Prolonged Blood Pressure Research Articles

Determinants of prolonged baseline blood pressure restoration following autonomic dysreflexia for individuals with spinal cord injuries

Objective This study aimed to identify the determinants affecting the time required for blood pressure (BP) restoration after autonomic dysreflexia (AD) and to propose a new method for BP measurement in individuals with cervical spinal cord injury (SCI) who experience AD. Methods In a prospective, single-center observational study, participants’ bladders were filled with body-temperature saline until reaching cystometric capacity, as confirmed by previous urodynamic studies. Restoration time (RT), defined as the time from the onset of voiding until BP returned to baseline, was measured during the morning voiding session. This session involved the use of a 10F hydrophilic transurethral catheter. Data were then compared with various clinical determinants including demographic, urodynamic, and cystographic variables. Results The study included 29 individuals with cervical SCI. Notable variations in RT were observed among individuals with differing levels of detrusor overactivity (DO) and bladder compliance. An inverse correlation was noted between RT and bladder compliance, whereas positive correlations were identified with maximal detrusor pressure, peak systolic BP (SBP), and the magnitude of BP changes. Factors associated with prolonged RT included injury completeness, bladder trabeculation, vesicoureteral reflux (VUR), DO, and changes in SBP. Conclusions A significant association was found between BP elevation and prolonged RT. Determinants such as the severity of the SCI, bladder trabeculation, VUR, and DO were correlated with prolonged RT, considering their importance in the assessment of baseline BP following AD.

D-dimer relation with hypertension and non-hypertension in covid-19 patient

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by SARS-CoV-2. It mainly affects lungs, but it also affects other systems too including cardiovascular system. Apparently, comorbidity may exacerbate the COVID-19 symptoms. Hypertension is the most common comorbidities in COVID-19 patients. Some COVID-19 patients have increased their d-dimer level which is a test to detect coagulation. It is suspected that prolonged high blood pressure might cause inflammation in the endothel and release inflammatory markers. Thus, the blood viscosity might also increase. The purpose of this research is to understand the association between d-dimer with hypertension in patients with COVID-19 at Dr.Soetomo General Academic Hospital from March – June 2021. The study design of this research is retrospective cross-sectional model which use medical records of COVID-19 patients at Dr. Soetomo General Academic Hospital, Surabaya, Indonesia in March 2021-June 2021. From 86 data which fulfil inclusion criteria will be tested using Chi-square. Most COVID-19 patients were aged between 30-60 years (68.6%). Based on sex distribution, the majority of patient was male (54.7%). There were no significant differences of d-dimer level based on hypertension (p=0.890), age (p=0.494), and sex (0.305). There was no correlation between d-dimer and hypertension comorbidity.

The Effect of Sitting Duration on Peripheral Blood Pressure Responses to Prolonged Sitting, With and Without Interruption: A Systematic Review and Meta-Analysis.

A previous meta-analysis reported that: (i) an acute bout of prolonged uninterrupted sitting induces a significant increase in peripheral blood pressure (BP) and (ii) the increase in BP can be offset by interrupting the sitting bout with light aerobic activities such as walking. However, the temporal association between prolonged uninterrupted sitting and BP was not determined. A better understanding of temporality, for example, how long it takes BP to increase, will assist in prescribing sitting interruption strategies. We aimed to determine: (1) the temporal association between the duration of uninterrupted sitting and BP and (2) whether regular sitting interruptions moderate the association between uninterrupted sitting and BP. Electronic databases (PubMed, Web of Science, SPORTDiscus) were searched from inception to July 2022. Reference lists of eligible studies and relevant reviews were also screened. Inclusion criteria for objective (1) were: (i) participants aged ≥ 18years; (ii) a prolonged sitting bout ≥ 1h; and (iii) peripheral BP measurements (systolic BP, diastolic BP, and/or mean arterial pressure) at more than two timepoints during the sitting bout. Additional criteria for objective (2) were: (i) the sitting interruption strategy was implemented during the sitting bout (i.e., not prior to engaging in sitting) and (ii) the study included a control (uninterrupted sitting) condition or group. There were 1555 articles identified, of which 33 met inclusion criteria for objective (1). Of those articles, 20 met inclusion criteria for objective (2). To investigate the effect of sitting duration on the BP response, unstandardized b coefficients (mmHg/h) and 95% confidence intervals (CIs) were calculated using a three-level mixed-effect meta-regression. Increased sitting duration was positively associated with systolic BP (b = 0.42mmHg/h, 95% CI 0.18-0.60), diastolic BP (b = 0.24mmHg/h, 95% CI 0.06-0.42), and mean arterial pressure (b = 0.66mmHg/h, 95% CI 0.36-0.90). In trials where sitting was interrupted, there was a significant decrease in systolic BP (b = - 0.24mmHg/h, 95% CI - 0.42 to - 0.06) and diastolic BP (b = - 0.24mmHg/h, 95% CI - 0.42 to - 0.12), and a non-significant change in mean arterial pressure (p = 0.69). Increased uninterrupted sitting duration results in greater increases in BP; however, regularly interrupting sitting may offset negative effects.

Assessment of the Role of Endothelial and Vascular Smooth Muscle EGFR for Acute Blood Pressure Effects of Angiotensin II and Adrenergic Stimulation in Obese Mice.

(1) Background: Obesity is associated with hypertension because of endocrine dysregulation of the adrenergic and the renin-angiotensin-aldosterone systems. The epidermal growth factor receptor (EGFR) is an important signaling hub in the cardiovascular system. In this study, we investigate the role of smooth muscle cell (VSMC) and endothelial cell (EC) EGFRs for blood pressure homeostasis and acute vascular reactivity in vivo. (2) Methods: Mice with deletion of the EGFR in the respective cell type received either a high-fat (HFD) or standard-fat diet (SFD) for 18 weeks. Intravascular blood pressure was measured via a Millar catheter in anesthetized animals upon vehicle load, angiotensin II (AII) and phenylephrine (PE) stimulation. (3) Results: We confirmed that deletion of the EGFR in VSMCs leads to reduced blood pressure and a most probably compensatory heart rate increase. EC-EGFR and VSMC-EGFR had only a minor impact on volume-load-induced blood pressure changes in lean as well as in obese wild-type animals. Regarding vasoactive substances, EC-EGFR seems to have no importance for angiotensin II action and counteracting HFD-induced prolonged blood pressure increase upon PE stimulation. VSMC-EGFR supports the blood pressure response to adrenergic and angiotensin II stimulation in lean animals. The responsiveness to AII and alpha-adrenergic stimulation was similar in lean and obese animals despite the known enhanced activity of the RAAS and the sympathetic nervous system under a high-fat diet. (4) Conclusions: We demonstrate that EGFRs in VSMCs and to a lesser extent in ECs modulate short-term vascular reactivity to AII, catecholamines and volume load in lean and obese animals.

POSSIBILITIES OF PROLONGED BLOOD PRESSURE MONITORING IN ASSESSMENT OF THE EFFICACY AND SAFETY OF COMBINED ANTIHYPERTENSIVE THERAPY IN EMERGENCY CARE

<b>Introduction.</b> At the stage of emergency medical care, the time of observation of a patient receiving antihypertensive therapy is limited to the time of stay of the emergency medical service team with this patient. Therefore, assessing the efficacy and safety of prescribing a particular antihypertensive treatment pattern is a relevant task. <br><b>Patients and Methods.</b> In this study, we used three two-component combinations of antihypertensive drugs (captopril and furosemide, moxonidine and furosemide, moxonidine and nifedipine) and prolonged blood pressure monitoring. We included 105 patients with a history of primary arterial hypertension who called an ambulance because of an increase in blood pressure and signed a voluntary informed consent. Evaluation of the results of prolonged blood pressure monitoring was carried out in 91 patients. The comorbidity, the clinical condition of the patient, blood pressure monitoring parameters, the efficacy and safety of antihypertensive therapy at the prehospital stage were evaluated. <br><b>Results.</b> The most pronounced and somewhat excessive hypotensive effect developed when using a combination of moxonidine with nifedipine. The index of excessive decrease in blood pressure below 120/70 mm Hg in this group was 51.6% (p<0.05), as compared to the combinations of captopril with furosemide and moxonidine with furosemide (10.3% and 7.8%, respectively). <br><b>Conclusion.</b> The use of blood pressure monitoring in patients with a clinically significant increase in blood pressure on prehospital stage allows us to assess the dynamics of blood pressure, the effectiveness and safety of prescribing various combinations of antihypertensive drugs.

Impact of endoscopist experience, patient age and comorbidities on dose of sedation and sedation-related complications by endoscopic ultrasound.

The aim of the study is to investigate the influence of endosonographer experience and patient-related factors on the dose of sedation and sedation-related complications during endoscopic ultrasound (EUS). Our retrospective analysis included EUS investigations performed between 2015 and 2018 at our institution. Sedation-related complications were defined as cardiorespiratory instability with oxygen saturation drop below 90% or prolonged low blood pressure or bradycardia. In total, 537 EUS examinations were analyzed (37.3% interventional). The median dose of propofol and midazolam were: 140 (30-570) and 3(1-7) mg, respectively. Sedation-related complications were documented in 1.8% of cases. All patients had transient, nonfatal respiratory insufficiency. Totally, 60% of the patients who developed complications were >75 years and 70% were male. The presence of cardiac and/or pulmonary comorbidities was associated with an OR = 8.77 [95% confidence interval (CI), 1.8-41.7] and American Society of Anesthesiologists class III with an OR = 7.64 (95% CI, 1.60-36.3) for the occurrence of sedation-related complications. Endosonographer experience did not influence the rate of sedation-related complications. In both diagnostic and interventional EUS, patients with comorbidities and older age received significantly less sedation. Experienced endosonographers used less sedation than trainees. Endosonographer experience, patient age and the presence of comorbidities had a significant influence on sedation dose. Sedation-related complications occurred only in 1.8% of cases.

Management of primary aldosteronism and mineralocorticoid receptor-associated hypertension.

Resistant hypertension is associated with a poor prognosis due to organ damage caused by prolonged suboptimal blood pressure control. The concomitant use of mineralocorticoid receptor (MR) antagonists with other antihypertensives has been shown to improve blood pressure control in some patients with resistant hypertension, and such patients are considered to have MR-associated hypertension. MR-associated hypertension is classified into two subtypes: one with a high plasma aldosterone level, which includes primary aldosteronism (PA), and the other with a normal aldosterone level. In patients with unilateral PA, adrenalectomy may be the first-choice procedure, while in patients with bilateral PA, MR antagonists are selected. In addition, in patients with other types of MR-associated hypertension with high aldosterone levels, MR antagonists may be selected as a first-line therapy. In patients with normal aldosterone levels, ARBs or ACE inhibitors are used as a first-line therapy, and MR antagonists may be used as an add-on agent. Since MR antagonist therapy may have efficacy as a first-line or add-on agent in these patients, it is important to recognize this type of hypertension. Further studies are needed to elucidate the pathogenesis and management of MR-associated hypertension in more detail to improve the clinical outcomes of patients with MR-associated hypertension.

P251 Right ventricular free wall dissection clearly detected and recorded by echocardiography: a fatal complication after inferior myocardial infarction

Abstract An 81-year-old man was transferred to our institution by ambulance because of poor feeding, general fatigue and slight disorientation lasting for a week. On arrival, he was awake and able to speak, however, his blood pressure was low at 61/43 mmHg in spite of his medical history of hypertension. His ECG showed abnormal Q waves and ST elevation in II, III, aVF leads. The echo exam detected severe hypokinesis in the left ventricular inferior wall and reduced ejection fraction at 30%. Pericardial effusion was not observed in the first echo exam. The patient was diagnosed as cardiogenic shock due to recent inferior myocardial infarction. Coronary angiography was performed, which detected total occlusion of mid right coronary artery, followed by a successful percutaneous coronary intervention (PCI) with a drug-eluting stent under the support of intra-aortic balloon pumping. Nevertheless, his blood pressure remained low and intravenous adrenaline administration was necessary during and even after PCI. To detect the cause of prolonged low blood pressure, echo was performed again immediately after PCI. The echo exam detected new findings: right ventricular posterior free wall was dissected and abnormal shunt flows were obviously observed from left ventricle to right atrium through the dissection cavity during systole. An urgent surgical repair was considered as the only option for his survival, however, his family did not accept it because the operation itself was too risky. On the next day of his admission, he passed away. Right ventricular free wall dissection is a very rare but fatal complication after inferior myocardial infarction, nevertheless, we could detect it by echocardiography with clearly recorded images. Abstract P251 Figure.

Abstract 116: Acute and Chronic Anti-Arrhythmogenic Effect of Liposome-Encapsulated Hemoglobin (HbV) on the Myocardium Through Improving Myocardial Electrical Remodeling and the Arrhythmogenic Substrate in Hemorrhagic Shock-Induced Heart

Introduction: Prolonged blood pressure < 40 mmHg in hemorrhagic shock (HS) causes irreversible heart dysfunction, “Shock Heart Syndrome” (SHS), which is associated with lethal arrhythmias (VT/VF). Methods: To investigate whether liposome-encapsulated human hemoglobin (HbV) is comparable to washed red blood cells (wRBCs) for improving arrhythmogenesis in SHS in either acute or chronic phase, optical mapping analysis (OMP), electrophysiological study (EPS) and pathological examinations were performed in Sprague-Dawley rat hearts, being obtained from both acute and chronic phase when each rat survived. The first, they were subjected to acute HS by withdrawing 30% of total blood volume. After HS, rats were immediately resuscitated by transfusing exactly same amount of 5% albumin (5%ALB, n=13), HbV (n=13), or wRBCs (n=13). All rats in chronic phase survived at least several weeks. After excising heart, OMP and EPS were performed in Langendorff-perfused hearts. Results: In both acute and chronic phase, OMP showed tendency for abnormal conduction and significantly impaired action potential duration dispersion (APDd) in left ventricle with 5%ALB (25±9 / 24±10 ms, Acute / Chronic phase). In contrast, myocardial conduction and APDd were substantially preserved with HbV (14±3 / 13±5 ms) and wRBCs (14±3 / 15±3 ms) as shown in Figure . Sustained VT/VF was easily provoked by burst pacing stimulus to left ventricle with 5%ALB. No VT/VF was induced with HbV and wRBCs. Pathology showed myocardial structural damage characterized by worse myocardial cell damage and Connexin43 with 5%ALB, whereas it was attenuated with HbV and wRBCs in both acute and chronic phase. Conclusions: Ventricular structural remodeling after HS causes VT/VF in the presence of APDd. Transfusion of HbV prevents acutely and chronically VT/VF, similarly to transfusion of wRBCs, by preventing chronic electrical remodeling of APDd and preserving myocardial structures in HS-induced SHS

Myocardial Electrical Remodeling and the Arrhythmogenic Substrate in Hemorrhagic Shock-Induced Heart: Anti-Arrhythmogenic Effect of Liposome-Encapsulated Hemoglobin (HbV) on the Myocardium.

Prolonged low blood pressure <40 mmHg in hemorrhagic shock (HS) causes irreversible heart dysfunction, 'Shock Heart Syndrome' (SHS), which is associated with lethal arrhythmias (ventricular tachycardia or ventricular fibrillation [VT/VF]) leading to a poor prognosis. To investigate whether the liposome-encapsulated human hemoglobin oxygen carrier (HbV) is comparable in effectiveness to autologous washed red blood cells (wRBCs) for improving arrhythmogenic properties in SHS, optical mapping analysis (OMP), electrophysiological study (EPS), and pathological examinations were performed in Sprague-Dawley rat hearts obtained from rats subjected to acute HS by withdrawing 30% of total blood volume. After acute HS, the rats were immediately resuscitated by transfusing exactly the same amount of saline (SAL), 5% albumin (5% ALB), HbV, or wRBCs. After excising the heart, OMP and EPS were performed in Langendorff-perfused hearts. OMP showed a tendency for abnormal conduction and significantly impaired action potential duration dispersion (APDd) in both ventricles with SAL and 5% ALB. In contrast, myocardial conduction and APDd were substantially preserved with HbV and wRBCs. Sustained VT/VF was easily provoked by a burst pacing stimulus to the left ventricle with SAL and 5% ALB. No VT/VF was induced with HbV and wRBCs. Pathology showed myocardial structural damage characterized by worse myocardial cell damage and Connexin43 with SAL and 5% ALB, whereas it was attenuated with HbV and wRBCs. Ventricular structural remodeling after HS causes VT/VF in the presence of APDd. Transfusion of HbV prevents VT/VF, similarly to transfusion of wRBCs, by preventing electrical remodeling and preserving myocardial structures in HS-induced SHS.

Modern Aspects of Hypertensive Angioretinopathy

This literature review is devoted to modern problems of hypertensive retinopathy with arterial hypertension, as well as hypertensive retinopathy in combination diseases. The latest world studies were analyzed. Particular attention is paid to the clinical disease characteristics at the present stage with the analysis of the arterio-venous ratio, optic nerve edema (with high blood pressure figures) using an automated system, vector analysis, suggesting a new arteriovenous classification, called Web Integration (Wivern). The modern pathogenesis of hypertensive retinopathy, namely the ratio of proangiogenic and anti-angiogenic factors, the role of inflammation (C-reactive protein), the role of endothelin-1, endostatin, interleukin-8 (IL-8), and the main fibroblast growth factor (bFGF ), angiogenin and uric acid. The special importance of fundus registration is reflected with the help of the newest equipment at high figures of arterial pressure in patients with hypertensive retinopathy. It is known that according to the World Health Organization (WHO), mortality rate from cardiovascular diseases is 31 %. Hypertension is the main risk factor for coronary heart disease, myocardial infarction, heart failure, stroke, kidney disease and early death. Questions of eye blood flow in hypertensive angioretinopathy in patients with arterial hypertension (AH) are covered. Hypertensive retinopathy (HR) is a retinal disease that is caused by a prolonged increase blood pressure (BP) and leads to a decrease in vision. The data of pathophysiology are analyzed (arterial hypertension (AH) leads to thickening of the vessels of the inner membrane (intima), to thickening of the medial membrane (media) — hyperplasia of the muscular tissue followed by hyaline degeneration with the development of sclerotic changes). The questions of modern diagnostics with retinal morphological status evaluation (OCT), detection of eye fundus condition with newest fundus camers, pathogenetic aspects are discussed. This review will help to prevent the development of more severe forms of hypertensive retinopathy. This information will allow us to identify the most significant indicators in the early diagnosis of hypertension angioretinopathy.

Blood Pressure Reactivity and Recovery to Anger Recall in Hypertensive Patients with Type D Personality.

Type D, otherwise known as distressed personality type, has been associated with an increased risk of cardiovascular morbidity and mortality. Blood pressure reactivity and recovery to stress could be a possible underlying pathway linking type D personality and cardiovascular events. A total of 41 patients with hypertension were recruited from a regional hospital in southern Taiwan. Demographic and clinical characteristics were obtained from all participants. Type D personality was assessed using the 14-item Type D Scale-Taiwanese version. Systolic blood pressure, diastolic blood pressure, and heart rate were measured at the end of baseline, anger recall, verbal, and recovery phases of an anger recall task. Analysis of covariance was used to examine differences in blood pressure and heart rate at the anger recall, verbal, and recovery phase between patients with or without type D personality. After adjusting for baseline measurements, sex, and age, systolic blood pressure (p = 0.002) and diastolic blood pressure (p = 0.011) at the recovery phase were significantly higher in the patients with type D personality. No significant differences in blood pressure or heart rate were observed in the anger recall or verbal phase between the two groups of patients. The findings of this study support the notion that prolonged blood pressure recovery rather than high reactivity could be an underlying pathway linking type D personality and the risk of future cardiovascular events among patients with hypertension.

Influence of non-invasive blood pressure measurement intervals on the occurrence of intra-operative hypotension.

The American Society of Anesthesiologists Standards for Basic Monitoring recommends blood pressure (BP) measurement every 5min. Research has shown distractions or technical factors can cause prolonged measurement intervals exceeding 5min. We investigated the relationship between prolonged non-invasive BP (NIBP) measurement interval and the incidence of hypotension, detected post-interval. Our secondary outcome was to determine independent predictors of these prolonged NIBP measurement intervals. Retrospective data were analyzed from 139,509 general anesthesia cases from our institution's Anesthesia Information Management System (AIMS). Absolute hypotension (AH) was defined a priori as a systolic BP < 80mmHg and relative hypotension (RH) was defined as a 40% decrease in systolic BP from the preoperative baseline. Odds ratios (OR) with 95% confidence intervals and Pearson's Chi square Test reported the association of prolonged NIBP measurement intervals on hypotension detected post-NIBP measurement interval. Logistic regression models were developed to determine independent predictors of NIBP measurement intervals. The analysis revealed that NIBP measurement intervals greater than 6 and 10min are associated with an approximately four times higher incidence of a patient transitioning into hypotension (AH/RH > 6min OR 4.0 / 3.6; AH/RH > 10min OR 4.3 / 3.9; p < 0.001). A key finding was that the "> 10-minute AH model" indicated that age 41-80, increased co-morbidity profile, obesity and turning (repositioning) of the operative room table were significant predictors of prolonged NIBP measurement intervals (p < 0.001). While we do not suggest NIBP measurement intervals cause hypotension, intervals greater than 6 and 10min are associated with a fourfold increase in the propensity of an undetected transition into both RH or AH. These data support current monitoring guidelines.

Plastics and cardiovascular health: phthalates may disrupt heart rate variability and cardiovascular reactivity.

Plastics have revolutionized medical device technology, transformed hematological care, and facilitated modern cardiology procedures. Despite these advances, studies have shown that phthalate chemicals migrate out of plastic products and that these chemicals are bioactive. Recent epidemiological and research studies have suggested that phthalate exposure adversely affects cardiovascular function. Our objective was to assess the safety and biocompatibility of phthalate chemicals and resolve the impact on cardiovascular and autonomic physiology. Adult mice were implanted with radiofrequency transmitters to monitor heart rate variability, blood pressure, and autonomic regulation in response to di-2-ethylhexyl-phthalate (DEHP) exposure. DEHP-treated animals displayed a decrease in heart rate variability (-17% SD of normal beat-to-beat intervals and -36% high-frequency power) and an exaggerated mean arterial pressure response to ganglionic blockade (31.5% via chlorisondamine). In response to a conditioned stressor, DEHP-treated animals displayed enhanced cardiovascular reactivity (-56% SD major axis Poincarè plot) and prolonged blood pressure recovery. Alterations in cardiac gene expression of endothelin-1, angiotensin-converting enzyme, and nitric oxide synthase may partly explain these cardiovascular alterations. This is the first study to show an association between phthalate chemicals that are used in medical devices with alterations in autonomic regulation, heart rate variability, and cardiovascular reactivity. Because changes in autonomic balance often precede clinical manifestations of hypertension, atherosclerosis, and conduction abnormalities, future studies are warranted to assess the downstream impact of plastic chemical exposure on end-organ function in sensitive patient populations. This study also highlights the importance of adopting safer biomaterials, chemicals, and/or surface coatings for use in medical devices.NEW & NOTEWORTHY Phthalates are widely used in the manufacturing of consumer and medical products. In the present study, di-2-ethylhexyl-phthalate exposure was associated with alterations in heart rate variability and cardiovascular reactivity. This highlights the importance of investigating the impact of phthalates on health and identifying suitable alternatives for medical device manufacturing.

Beneficial effects of prolonged blood pressure control after carotid artery stenting.

ObjectivesThe main purpose of this study was to investigate whether carotid artery stenting (CAS) plus medicine in patients with severe carotid artery stenosis provide a better long-term blood pressure (BP) control compared to other medical treatments alone. The other aim was to explore the correlation between post-CAS hypotension within 6 h and long-term BP reductions after CAS.Materials and methodsPatients with severe carotid stenosis were recruited either in the CAS group or in the medication group. BPs and the number of classes of antihypertensive agents were recorded at baseline, 6, and 12 months. Extra BP information was collected at 6 h, 3 days, and 1 month after CAS. Univariate and multivariate linear regressions were performed to test the relationship of BP changes among CAS and medication groups after 6 and 12 months of follow-up. Univariate linear regressions were also used to determine the correlations between the mean or maximal systolic BP (SBP) reductions at 6 h and 1 year post-CAS.ResultsIn total, 72 members in the CAS group and 82 members in the medication group were recruited. Compared with the medication group, patients in the CAS group had greater BP reductions at 6 and 12 months of follow-up after adjusting for confounding factors (13.56 mmHg at 6 months, P=0.0002; 16.98 mmHg at 12 months, P<0.0001). This study also shows significant positive correlations between the mean or maximal SBP reductions 6 h post-CAS and SBP reductions 1 year post-CAS (β =0.20±0.07, P=0.0067 and β =0.47±0.10, P<0.0001, respectively).ConclusionAs compared to medical treatment alone, CAS may provide significant beneficial effect on long-term BP control 1 year post-CAS. Furthermore, SBP reductions 6 h post-CAS may predict the SBP reductions 1 year post-CAS.

Blood Pressure Elevation Lasting Longer Than 1 Year Among Public Employees After the Great East Japan Earthquake: The Watari Study.

We have previously reported that the public employees of Watari town showed significantly greater elevations in both systolic and diastolic blood pressure than the general population 4-8 months after the Great East Japan Earthquake, which occurred on 11 March 2011. To examine whether these differences persisted thereafter, we conducted a follow-up study for both the public employees and the general population of Watari town over 1 year. Among 225 public employees and 1232 individuals from the general population of the town who received consecutive annual health checkups from 2010 to 2012, 89 pairs were matched for age and sex according to a propensity score. The baseline characteristics (predisaster) did not statistically differ between the paired groups. The public employees showed significantly higher systolic and diastolic blood pressure in 2011 (postdisaster) compared with the general population (129.8 ± 14.0/78.0 ± 11.7 vs. 117.0 ± 14.4/71.6 ± 11.4 mm Hg, P < 0.001 for both). Furthermore, the systolic blood pressure of the public employees remained significantly higher than that of the general population in 2012 (125.3 ± 16.0 vs. 119.9 ± 15.5 mm Hg, P = 0.023). Prolonged blood pressure elevation among the public employees was observed for more than 1 year after the disaster, suggesting a need for close blood pressure monitoring of public employees engaged in long-term disaster relief operations.

Abstract 099: Functional Remodeling of the Renal Vasculature Precedes the Establishment of Salt-sensitive Hypertension in Eln-deficient Mice

Vascular stiffening due to elastin deficiency is a leading risk for hypertension and chronic kidney disease (CKD). However, the mechanisms by which elastin deficiency is involved in the pathogenesis of hypertension and/or CKD are poorly understood. Here, we used elastin heterozygous mice ( Eln+/- ), an animal model of elastin insufficiency, to test the hypothesis that renal dysfunction due to elastin deficiency occurs independently of and precedes the development of hypertension in this mouse model. We assessed blood pressure (BP) and renal hemodynamics in 30-day (P30) and 12-week old anesthetized male and female mice. At P30, mean blood pressure of Eln+/- was similar to wild type (WT) controls ( Eln+/- , 79 ± 5 vs. WT, 69±3 mmHg, P = 0.06); however, renal blood flow was lower ( Eln+/- 2.9 ± 0.2 vs. WT 4.0 ± 0.5 mL/min/g KW, P = 0.03) whereas renal vascular resistance (RVR; Eln+/- 29 ± 3 vs. WT 18 ± 3 mmHg/mL/min/g KW, P = 0.03) was augmented at baseline in Eln+/- mice. At 12 wks old, RVR remained elevated while filtration fraction was higher in male Eln+/- relative to WT mice ( Eln+/- 44 ± 3 vs. WT 38±5 % P = 0.07). Eln+/- mice showed isolated systolic hypertension that was evident only at nighttime ( Eln+/- 136 ± 2 vs. WT 112 ± 6 mmHg, P &lt;0.01). Acute salt loading with 6% dietary sodium increased daytime systolic blood pressure only in male Eln+/- mice ( Eln+/- 118 ± 5 vs. WT 102 ± 6 mmHg, P = 0.03), causing a rightward shift and blunted slope of the pressure-natriuresis curve. Renal interlobar artery basal tone and myogenic response to increasing intraluminal pressure at P10 were similar ( Eln+/- 78 ± 3 vs. WT 67 ± 6 % P = 0.06) whereas they were augmented at P30 ( Eln+/- 63 ± 4 vs. WT 49 ± 6 % P = 0.05) and at 12 wks old in Eln+/- mice ( Eln+/- 50 ± 2 vs. WT 33 ± 3 % P &lt; 0.01), and normalized by the AT1R blocker, candesartan ( Eln+/- 22 ± 9 vs. WT 8 ± 5 % P = 0.10). We conclude that AT1R mediates augmented mechanotransduction and renal vascular dysfunction due to Eln insufficiency that in turn contribute to altered renal sodium handling and increased BP. Such prolonged systemic BP elevation leads to glomerular structural damage due to high renal perfusion pressure. Therefore, therapies that target the AT1R to control BP in patients with elastin deficiency may be beneficial in preventing hypertension-evoked kidney damage.

Protective Role of Kallistatin in Vascular and Organ Injury.

Kallistatin is an endogenous protein that exerts pleiotropic effects, including vasodilation and inhibition of angiogenesis, inflammation, oxidative stress, apoptosis, fibrosis, and tumor progression. Through its 2 functional domains—an active site and a heparin-binding site—kallistatin regulates differential signaling pathways and a wide spectrum of biological functions. Kallistatin’s active site is key for inhibiting tissue kallikrein activity and stimulating the expression of endothelial nitric oxide (NO) synthase (eNOS), sirtuin 1 (SIRT1), and suppressor of cytokine signaling 3 (SOCS3). Kallistatin via its heparin-binding site blocks signaling pathways mediated by growth factors and cytokines, such as vascular endothelial growth factor (VEGF), tumor necrosis factor-α (TNF-α), high-mobility group box-1 (HMGB1), Wnt, transforming growth factor-β (TGF-β), and epidermal growth factor. Kallistatin gene or protein delivery protects against the pathogenesis of hypertension, heart and kidney damage, arthritis, sepsis, influenza virus infection, tumor growth, and metastasis in animal models. Conversely, depletion of endogenous kallistatin by neutralizing antibody injection exacerbates cardiovascular and renal injury in hypertensive rats. Kallistatin levels are markedly reduced in rodents with hypertension, sepsis, streptozotocin-induced diabetes mellitus, and cardiac and renal injury. Kallistatin levels are also diminished in patients with liver disease, septic syndrome, diabetic retinopathy, severe pneumonia, inflammatory bowel disease, obesity, and prostate, and colon cancer. Therefore, circulating kallistatin levels may serve as a new biomarker for human diseases. This review summarizes kallistatin’s protective roles and mechanisms in vascular and organ injury and highlights the therapeutic potential of kallistatin for multiple disease states. Kallistatin was discovered in human plasma as a tissue kallikrein–binding protein.1 Sequence analysis indicated that tissue kallikrein–binding protein is a novel serine proteinase inhibitor (serpin) and was later designated kallistatin because of its ability to inhibit tissue kallikrein activity.2–9 Tissue kallikrein is a serine proteinase that cleaves low–molecular weight kininogen substrate to release vasoactive kinin peptides.10 The …

Hypertension Mechanisms: Elastin Haploinsufficiency Alters Renal Structure and Function

Hypertension is a hallmark of Williams syndrome, an autosomal‐dominant disease caused partly by loss‐of‐function mutations or gene deletions resulting in elastin (Eln) haploinsufficiency. Hypertension is a leading risk for several cardiovascular diseases including heart failure, stroke, chronic kidney disease, and renal failure. The mechanisms underlying hypertension due to elastin insufficiency are poorly understood. Because the kidney plays a critical role in long‐term blood pressure (BP) control, we determined whether Eln haploinsufficiency affects renal structure and function to contribute to hypertension development. We determined the effects of hypertension on wild type (WT) and Eln+/− mouse kidney structure using histology and electron microscopy. Kidney function was assessed by measuring renal blood flow, glomerular filtration rate (GFR), urine output, sodium and potassium excretion, and proteinuria. We found that Eln+/− mice had glomerular podocyte effacement accompanied by increased BP, renal vascular resistance (RVR), urine output and sodium excretion rate. However, GFR was only slightly elevated in Eln+/− mice. Systemic angiotensin type 1 receptor blockade with candesartan decreased RVR and BP in female Eln+/− mice to levels in WT controls. Ex vivo pressurized vessel studies showed increased myogenic tone accompanied by increased wall tension and wall strain in interlobar arteries from Eln+/− mice. We conclude that Eln haploinsufficiency causes renal vascular dysfunction, which contributes to the development of hypertension. Such a prolonged systemic BP elevation leads to glomerular structural damage due to high renal perfusion pressure. Therefore, therapies that control BP in patients with elastin deficiency may be beneficial in preventing hypertension‐evoked kidney damage.Support or Funding InformationMargaret Q. Landenberger Research Foundation Grant

Heart-Healthy Nutrition Approach for Chronic Kidney Disease Patients

CHRONIC KIDNEY DISEASE (CKD) patients have a higher risk of developing cardiovascular disease (CVD) in comparison to the general population. There is a well-established link between CKD and CVD risk factors in this population. CVD is the leading cause of morbidity and mortality in the CKD population. This increased risk and associated link emphasizes the need to further educate patients about the importance of a hearthealthy nutrition intake, placing the focus on CKD patients who exhibit risk factors or already have CVD. CVD encompasses a group of diseases that involve the heart and/or the blood vessels: Coronary heart disease is one of the most common forms of CVD. This affects blood vessels of the heart and may cause angina (chest pain) and heart attacks. Heart failure or congestive heart failure occurs when the heart is not able to pump blood around the body as well as it should. This develops slowly over time and may limit the ability to perform daily activities of living. Ischemic heart disease may be characterized by atherosclerosis and result in myocardial infarction or angina. Left ventricular hypertrophy is an abnormal enlargement of the left ventricle and most commonly the result of prolonged high blood pressure. Stroke is the lack of blood flow to the brain. A stroke may be caused by a blood clot or bleeding in the brain from a broken blood vessel. What are some of the strategies that registered dietitian nutritionists (RDNs) with expertise in renal nutrition and