areas presenting spatial overlap. In particular, the BRS assessed during hypotension was strongly correlated with FA and RD when compared with hypertension. Executive function performance was associated with FA and RD in the areas that correlated with cfPWV and BRS. These findings suggest that baroreflex-mediated control of systemic arterial perfusion, especially during hypotension, may play a crucial role in maintaining neuronal fiber integrity of brain WM in older adults.
| S-EPMC4380707 | biostudies-literature
Project description:Background and purposeArterial stiffening is associated with hypertension, stroke, and cognitive decline; however, the effects of aging and cardiovascular disease risk factors on carotid artery stiffening have not been assessed prospectively in a large multiethnic longitudinal study.MethodsDistensibility coefficient and the Young's elastic modulus (YEM) of the right common carotid artery were calculated at baseline and after a mean of 9.4 (standard deviation [SD], 0.5) years in 2650 participants. Effects of age and cardiovascular disease risk factors were evaluated by multivariable mixed regression and ANCOVA models.ResultsAt baseline, participants were 59.9 (SD, 9.4) years old (53% women; 25% black, 22% Hispanic, 14% Chinese). YEM increased from 1581 (SD, 927) to 1749 (SD, 1306) mm Hg (P<0.0001), and distensibility coefficient decreased from 3.1 (SD, 1.3) to 2.7 (SD, 1.1)×10(-3) mm Hg(-1) (P<0.001), indicating progressive arterial stiffening. YEM increased more among participants who were aged>75 years old at baseline (P<0.0001). In multivariable analyses, older age and less education independently predicted worsening YEM and distensibility coefficient. Stopping antihypertensive medication during the study period predicted more severe worsening of YEM (β=360.2 mm Hg; P=0.008). Starting antihypertensive medication after examination 1 was predictive of improvements in distensibility coefficient (β=1.1×10(-4) mm Hg(-1); P=0.024).ConclusionsArterial stiffening accelerates with advanced age. Older individuals experience greater increases in YEM than do younger adults, even after considering the effects of traditional risk factors. Treating hypertension may slow the progressive decline in carotid artery distensibility observed with aging and improve cerebrovascular health.
| S-EPMC3888489 | biostudies-literature
Project description:James Parkinson first described the motor symptoms of the disease that took his name over 200 years ago. While our knowledge of many of the changes that occur in this condition has increased, it is still unknown what causes this neurodegeneration and why it only affects some individuals with advancing age. Here we review current literature to discuss whether the mitochondrial dysfunction we have detected in Parkinson's disease is a pathogenic cause of neuronal loss or whether it is itself a consequence of dysfunction in other pathways. We examine research data from cases of idiopathic Parkinson's with that from model systems and individuals with familial forms of the disease. Furthermore, we include data from healthy aged individuals to highlight that many of the changes described are also present with advancing age, though not normally in the presence of severe neurodegeneration. While a definitive answer to this question may still be just out of reach, it is clear that mitochondrial dysfunction sits prominently at the centre of the disease pathway that leads to catastrophic neuronal loss in those affected by this disease.
| S-EPMC6627981 | biostudies-literature
Project description:Concerns exist that the positive association of physical activity with better lung function, which has been suggested in previous longitudinal studies in smokers, is due to reverse causation. To investigate this, we applied structural equation modeling (SEM), an exploratory approach, and marginal structural modeling (MSM), an approach from the causal inference framework that corrects for reverse causation and time-dependent confounding and estimates causal effects, on data from participants in the European Community Respiratory Health Survey (ECRHS, a multicentre European cohort study initiated in 1991-1993 with ECRHS I, and with two follow-ups: ECRHS II in 1999-2003, and ECRHS III in 2010-2014). 753 subjects who reported current smoking at ECRHS II, with repeated data on lung function at ECRHS I, II and III, physical activity at ECRHS II and III, and potential confounders at ECRHS I and II, were included in the analyses. SEM showed positive associations between physical activity and lung function in both directions. MSM suggested a protective causal effect of physical activity on lung function (overall difference in mean β (95% CI), comparing active versus non-active individuals: 58 mL (21-95) for forced expiratory volume in one second and 83 mL (36-130) for forced vital capacity). Our results suggest bi-directional causation and support a true protective effect of physical activity on lung function in smokers, after accounting for reverse causation and time-dependent confounding.
| S-EPMC7446897 | biostudies-literature