Increased Pulse Pressure Research Articles

Serum leptin is associated with increased pulse pressure and the development of arterial stiffening in adult men: results of an eight-year follow-up study

High leptin levels are associated with an unfavorable cardiometabolic risk profile. A number of studies found a positive association between leptin and vascular damage, but to date, no observational study has evaluated a potential predictive role of leptin for arterial stiffening. Therefore, the aim of this study was to estimate the role of leptin in the incidence of arterial stiffening (pulse pressure >60 mmHg) and changes in pulse pressure in an 8-year follow-up of a sample of adult men (The Olivetti Heart Study). The analysis included 460 men without baseline arterial stiffening and antihypertensive treatment at baseline and at follow-up (age: 50.0 years, BMI: 26.5 kg/m2). At the end of the follow-up period, the incidence of arterial stiffening was 8%. Baseline leptin was significantly greater in the group that developed arterial stiffening and was significantly correlated with pulse pressure changes over time (p < 0.05). According to the median plasma leptin distribution of the whole population, the sample was stratified into two groups: one with leptin levels above the median and the other with leptin levels below the median. Those who had baseline leptin levels above the median had a greater risk of developing arterial stiffening (odds ratio: 2.5, p < 0.05) and a greater increase in pulse pressure over time (beta: 2.1, p < 0.05), also after adjustment for confounders. The results of this prospective study indicate a predictive role of circulating leptin levels for vascular damage, independent of body weight and blood pressure.

Multi-centre cross-sectional study on vascular remodelling in children following successful coarctation correction.

Coarctation of the aorta is an arteriopathy with life-long sequelae, with remarkably increased cardiovascular events in young adults even after successful repair and despite blood pressure status. There are data on arterial remodelling in adults after coarctation correction, however, these data are scarce in childhood. Thus, the aim of this cross-sectional study was to evaluate changes in arterial wall function and morphology in children following successful coarctation repair and to compare these changes among patients with different blood pressure status and coarctation correction modes. Blood pressure status, echocardiographic parameters, arterial wall structure and stiffness, endothelial function and central blood pressure measurements were evaluated in 110 children aged 6-18 years following successful coarctation repair with right arm blood pressure not exceeding leg blood pressure by ≥20 mmHg. The prevalence of arterial hypertension was 50%. The mean carotid intima-media thickness SDS was 3.1 ± 1.5 and above 1.65 SDS in 91 of 110 patients. Increased right carotid intima-media thickness was associated with left ventricular hypertrophy, office blood pressure difference between leg and right arm, recoarctation in the past and interventional coarctation correction. Increased local common carotid artery stiffness was associated with increased pulse pressure and central systolic blood pressure. Potentially decreased endothelial function was related to a slight increase of peak and mean systolic gradient in the descending aorta. After successful coarctation repair and with a low blood pressure gradient, children still have a high prevalence of arterial hypertension and significant arterial remodelling, indicating accelerated biological age and advanced arteriosclerosis.

Characteristics and Determinants of Pulse Pressure-Age Relationship in Healthy and Non-treated Hypertensive Subjects of Argentinean Population.

The relationship between the increases in pulse pressure (PP) and arterial stiffness determined by aging or systemic hypertension has been widely reported. These findings are supported by large-cohort analyzes conducted in well-known populations, such as Framingham Study. However, there is evidence that an age-PP curvilinear relationship may exist in hypertensive subjects. This study aimed to evaluate the age-related change in pulse pressure and arterial stiffness in a population-based study. Carotid-femoral Pulse Wave Velocity (cfPWV) were obtained in 2075 subjects. Age-related changes of PP showed a curvilinear relationship (R=0.39, p<0.0001) in normotensive subjects, with a nadir at around 50 years of age. On the other hand, the age-cfPWV relationship showed a linear and positive correlation (R=0.72, p<0.0001). PP also showed a curvilinear relationship with age (R=0.36, p<0.0001) in hypertensive subjects, with a nadir around 50 years of age. The age-cfPWV relationship showed a linear and positive correlation (R=0.55, p<0.0001). Similar results were observed in the adult population (age≥16 years). Multivariate analysis showed that age, sex, cfPWV, and mean arterial pressure are determinants of PP values in the entire population; however, this result was not uniform when different subgroups were analyzed. In conclusion, age-related changes in PP showed a curvilinear relationship and no parallelism with the age-cfPWV relationship for both normotensive and hypertensive subjects. The determinants of PP impact it differently depending on age and the pathological condition of the subject.

Association between pulse pressure and new-onset diabetes in hypertensive patients

Objective: To determine the association between pulse pressure and the risk of new-onset diabetes in hypertensive patients. Methods: In this prospective cohort study, hypertensive patients from the Kailuan Study, who were diagnosed in 2006-2007 check-up, were screened for enrollment. Participants who finished the biennial follow-up until December 31, 2017 were finally included in this analysis. The primary outcome was incident diabetes development. The pulse pressure variables were divided into quartiles (Q1-Q4), and the Kaplan-Meier curve was used to examine and estimate the cumulative incidence of new-onset diabetes among quartiles. Cox proportional hazards regression model was performed to explore the association between pulse pressure and the risk of new-onset diabetes in hypertensive patients. Results: During an average follow-up of 8.17 years, 6 617 new-onset diabetes were identified out of the 32 917 hypertensive patients with no history or evidence of diabetes in 2006-2007 check-up. Participants were classified into quartiles according to pulse pressure levels as follows: Q1 group(<41 mmHg (1mmHg=0.133kPa))(n=7 995); Q2 group(41-<51 mmHg) (n=8 196); Q3 group (51-<61 mmHg) (n= 8 270); Q4 group (≥61 mmHg) (n=8 456). The cumulative incidences of new-onset diabetes across the quartiles were 16.94%, 19.61%, 21.07%, and 22.33%, respectively, with the incidence density was 20.27, 23.20, 24.92, and 26.10 per 1 000 person-years, respectively. The cumulative incidence of new-onset diabetes increased in proportion with increasing pulse pressure levels (P<0.01 by the Log-rank test). After multivariate adjustment, compared with the first quartile, the hazard ratios for new-onset diabetes in the third and fourth quartiles were 1.13 (95%CI 1.04-1.22, P<0.01) and 1.14 (95%CI 1.05-1.24, P<0.01), respectively. The risk of new-onset diabetes increased 5%(HR=1.05, 95%CI 1.02-1.08, P<0.01) with the fractional pulse pressure increased per 1 SD (0.13). Findings from the three sensitivity analyses were consistent with the main results in this cohort. Conclusions: Pulse pressure at baseline is positively associated with the incidence of new-onset diabetes among hypertensive individuals, and pulse pressure is an independent risk factor for the development of diabetes in hypertensive patients.

Regular physical activity: a major component of isolated systolic hypertension in the young.

In the last few decades there has been much debate about the clinical significance of isolated systolic hypertension in youth (ISHY). Purpose of this article is to discuss the epidemiology and pathophysiology of ISHY focusing on the relationship between ISHY and aerobic exercise. There is evidence to suggest that regular physical activity produces favourable long-standing cardiovascular effects in young individuals including the improvement of arterial elasticity as measured from carotid-femoral pulse wave velocity and from small artery compliance. A recent ESH document recognises the heterogeneity of ISHY which may be associated with multiple factors that can interact to determine this BP phenotype. Several studies have shown that long-term training in aerobic sports is one main factor contributing to ISHY. In the athlete, the increased stroke volume secondary to low heart rate and the high arterial elasticity causes an increase in peripheral pulse pressure. This explains why ISHY is more common in physically trained than in sedentary individuals and is considered by some authors as a spurious hypertension. Recent results from the HARVEST study confirm the existence of an association between ISHY and endurance training. In that study the prevalence of ISHY was directly related to physical activity habits being 8.8% in the sedentary subjects and 25.7% in the athletes. Eligibility to competitive athletics of athletes with ISHY should be based on the results of 24-hour ambulatory BP monitoring and careful clinical assessment of all cardiovascular risk factors and target organ involvement in order to establish the global level of risk.

MO570PULSE PRESSURE: A PREDICTOR OF CARDIOVASCULAR CALCIFICATION AND CARDIOVASCULAR MORTALITY IN HEMODIALYSIS PATIENTS

Abstract Background and Aims The mortality rate is extremely high in chronic kidney disease (CKD), primarily due to the high prevalence of cardiovascular disease (CVD). Increased pulse pressure (PP), defined as the difference between inappropriately elevated systolic blood pressure (SBP) and reduced diastolic blood pressure (DBP) at any value of mean arterial pressure (MAP), is a surrogate measure of increased arterial stiffness of central elastic arteries (aorta and its major branches). CKD-MBD anomalies leading to calcification contribute to increased arterial stiffness and pulse pressure. This study aimed to evaluate the relationship of pulse pressure parameter with valve calcification and abdominal aortic calcification in hemodialysis patients and its impact on cardiovascular mortality. Method We performed a prospective case series study with 3 years follow- up. Plain X-ray images of the lateral lumbar spine from all subjects were studied to obtain images of the lower abdominal aorta using semiquantitative scores as described by Kauppila et al. Cardiac valve calcifications were evaluated by two-dimensional echocardiography with an HDI 5000 Sono CT echocardiographic machine with a 3.3-MHz multiphase array probe in subjects lying in the left decubitus position an according to the recommendations of the European Association of Echocardiography. The patient was evaluated as having vascular calcification if he had the presence of calcification in at least one of the site examined: a mitral valve, aortic valve or abdominal aorta. Results We studied 85 chronic stable hemodialysis patients. Mean age and meantime is therapy was 49.9±12.4 years and 51.5±28.7 months, respectively. Mean pulse pressure was 55.72±14.2 mmHg. Fifty-nine patients (69.4%) were identified with aortic abdominal calcification, and the mean Kauppila score was 4.91 ± 4.05. Sixty patients (70.5%) had at least one valve calcified, while thirty-three patients (38.8%) had both valves calcified. Univariate analysis revealed that every 1 mmHg increase in pulse pressure was associated with increased cardiovascular calcification risk p=0.020. In multivariate analysis, after adjustment for age, gender, diabetes mellitus, cholesterol, and triglyceride serum levels, the association also remained strong, where every increase of 1 mm Hg in pulse pressure was associated with increased risk for cardiovascular calcification (HR 1.02, 95% CI (1.00-1.03), p= 0.038). Besides, pulse pressure was an independent predictor for cardiovascular mortality (HR 1.03, 95% CI (1.02-1.05), p=0.002). Conclusion Pulse pressure may identify hemodialysis patients with subclinical cardiovascular calcification who need further evaluation. Wide pulse pressure is associated with increased cardiovascular mortality.

Mechanisms for the Age‐Related Differences in Cerebral Artery Endothelial Function After Exposure to Elevated Pulse Pressure

Greater large artery stiffness is correlated with increased cerebrovascular dysfunction and damage. One possible mechanism for this correlation is increased pulse pressure in cerebral resistance arteries, a result of less dampening of pulse pressure by the large arteries, leading to reduced cerebral artery endothelial function. Old age is associated with increases in large artery stiffness and cerebrovascular impairment; however, the effect of age on the response to elevated pulse pressure in cerebral arteries is unclear. Thus, we hypothesized that cerebral resistance arteries exhibit an age-related decline in endothelial function following exposure to pulsatile pressure. In young (n=41, 5-10 mo.) and old (n=26, 25-30 mo.) male C57BL6 mice, we measured cerebrovascular function by the ex vivo endothelium-dependent dilation (EDD) to acetylcholine (ACh) in isolated posterior cerebral arteries following exposure to static pressure (50 mmHg), low pulse pressure (50-75 mmHg), or high pulse pressure (37.5-87.5 mmHg)(400bpm). We also determined the effects of nitric oxide synthase inhibition (L-NAME) and decomposition of hydrogen peroxide (PEG-catalase) on the response to ACh. We measured endothelium-independent dilation (EID) by the dose response to sodium nitroprusside. We also measured posterior cerebral artery wall thickness in young and old mice using histological analysis. Compared with young mice, cerebral arteries from old mice had a 37.3% lower maximal EDD during exposure to static pressure (p<0.001), but EID did not differ with age (p=0.86). Exposure to low pulse pressure did not affect maximal EDD for either young or old cerebral arteries (p>0.05). In young cerebral arteries, maximal EDD was 43.9% lower after exposure to high pulse pressure compared with static pressure (p<0.005); however, high pulse pressure had no effect on maximal EDD in old cerebral arteries (p=0.39). Addition of L-NAME reduced maximal EDD in both old (p=0.001) and young (p<0.001) cerebral arteries during all pressure conditions, such that maximal EDD was no longer different between groups (p>0.05). In young cerebral arteries, the presence of PEG-catalase led to a lower maximal EDD in the static pressure (p=0.045) and low pulse pressure (p=0.001) conditions and trended towards greater maximal EDD in the high pulse pressure condition (p=0.08). Cerebral arteries from old mice had a 22% greater wall thickness compared with cerebral arteries from young mice (p=0.047). In conclusion, these results suggest high pulse pressure impairs endothelial function in cerebral resistance arteries from young mice, and this impairment results from lowered bioavailability of the products of nitric oxide synthase and reduced contribution by hydrogen peroxide to vasodilation. Contrary to our hypothesis, cerebral arteries from old mice were protected from the deleterious effects of high pulse pressure, perhaps as a result of arterial remodeling in response to chronic exposure to higher pulse pressure in vivo.

Nox5 in Vascular Smooth Muscle Cells Mediates Ang II‐Induced Renal Fibrosis and Inflammation

Introduction Mice expressing human Nox5 (hNox5) in vascular smooth muscle cells (VSMC) exhibit increased contraction, ROS generation, cardiac fibrosis and increased pulse pressure. In kidneys, hNox5 in podocytes is associated with albuminuria, hypertension and inflammation. Here we questioned whether VSMC Nox5 influences kidney function and damage in Ang II-induced hypertension. Methods Wildtype (WT) and mice expressing hNOX5 in SMC (Nox5+SM22+) were studied. Mice were infused with Ang II (600 ng/Kg/day) for 28 days. Blood pressure was assessed by tail-cuff, kidney damage by histology, and mRNA and protein expression by qPCR and western-blotting, respectively. Inflammatory infiltrate was assessed by FACS. Results Ang II increased blood pressure (mmHg) in WT (162.7±9) and Nox5+SM22+ (162.3±10). Albuminuria was increased in Nox5+SM22+ versus WT mice (10.2±6 vs 1.27±0.3 mg/mmol, p<0.05) and by Ang II in both groups (Nox5: 44.8±18; WT: 58.7±12 mg/mmol). Kidneys from Ang II-infused Nox5+SM22+ mice exhibited significant perivascular fibrosis and inflammatory cell infiltration compared to WT. Kidney expression of vimentin (AU: 1.01±0.05 vs WT 0.85±0.03) and αSMA (AU: 0.44±0.03 vs WT 0.33±0.01), markers of myofibroblast differentiation, was increased in Nox5 mice (p<0.05), an effect that was augmented by Ang II. In kidneys from Nox5+SM22+ mice, levels of macrophage F4/80+ cells were increased (%: 24±2 vs WT 18±1, p<0.05). Ang II increased macrophage homing in kidneys from WT mice (34±3%, p<0.05 vs non-treated), but did not further increase it in Nox5 mice (35±5%). Levels of cytotoxic CD8+ T cells and expression of IL-1b and IRAK were increased by Ang II in Nox5 mice. Conclusion Our study suggests that Nox5 in VSMCs induces renal fibrosis and pro-inflammatory signalling by Ang II, likely through increased ROS generation.

Relationship between arylesterase activity and pulse pressure index in patients with an acute ischemic stroke

Stroke is a multifactorial disease. Arylesterase (ARE) activities have been considered as an anti-atherosclerosis factor. Increased pulse pressure (PP) may lead to a high risk of coronary artery disease and neurovascular morbidity and mortality. Nevertheless, there are limitations for PP as an evaluation index. In order to overcome the defects of PP, there is a novel parameter, “pulse pressure/systolic pressure” named “pulse pressure index (PPI)” for evaluation of cardiovascular effect. We researched the relationship between ARE activities and pulse pressure index (PPI) in acute ischemic stroke patients. We evaluated and compared the ARE activity and PPI in 87 ischemic stroke patients and 48 control patients. ARE activity was measured with the ultraviolet (UV) spectrophotometric method by using “Rel Assay Diagnostic” kits. Pulse pressure was measured by subtraction of diastolic blood pressure from systolic blood pressure. PPI was calculated as “pulse pressure / systolic pressure”. Hypertension, age, diabetes mellitus, dyslipidemia importantly higher in ischemic stroke patients than the control group (p&lt;0.05). PPI was significantly higher in ischemic stroke patients than the control group (0.486±0.075 and 0.417±0.051, p&lt;0.05). ARE activity was significantly lower in ischemic stroke patients than in the control group (511.59 ± 68.51 and 584.16 ± 81.74 p=0.019). This study demonstrated that ARE activity is lower and PPI is higher in acute ischemic stroke patients than control subjects. Our results suggested that, ARE activity and PPI are important risk factors in acute ischemic stroke patients.

Contributions of Cerebral Blood Flow to Associations Between Blood Pressure Levels and Cognition: The Age, Gene/Environment Susceptibility-Reykjavik Study.

[Figure: see text].

ROLE OF VASCULAR NOX5 IN ANG II-MEDIATED PRO-FIBROTIC AND PRO-INFLAMMATORY SIGNALLING IN THE KIDNEY

Objective: Mice expressing human Nox5 (hNox5) in vascular smooth muscle cells (VSMC) exhibit increased contraction, ROS generation, cardiac fibrosis and increased pulse pressure. In kidneys, hNox5 in podocytes is associated with albuminuria, hypertension and inflammation. Here we questioned whether VSMC Nox5 influences kidney function and damage in Ang II-induced hypertension. Design and method: Wildtype (WT) and mice expressing hNOX5 in SMC (Nox5+SM22+) were studied. Mice were infused with Ang II (600 ng/Kg/day) for 28 days. Blood pressure was assessed by tail-cuff, kidney damage by histology, and mRNA and protein expression by qPCR and western-blotting, respectively. Inflammatory infiltrate was assessed by FACS. Results: Ang II increased blood pressure (mmHg) in WT (162.7 ± 9) and Nox5+SM22+ (162.3 ± 10). Albuminuria was increased in Nox5+SM22+ versus WT mice (10.2 ± 6 vs 1.27 ± 0.3 mg/mmol, p &lt; 0.05) and by Ang II in both groups (Nox5: 44.8 ± 18; WT: 58.7 ± 12 mg/mmol). Kidneys from Ang II-infused Nox5+SM22+ mice exhibited significant perivascular fibrosis and inflammatory cell infiltration compared to WT. Kidney expression of vimentin (AU: 1.01 ± 0.05 vs WT 0.85 ± 0.03) and aSMA (AU: 0.44 ± 0.03 vs WT 0.33 ± 0.01), markers of myofibroblast differentiation, was increased in Nox5 mice (p &lt; 0.05), an effect that was augmented by Ang II. In kidneys from Nox5+SM22+ mice, levels of macrophage F4/80+ cells were increased (%: 24 ± 2 vs WT 18 ± 1, p &lt; 0.05). Ang II increased macrophage homing in kidneys from WT mice (34 ± 3%, p &lt; 0.05 vs non-treated), but did not further increase it in Nox5 mice (35 ± 5%). Levels of cytotoxic CD8+ T cells and expression of IL-1b and IRAK were increased by Ang II in Nox5 mice. Conclusions: Our study suggests that Nox5 in VSMCs induces renal fibrosis and pro-inflammatory signalling by Ang II, likely through increased ROS generation.

Increased Pulse Pressure Variability Within the First 24 Hours Leads to Poor Disposition in Subarachnoid Hemorrhage Patients.

Aneurysmal subarachnoid hemorrhage (SAH) continues to be associated with significant morbidity and mortality despite treatment advancements. Although high blood pressure (BP) remains a significant risk factor in aneurysmal SAH and rerupture, the role of BP parameters and fluctuation in prognostication remains unclear. We sought to define how BP parameters and variability within 24 hours of hospitalization in acute-onset SAH affects patient discharge outcomes. We retrospectively analyzed a prospectively collected cohort of SAH patients. Hourly BP parameters, including systolic BP (SBP), diastolic BP, pulse pressure (PP), and their corresponding variability (delineated by SD), were collected to investigate associations with the primary endpoint of discharge disposition. One hundred and seventy-four SAH patients were included in the study. On bivariate analysis, Hunt-Hess (HH) score, Fisher grade, intraventricular hemorrhage, external ventricular drain placement, and SBP and PP variability were significantly associated with a poor disposition. Poor disposition was significantly associated with age, HH score, intraventricular hemorrhage, and PP variability on multivariate analysis. PP variability remained an independent predictor for poor disposition (odds ratio 1.11, 95% confidence interval, 1.02-1.21, P = 0.02) when adjusting for potential confounders. Increased BP and PP variability within the first 24 hours of admission portends a poor discharge disposition for aneurysmal SAH patients.

Association of Low BMI with Aortic Stiffness in Young Healthy Individuals

Increased arterial stiffness is an independent predictor of cardiovascular morbidity and mortality. It is unknown whether low BMI has any detrimental effect on the arterial wall during young age. The present study was aimed to determine if low BMI can increase arterial stiffness in young, healthy individuals. A cross-sectional study was conducted on young, healthy subjects (n=100) with low BMI <18.5 (n=50) and normal BMI: 18.5-24.9 (n=50) with ages ranging between 15-23 years. BMI, heart rate, blood pressure, and arterial stiffness indices such as regional pulse wave velocity (PWV) between brachial-ankle (baPWV), carotid-femoral (cfPWV), heart-ankle (haPWV), heartbrachial (hbPWV) were measured. A significantly increased pulse pressure (p=0.014), baPWV (1059.2 ± 140.26 cm/s vs 994.66 ± 129.23 cm/s; p=0.019) and cfPWV (641.03 ± 113.83 cm/s vs 583.96 ± 120.48 cm/s; p=0.017) was found in individuals with low BMI than normal BMI group. There was a significant negative correlation between BMI and central arterial PWV. Further multiple regression analysis showed that BMI was robustly associated with cf-PWV (p=0.004) and baPWV (p=0.016) even after multiple adjustments with potential confounders using several models. These findings show a significant increased aortic stiffness and pulse pressure in low BMI subjects compared to those with normal BMI. Low BMI was inversely and independently associated with central arterial or aortic stiffness. These findings suggest that low BMI may be a risk factor for aortic stiffness in young, healthy individuals.

Age and Sex Differences in the Associations of Pulse Pressure With White Matter and Subcortical Microstructure.

Midlife vascular disease increases risk for dementia and effects of vascular dysfunction on brain health differ between men and women. Elevated pulse pressure, a surrogate for arterial stiffness, contributes to cerebrovascular pathology and white matter damage that may advance cognitive aging; however, it remains unclear how associations between pulse pressure and neural integrity differ by sex and age. This study used restriction spectrum imaging to examine associations between pulse pressure and brain microstructure in community-dwelling women (N=88) and men (N=55), aged 56 to 97 (mean, 76.3) years. Restricted isotropic (presumed intracellular), hindered isotropic (presumed extracellular), neurite density, and free water diffusion were computed in white matter tracts and subcortical regions. After adjustment for age and sex, higher pulse pressure correlated with lower restricted isotropic diffusion in global white matter, with more pronounced associations in parahippocampal cingulum, as well as in thalamus and hippocampus. Subgroup analyses demonstrated stronger correlations between pulse pressure and restricted isotropic diffusion in association fibers for participants ≤75 years than for older participants, with stronger effects for women than men of this age group. Microstructure in parahippocampal cingulum and thalamus differed by pulse pressure level regardless of antihypertensive treatment. Increased pulse pressure may lead to widespread injury to white matter and subcortical structures, with greatest vulnerability for women in late middle to early older age. Restriction spectrum imaging could be useful for monitoring microstructural changes indicative of neuronal loss or shrinkage, demyelination, or inflammation that accompany age-related cerebrovascular dysfunction.

Cold Pressor Test Influences the Cardio-Ankle Vascular Index in Healthy Overweight Young Adults

Objective: The cold pressor test (CPT) has been shown a potential sympathoexcitatory stimulus which increases aortic pulse wave velocity and the aortic augmentation index, suggesting that noninvasively, arterial stiffness parameters are altered by the CPT. The cardio-ankle vascular index (CAVI) is widely used for reflecting arterial stiffness, and the ankle-brachial index (ABI) for evaluating peripheral artery disease in obesity. We aimed to assess CAVI and ABI in overweight young adults in the context of sympathetic activation by using the CPT. Methods: 160 participants were divided into 2 groups: 86 normal-weight (body mass index [BMI] 18.50–22.99 kg/m²) and 74 overweight (BMI ≥23 kg/m²). The CPT was performed by immersing a participant’s left hand into cold water (3–5°C) for 3 min, and CAVI and ABI assessment. Results: At baseline, the CAVI in the overweight group was significantly less than that in the normal-weight group (5.79 ± 0.85 vs. 6.10 ± 0.85; p < 0.05). The mean arterial pressure (MAP) for overweight was significantly greater than that for normal-weight subjects (93.89 ± 7.31 vs. 91.10 ± 6.72; p < 0.05). During the CPT, the CAVI increased in both normal-weight and overweight subjects, the CAVI value was greater during the CPT in overweight subjects by 14.36% (6.62 ± 0.95 vs. 5.79 ± 0.85, p < 0.05) and in normal-weight subjects by 8.03% (6.59 ± 1.20 vs. 6.10 ± 0.85, p < 0.05) than those baseline values. The CPT evoked an increase in systolic blood pressure (SBP), diastolic BP (DBP), heart rate (HR,) and pulse pressure (PP) in both groups. After a 4-min CPT period, the CAVI returned values similar to the baseline values in both groups, and the SBP, DBP, MAP, and PP in overweight participants were significantly higher than those in normal-weight participants. However, there was no significant difference in the ABI at baseline, during CPT, and post-CPT in either group. Conclusions: Our results indicated that the CAVI was influenced by sympathetic activation response to the CPT in both normal-weight and overweight young adults. Specifically, during the CPT, the percentage change of the CAVI in overweight response was greater in normal-weight participants than baseline values in each group. The ABI was not found significantly associated with CPT. These findings suggesting that sympathoexcitatory stimulus by CPT influence CAVI results.

Relationship Between Paraoxonase-1 Activity and Pulse Pressure Index in Patients with a Acute Ischemic Stroke

Objectives: Stroke is a multifactorial disease. Oxidative stress and blood pressure were found to be closely related with cardiovascular and cerebrovascular diseases. Paraoxonase-1 (PON1) has been considered as an anti-atherosclerosis factor. Increased pulse pressure (PP) may lead to an increased risk of cardiovascular and cerebrovascular morbidity and mortality. Nevertheless, there are limitations for PP as an evaluation index. In order to overcome the defects of PP, there is a novel parameter, “pulse pressure/systolic pressure” called “pulse pressure index (PPI)” for evaluation of cardiovascular outcomes. We investigated the association between Paraoxonase-1 (PON1) activities and pulse pressure index (PPI) in acute ischemic stroke patients.&#x0D; Methods: We evaluated and compared the PON-1 activity and PPI in 46 ischemic stroke patients and 32 control patients. PON1 activitity was measured with UV spectrophotometric method by using “Rel Assay Diagnostic” kits. Pulse pressure was calculated by subtraction of diastolic blood pressure from systolic blood pressure. PPI was calculated “pulse pressure / systolic pressure”.&#x0D; Results: Hypertension, age, diabetes mellitus, dyslipidemia signficantly higher in ischemic stroke patients than control group (p

Cardiometabolic Risk and Biomarker Trajectories Among Older Adults: Findings From the Health and Retirement Study

The deterioration of the cardiovascular system is a process associated with aging. Most of the prior works have examined changes in cardiometabolic risk (CMR) while aging at the population level using cross-sectional data, but we study within-person changes for total CMR and separate risk factors, including pulse pressure, resting heart rate, C-reactive protein, glycosylated hemoglobin (HbA1c), high-density lipoprotein cholesterol, total cholesterol, waist circumference, and obesity. We examine 8-year changes (from 2006 to 2014) among respondents from the Health and Retirement Study biomarker sample (n=19,776). We use growth curve models to identify differences at baseline and the changes while aging, by age, gender, race/ethnicity, and education. Blacks, the old-old, the less educated, and current smokers have higher baseline CMR. The total CMR increases while people age over 8 years. HbA1c, waist circumference, and pulse pressure increase significantly with age. A reduction in total cholesterol can be observed and is likely due to medication. The CMR increase is no longer significant after accounting for socioeconomic status. The next step of this study is to focus on the disparity of risk distribution, in order to identify the individuals that are most in need of specific care and support.

Some Aspects of Role of Nitric Oxide in the Mechanisms of Hypertension (Experimental Study).

BackgroundModulation of endothelial function is a therapeutic option to reduce some of the significant complications of hypertension. However, the relationship between endothelial dysfunction reduced nitric oxide (NO) production, and the development of hypertension is not fully understood. To establish a potential pathogenetic link between impaired NO synthesis and hypertension, we investigated the results of competitive interaction of the substrate of NO synthase, L-arginine, and its analog, an non-selective inhibitor of NO synthase, N-nitro-methyl ether-L-arginine (L-NAME), in experimental rats.MethodsArterial hypertension was induced in male Wistar rats by intraperitoneal administration of L-NAME (Sigma-Aldrich) for 4 - 7 weeks. During the last 3 weeks, to a separate group of animals simultaneously with L-NAME, L-arginine (Sigma-Aldrich) was administered. In animals monitored for systolic and diastolic pressure, the level of NO in blood samples was determined spectrophotometrically using a Griess reagent.ResultsAdministration of L-NAME for 4 - 7 weeks induced an irreversible decrease of NO content in blood, a reversible increase of systolic pressure (SP) and diastolic pressure (DP), and an irreversible increase in pulse pressure (PP). In rats against the background of 7 weeks of intraperitoneal administration of L-NAME, during the last 3 weeks, they were injected with L-arginine, the SP and DP indices returned to their initial values, PP decreased and the NO content in arterial blood increased.ConclusionsThe results of the study indicate the presence of residual endothelial dysfunction (characterized by insufficient NO) after the correction of hypertension. Therefore, in developing the new therapeutic approaches for the treatment of hypertension, it is necessary to include drugs that, in addition to correcting blood pressure, will support normalization, and potentiation of endothelial function and endogenous NO synthesis.

Later-Onset Hypertension Is Associated With Higher Risk of Dementia in Mild Cognitive Impairment.

To investigate the correlation between hypertension development and the progression of mild cognitive impairment (MCI) to dementia in middle-aged and elderly people. A population-based longitudinal cognition survey of people aged 55+ was conducted. The hypertension onset age was estimated by self-reported information and medical insurance card records. To study the effect of later-onset hypertension on dementia, the incidence of dementia was compared between the two groups. Of 277 hypertensive MCI participants without dementia, 56 (20.22%) progressed to dementia (MCIp) over the 6-year follow-up. The proportion of MCIp participants in the old-age-onset hypertension group (≥65 years) was higher than that in the middle-age-onset hypertension group (27.0 vs. 15.4%, respectively; X2 = 5.538, P = 0.019). In the old-age-onset hypertension group, the proportion of MCIp without diabetes mellitus was higher than those with diabetes mellitus (24.7 vs. 12.6%, respectively; X2 = 5.321, P = 0.021) and those with increased pulse pressure was higher than those without increased pulse pressure (33.3 vs. 15.4%, respectively; X2 = 3.902, P = 0.048). However, the cox proportional hazard showed that older age was the only risk factor for MCIp (HR = 0.618, p = 0.000). These results suggest that individuals with later-onset hypertension may have greater cognition decline, even with blood pressure maintained at 130/80 mmHg with antihypertensive management.

Abstract 16912: Cardiac Microstructural Associations With Pulse Pressure Differ by Sex

Background: Alterations in the orientation and integrity of myocardial fibers can be assessed using ultrasonic image analysis. The ability to detect such microstructural abnormalities may shed light on sex differences in the progression from common risk factors, such as blood pressure elevation, to overt cardiac disease. Methods: In a community-based cohort of N=2510 adults (age 66±9 years, 56% women) without overt cardiovascular disease, we evaluated whether a novel echocardiography-based assessment of left ventricular myocardial microstructure, the signal intensity coefficient (SIC), could detect tissue-level alterations that are associated with blood pressure parameters including pulse pressure, an indirect measure of large artery stiffness and established correlate of adverse cardiac outcomes. Results: We observed that for every 10 mmHg increase in pulse pressure, women had a significantly greater degree of cardiac microstructural alteration (coeff 0.07; s.e. 0.02, P&lt;0.001), whereas this age-adjusted association was not seen in men (coeff -0.01; s.e. 0.02, P=0.65) ( Figure ). Although we observed similar results for systolic, diastolic, and mean arterial pressure, the sex interaction terms were non-significant (P&gt;0.05) for these other parameters. Conclusion: A novel index of myocardial tissue alteration is associated with incremental elevations in pulse pressure in women but not in men. Further research is needed to examine the extent to which cardiac microstructural abnormalities may mediate the risks for cardiac disease in women, particularly those conditions involving large artery stiffening such as heart failure with preserved ejection fraction.