Arterial Stiffness, Central Pulsatile Hemodynamic Load, and Orthostatic Hypotension.
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ABSTRACT:
SUBMITTER: Liu K
PROVIDER: S-EPMC8031559 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background: Orthostatic hypotension, defined as a decrease in blood pressure on standing, is associated with an increased risk of mortality and cardiovascular events in the general population. In addition, it has recently been suggested that arterial stiffness is independently associated with orthostatic hypotension, which may be due to a loss of the buffering effect of the ascending aorta and an early return of pressure waves. However, the specific mechanisms underlying this association remain unclear. Thus, we aimed to evaluate the association between orthostatic hypotension and arterial stiffness in the adult population. Methods: PubMed, Scopus, Web of Science, and Cochrane Library databases were searched from inception to 31 January 2022. The DerSimonian and Laird method was used to calculate pooled odds ratio (OR) estimates and their respective 95% confidence intervals (95% CI) for the association between orthostatic hypotension and arterial stiffness. Results: Overall, 11 studies were included, with a total of 10,611 subjects. Our results showed that increased arterial stiffness raises the risk of orthostatic hypotension (OR: 1.40, 95% CI: 1.28-1.54), with a stronger association at central arterial stiffness (OR: 1.50, 95% CI: 1.34-1.68) than at peripheral arterial stiffness (OR: 1.29, 95% CI: 1.17-1.43). Conclusion: Our findings showed that increased arterial stiffness raises the risk of orthostatic hypotension by 40% among the adult population. Considering that orthostatic hypotension, which is usually a consequence of antihypertensive treatment, has been widely associated with the risk of cardiovascular events, appropriate control of arterial stiffness could be a clinical strategy to prevent cardiovascular morbidity and mortality.
| S-EPMC10210150 | biostudies-literature
Project description:Measuring arterial stiffness has recently gained a lot of interest because it is a strong predictor for cardiovascular events and all-cause mortality. However, assessing blood vessel stiffness is not easy and the in vivo measurements currently used provide only limited information. Ex vivo experiments allow for a more thorough investigation of (altered) arterial biomechanical properties. Such experiments can be performed either statically or dynamically, where the latter better corresponds to physiological conditions. In a dynamic setup, arterial segments oscillate between two predefined forces, mimicking the diastolic and systolic pressures from an in vivo setting. Consequently, these oscillations result in a pulsatile load (i.e., the pulse pressure). The importance of pulse pressure on the ex vivo measurement of arterial stiffness is not completely understood. Here, we demonstrate that pulsatile load modulates the overall stiffness of the aortic tissue in an ex vivo setup. More specifically, increasing pulsatile load softens the aortic tissue. Moreover, vascular smooth muscle cell (VSMC) function was affected by pulse pressure. VSMC contraction and basal tonus showed a dependence on the amplitude of the applied pulse pressure. In addition, two distinct regions of the aorta, namely the thoracic descending aorta (TDA) and the abdominal infrarenal aorta (AIA), responded differently to changes in pulse pressure. Our data indicate that pulse pressure alters ex vivo measurements of arterial stiffness and should be considered as an important variable in future experiments. More research should be conducted in order to determine which biomechanical properties are affected due to changes in pulse pressure. The elucidation of the underlying pulse pressure-sensitive properties would improve our understanding of blood vessel biomechanics and could potentially yield new therapeutic insights.
| S-EPMC8569808 | biostudies-literature
Project description:PURPOSE OF REVIEW:This article reviews the management of orthostatic hypotension with emphasis on neurogenic orthostatic hypotension. RECENT FINDINGS:Establishing whether the cause of orthostatic hypotension is a pathologic lesion in sympathetic neurons (ie, neurogenic orthostatic hypotension) or secondary to other medical causes (ie, non-neurogenic orthostatic hypotension) can be achieved by measuring blood pressure and heart rate at the bedside. Whereas fludrocortisone has been extensively used as first-line treatment in the past, it is associated with adverse events including renal and cardiac failure and increased risk of all-cause hospitalization. Distinguishing whether neurogenic orthostatic hypotension is caused by central or peripheral dysfunction has therapeutic implications. Patients with peripheral sympathetic denervation respond better to norepinephrine agonists/precursors such as droxidopa, whereas patients with central autonomic dysfunction respond better to norepinephrine reuptake inhibitors. SUMMARY:Management of orthostatic hypotension is aimed at improving quality of life and reducing symptoms rather than at normalizing blood pressure. Nonpharmacologic measures are the key to success. Pharmacologic options include volume expansion with fludrocortisone and sympathetic enhancement with midodrine, droxidopa, and norepinephrine reuptake inhibitors. Neurogenic supine hypertension complicates management of orthostatic hypotension and is primarily ameliorated by avoiding the supine position and sleeping with the head of the bed elevated.
| S-EPMC7339914 | biostudies-literature
Project description:Background/objectivesWhite matter hyperintensities (WMH) in magnetic resonance imaging (MRI) scans of the brain, and orthostatic hypotension (OH) are both common in older people. We tested the hypothesis that OH is associated with WMH.DesignCross-sectional study.SettingSecondary care outpatient clinics in geriatric medicine and old age psychiatry in western Norway.Participants160 older patients with mild dementia, diagnosed according to standardised criteria.MeasurementsOH was diagnosed according to the consensus definition, measuring blood pressure (BP) in the supine position and within 3 minutes in the standing position. MRI scans were performed according to a common protocol at three centres, and the volumes of WMH were quantified using an automated method (n=82), followed by manual editing. WMH were also quantified using the visual Scheltens scale (n=139). Multiple logistic regression analyses were applied, with highest vs. lowest WMH quartile as response.ResultsThere were no significant correlations between WMH volumes and systolic or diastolic orthostatic BP drops, and no significant correlations between Scheltens scores of WMH and systolic or diastolic BP drops. In the multivariate analyses, only APOE?4 status remained a significant predictor for WMH using the automated method (p=0.037, OR 0.075 (0.007-0.851)), whereas only age remained a significant predictor for WMH scores (p=0.019, OR 1.119 (1.018-1.230)).ConclusionWe found no association between OH and WMH load in a sample of older patients with mild dementia.
| S-EPMC3526570 | biostudies-literature
Project description:BackgroundIncreased arterial stiffness leads to increased pulsatile load on the heart. We investigated associations of components of pulsatile load with a measure of left ventricular (LV) systolic function-global longitudinal strain (GLS), in a community-based cohort ascertained based on family history of hypertension.MethodsArterial tonometry and echocardiography with speckle tracking were performed in 520 adults with normal LV ejection fraction (EF) (age 67±9 years, 70% hypertensive) to quantify measures of pulsatile load (characteristic aortic impedance (Zc), total arterial compliance (TAC), and augmentation index (AI)) and GLS. The associations of log-Zc, log-TAC, and AI with GLS were assessed using sex-specific z-scores for each measure of arterial load.ResultsIn univariable analyses, higher Zc was associated with worse GLS (less negative) and higher TAC and AI were associated with better GLS (all P < 0.001). In a multivariable model including age, sex, heart rate (HR), LVEF, mean arterial load (systemic vascular resistance), and measures of pulsatile load, Zc remained associated with GLS (? = 0.28, P < 0.001), while the associations of TAC and AI were no longer significant (P > 0.5). Additional adjustment for cardiovascular risk factors and history of coronary heart disease and stroke did not attenuate the association of Zc with GLS; Zc, sex, HR, LVEF remained associated with GLS after stepwise elimination (all P < 0.001).ConclusionsGreater proximal aortic stiffness, as manifested by a higher Zc, is independently associated with worse LV longitudinal function.
| S-EPMC4715245 | biostudies-literature
Project description:Orthostatic hypotension (OH) is a sustained fall in blood pressure on standing that can cause symptoms of organ hypoperfusion. OH is associated with increased morbidity and mortality and leads to a significant number of hospital admissions. OH can be caused by volume depletion, blood loss, cardiac pump failure, large varicose veins, medications, or defective activation of sympathetic nerves and reduced norepinephrine release upon standing. Neurogenic OH is a frequent and disabling problem in patients with synucleinopathies such as Parkinson disease, multiple system atrophy, and pure autonomic failure, and it is commonly associated with supine hypertension. Several therapeutic options are available.
| S-EPMC7029426 | biostudies-literature
Project description:Purpose:This study aimed to assess the effects of exercise with dietary restriction on arterial stiffness, central hemodynamics, and cardiac autonomic function in obese adolescents. Patients and methods:Twenty-one obese adolescents completed a 6-week exercise and dietary program. Body composition and metabolic parameters were measured. Carotid-femoral pulse wave velocity (cfPWV) and brachial-ankle pulse wave velocity (baPWV) were used to assess central and systemic arterial stiffness, respectively. Using applanation tonometry, the analyses of central hemodynamic parameters [central blood pressure, heart rate (HR), augmentation index normalized at 75 bpm (AIx75), and subendocardial viability ratio (SEVR)] were performed. To determine cardiac autonomic function, heart rate variability (HRV) was analyzed by standard deviation of normal R-R intervals (SDNN), root mean square of successive R-R interval differences (RMSSD), percentage of successive R-R intervals that differed by >50 ms (pNN50), total power (TP), low-frequency (LF) and high-frequency (HF) power, and LF/HF ratio. Results:Following the intervention, obese adolescents had reductions in body mass index, body fat percentage, brachial systolic and diastolic blood pressure, and HR; and they had shown improvements in lipid profiles. There were reductions in both cfPWV and baPWV following the intervention. Moreover, there were reductions in AIx75, aortic systolic and diastolic blood pressure and an augmentation in SEVR after intervention. The intervention increased cardiac autonomic function (determined by increased SDNN, RMSSD, pNN50, HF, and reduced LF/HF). Furthermore, we observed a correlation between increased cardiac autonomic function (SDNN, RMSSD, pNN50 and HF) and increased central hemodynamics, as measured by SEVR and AIx75. Conclusion:Obese adolescents had increased central hemodynamics and autonomic function with reduced arterial stiffness after exercise and dietary restriction. Moreover, a positive correlation between an enhancement of cardiac autonomic function and an augmentation in central hemodynamics was found after the intervention.
| S-EPMC6802540 | biostudies-literature
Project description:Orthostatic hypotension (OH) is relatively common in the early stage of Parkinson's disease (PD). It is divided into delayed OH and classical OH. Classical OH in PD has been investigated widely, however, the clinical implications of delayed OH in PD have seldom been studied. The purpose of this study is to characterize delayed OH in PD. A total of 285 patients with early drug-naïve PD were enrolled and divided into three groups according to orthostatic change: no-OH, delayed OH, and classical OH. The disease severity in terms of motor, non-motor, and cognitive functions was assessed. The cortical thickness of 82 patients was analyzed with brain magnetic resonance imaging. The differences among groups and linear tendency in the order of no-OH, delayed OH, and classical OH were investigated. Seventy-seven patients were re-evaluated. Initial and follow-up evaluations were explored to discern any temporal effects of orthostasis on disease severity. Sixty-four (22.5%) patients were defined as having delayed OH and 117 (41.1%) had classical OH. Between-group comparisons revealed that classical OH had the worst outcomes in motor, non-motor, cognitive, and cortical thickness, compared to the other groups. No-OH and delayed OH did not differ significantly. Linear trends across the pre-ordered OH subtypes found that clinical parameters worsened along with the orthostatic challenge. Clinical scales deteriorated and the linear gradient was maintained during the follow-up period. This study suggests that delayed OH is a mild form of classical OH in PD. PD with delayed OH has milder disease severity and progression.
| S-EPMC8047032 | biostudies-literature
Project description:Purpose Hyperadrenergic orthostatic hypotension is a subtype of orthostatic hypotension associated with elevated norepinephrine levels upon standing. Our previous study found that this subtype is characterized by less severe autonomic impairment compared to orthostatic hypotension with normal or low norepinephrine levels. However, long-term outcomes have not been determined. Thus, the purpose of this study was to evaluate the all-cause mortality and phenoconversion over 7 years. Methods In this prospective observational study, 92 patients with orthostatic hypotension were recruited from the Vanderbilt Autonomic Dysfunction Center. 34 patients with upright norepinephrine levels above 600 pg/mL were included in the hyperadrenergic cohort and 58 composed the orthostatic hypotension cohort. Both cohorts were followed for 7 years while assessing all-cause mortality and phenoconversion to neurodegenerative autonomic disorders. Results Hyperadrenergic patients showed an exaggerated orthostatic increase in norepinephrine to 938 ± 305 pg/mL upon head up tilt despite presenting with impaired autonomic reflexes. The 7-year mortality rate was 35% in the hyperadrenergic cohort compared to 22% in orthostatic hypotension (p = 0.01). The hyperadrenergic cohort had a greater phenoconversion rate to multiple system atrophy (p = 0.04), whereas the orthostatic hypotension cohort had greater phenoconversion to Parkinson's disease and dementia with Lewy bodies. Conclusions Despite having less severe autonomic impairment, our data suggests that hyperadrenergic orthostatic hypotension has worse clinical outcomes than neurogenic orthostatic hypotension. Patients with hyperadrenergic orthostatic hypotension require careful monitoring, given that this condition may be associated with negative outcomes.
| S-EPMC10543399 | biostudies-literature
Project description:Mean and pulsatile components of hemodynamic load are related to cardiovascular disease. Vascular growth factors play a fundamental role in vascular remodeling. The links between growth factors and hemodynamic load components are not well described. In 3496 participants from the Framingham Heart Study third generation cohort (mean age: 40±9 years; 52% women), we related 4 tonometry-derived measures of central arterial load (carotid femoral pulse wave velocity and forward pressure wave, mean arterial pressure, and the global reflection coefficient) to circulating concentrations of angiopoietin 2, its soluble receptor; vascular endothelial growth factor, its soluble receptor; hepatocyte growth factor; insulin-like growth factor 1; and its binding protein 3. Using multivariable linear regression models, adjusted for standard cardiovascular risk factors, serum insulin-like growth factor 1 concentrations were negatively associated with carotid femoral pulse wave velocity, mean arterial pressure, and reflection coefficient (P≤0.01 for all), whereas serum vascular endothelial growth factor levels were positively associated with carotid femoral pulse wave velocity and mean arterial pressure (P<0.04). Serum insulin-like growth factor binding protein 3 and soluble angiopoietin 2 receptor levels were positively related to mean arterial pressure and to forward pressure wave, respectively (P<0.05). In our cross-sectional study of a large community-based sample, circulating vascular growth factor levels were related to measures of mean and pulsatile hemodynamic load in a pattern consistent with the known physiological effects of insulin-like growth factor 1 and vascular endothelial growth factor.
| S-EPMC3336212 | biostudies-literature