bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract P115: The Epidemiological Profile Of CKD Among African American Men And Women: Findings From The Jackson Heart Study
Authors: Jones Kia Monique , Jones Kia Monique
Published: September 2020

The prevalence of CKD is paramount. CKD affects almost 1 in 7 adults in the United States and is associated with increased rates of cardiovascular disease. While African Americans make up about 13 percent of the population, they account for 35 percent of the people with kidney failure in the United States. The prevalence of early CKD is equivalent across racial and ethnic groups in the United States, but CKD progresses to end-stage renal disease far more rapidly in minority populations, with rates nearly four times higher in African Americans than in whites. The purpose of this study is to address the emergence of chronic disease complications in the African American community that focuses on associations with prevalent CKD outcomes in the JHS. Epidemiological study design used to access the preliminary data to derive conclusions about CKD. CKD was assessed by the JHS participants, who self-reported their CKD status/history. CKD was measured using the Renal form and History of CKD form that was given as a questionnaire within the JHS during Examination 1 Period. CKD was measured by Jackson Heart Study’s estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 to determine CKD status. African Americans have a disproportionate burden of CKD, which tends to have an earlier onset and a more rapid progression in this population. From a population health standpoint, CKD factors such as smoking, diabetes, history of hypertension, dietary patterns, physical activity, blood apolipoproteins and psychosocial factors account for more than 90% of the population-attributable risk. African American men and women with CKD is viewed among the highest-risk groups for cardiovascular events and disease. Race and ethnicity are associated with sociocultural and biologic variations that influence the risk and progression of CKD. Understanding these factors for minority populations can help in targeting interventions to decrease the disproportionately high rates of CKD progression and complications. As prevalence of chronic disease increased, public health’s focus on health- related behaviors and risk factors shifted the discipline’s attention to considering the neighborhood's influence on social determinants of health.
Abstract P120: Association Of Liver Transaminase Levels And Long-term Blood Pressure Variability In Military Young Males In Taiwan
Authors: Lin Gen-min , Liu Pang-yen
Published: September 2020

Background:
Elevated serum liver transaminases (AST and ALT), highly related to metabolic disorders, are paradoxically associated with lower risk of cardiovascular disease (CVD) and mortality. Blood pressure variability (BPV), a risk factor of CVD, has not been examined the relationship with serum liver transaminase.

Methods:
A prospective cohort of 1,112 military males, aged 32.2 years was collected in Taiwan. Serum AST and ALT were obtained from a 12 hour-fast blood sample of each participant. BPV was assessed by standard deviation (SD) and average real variability (ARV) of systolic and diastolic blood pressure (SBP and DBP), respectively across 4 visits during the study period (2012-14, 2014-15, 2015-16, and 2016-18). Multivariable linear regression analysis was used to determine the association adjusting for age, body mass index, SBP, DBP, lipid profiles, physical activity, alcohol and smoking status.

Results:
In the unadjusted model, serum ALT were positively correlated with SD
DBP
and ARV
DBP
(β (SE) =0.36 (0.16) and 0.24 (0.12), respectively), and so were AST (β= 0.19 (0.08) and 0.14 (0.06), respectively). However, all the associations were insignificant with adjustments. By contrast, the associations with systolic BPV were initially insignificant in the unadjusted model. With adjustments, serum ALT were negatively correlated with SD
SBP
and ARV
SBP
(β= -0.34 (0.16) and -0.24 (0.12), respectively) and so were AST (β= -0.14 (0.07) and -0.11 (0.06), respectively).

Conclusion:
Our findings suggest that liver transaminase levels were negatively correlated with long-term systolic BPV in young male adults, possibly accounting for the lower risk of CVD in previous studies.
Abstract P128: Age-related Patterns In Systolic And Diastolic Blood Pressure In Adults From The United States And India
Authors: Visaria Aayush , Lo David , Maniar Pranay
Published: September 2020

The purpose of this cross-sectional, exploratory analysis was to describe age-related patterns of blood pressure (BP) among participants in India (using the 2014 Annual Health Survey) and the United States (using National Health & Nutrition Examination Surveys 2011-2016). We included 10,759 U.S. and 790,641 Indian participants aged ≥20 years with ≥2 BP readings. We plotted mean systolic (SBP) and diastolic BP (DBP) across 5-year age groups and estimated best fit models. SBP increased linearly with age in both sexes and study populations (R
2
: 0.88-0.99; Fig. 1-2). Those with overweight/obese BMI had higher SBP and modestly higher rates of increase in SBP. DBP followed a quadratic curve (R
2
: 0.68-0.99), peaking in the 5-6th decade (45-49 years in U.S. and 50-59 in India) with higher and earlier peaks in those with elevated BMI. The models’ strong fit and similarity between study populations supports the notion that physical processes underly BP’s age-related changes.
Abstract P136: Effects Of Sex Hormones On The Hemodynamic And Sympathetic Responses To Centrally Administered Tumor Necrosis Factor-α In Rats
Authors: Cao Yiling , Xue Baojian , Yu Yang , Johnson Alan K , Wei Shun-Guang
Published: September 2020

Inflammation plays an important role in the pathophysiology of cardiovascular dysfunction and neurohumoral excitation in heart failure and hypertension. Growing evidence has demonstrated significant sex differences in the inflammatory response and immune processes, with estrogen exerting an anti-inflammatory effects and testosterone potentially having pro-inflammatory influence. We previously reported that central administration of tumor necrosis factor-α (TNF-α) elicited different effects on blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) in male and female rats. Whether the sex steroids estrogen and testosterone contribute to the observed differences in TNF-α-induced hemodynamic and sympathetic responses remains unknown. We hypothesized that estrogen protects against TNF-α-induced sympathetic excitation and pressor responses while testosterone enhances these excitatory outcomes in response to TNF-α. Female or male Sprague Dawley rats (10-12 weeks) anesthetized with ketamine plus xylazine underwent bilateral ovariectomy or castration, respectively, 2 weeks prior to study. Sham-operated (Sham) female or male animals served as controls. TNF-α (100 ng) was administered intracerebroventricularly (ICV). BP (mmHg), HR (bpm) and RSNA (% change) were recorded in urethane anesthetized rats. In ovariectomized female rats (n=6), ICV TNF-α induced significantly (*p<0.05 vs. Sham) larger increases in BP (19.3 ± 1.4* vs. 12.8 ± 1.2 ), HR (76.3 ± 4.8* vs. 51.5 ± 4.3) and RSNA (104.8 ± 6.9* vs. 72.4 ± 5.1), compared with Sham-female rats, that began within 20-30 mins and peaked at 90-120 mins after ICV injection. In castrated male rats (n=6), ICV TNF-α-elicited significantly smaller increases in BP (15.2 ± 1.3* vs. 21.8 ± 1.6), HR (57.7 ± 4.2* vs. 82.6 ± 4.1) and RSNA (72.6 ± 4.3* vs. 110.3 ± 4.7), compared with Sham-male animals. These data indicate a distinct role of sex hormones estrogen and testosterone in central inflammation-driven cardiovascular and sympathetic activation and suggest a protective effect of estrogen and a harmful effect of testosterone in the development of hypertension and heart failure.
Abstract P137: Knock Out Of Regulatory G Protein Signaling 2 Specifically In CD4 T Cells Prevents Angiotensin II Induced Hypertension
Authors: Scroggins Sabrina M , Gray Gabrielle , Myers Monica C , Miller Sarah N , Nakagawa Pablo , Santillan Donna A , Grobe Justin L , Santillan Mark K
Published: September 2020

Preeclampsia (PreE) is a hypertensive disorder in pregnancy. Aberrations of Regulator of G protein Signaling (RGS) family members are associated with PreE and hypertension (HTN). We previously observed a 9-fold increase in RGS2 in CD4+ T cells during PreE. In total, our work suggests that modulating T cells may be a therapeutic strategy for HTN. We hypothesize that reducing RGS2 specifically in CD4+ T cells will restore anti-inflammatory T cell responses and prevent HTN.

Utilizing an angiotensin (ANG) II infusion mouse model, we aimed to investigate 1) the impact of the loss of RGS2 in CD4+ T cells on cytokine production and 2) if the loss of RGS2 in CD4+ T cells will protect against the development of HTN. RGS2 was knocked-out in CD4+ T cells (CD4-Cre x RGS2
flox
mice;
KO
). CD4 RGS2
KO
(n=5) or littermate control mice (CTL, n=3) were administered 490 ng/kg/min ANG II for 21 days via mini-osmotic pump. Blood pressure was assessed by radiotelemetry. ELISAs were performed to determine pro- and anti- inflammatory cytokine levels in tissues from KO (n=9) and CTL (n=8) mice.

Pro-inflammatory cytokines IFNγ and IL-17 were not significantly different in the heart, kidney, liver or spleen of KO vs CTL mice. The anti-inflammatory cytokines IL-4 (KO 410 vs CTL 339 pg/mL, p<0.05) and TGFβ (KO 5.7x10
5
vs 5.0x10
5
pg/mL, p<0.05) were increased in the kidneys of KO mice compared to CTL mice. At baseline, KO and CTL mice showed no differences in 24-hr heart rate (HR), systolic or diastolic blood pressure (SBP and DBP, respectively). Throughout the study, KO mice had a significantly lower 24-hr SBP (Day 7: KO 132.3 vs CTL 149.7 mmHg, p<0.05; Day 14: KO 123.6 vs CTL 162.3 mmHg, p<0.05; Day 21: KO 118.3 vs 154.8 mmHg, p<0.05) and DBP (Day 7: KO 101.2 vs CTL 113.8 mmHg, p<0.05; Day 14: KO 98.4 vs CTL 121.8 mmHg, p<0.05; Day 21: KO 96.8 vs 116.4 mmHg, p<0.05) compared to CTL mice. The 24-hr HR was only significantly lower at three weeks ANG II (KO 493.4 vs CTL 540.6 bpm, p<0.05) compared to CTL mice.

The increased levels of IL-4 and TGFβ observed in KO mice support a role of RGS2 in anti-inflammatory immune responses. In accordance with our hypothesis, the loss of RGS2, specifically in CD4+ T cells prevented ANG II-induced hypertension. Therefore, RGS2 expression in CD4+ T cells plays a critical role in the development of HTN.
Abstract P140: Myeloid Activation in Hypertension and Effects on Bone: A New End Organ?
Authors: Do Carmo Luciana , Xiao Liang , Uppuganti Sasidhar , Florian David , Nyman Jeffry , Guelcher Scott , Harrison David G
Published: September 2020

Hypertension affects approximately one-half of the adult population. Another common disease is osteoporosis, which affects 53 million people in the United States. Clinical studies have shown an association between hypertension and bone loss. We hypothesized that experimental hypertension would be associated with osteoporosis. In Angiotensin (Ang) II-induced hypertension, there is an increase in hematopoietic stem cells (HSCs) expressing the master myeloid transcription factor PU.1 (2.99 ± 0.92) vs. sham (0.17 ± 0.04,p=0.007). Here we reported an increase an osteoclasts number per mm
2
by Tartrate-resistant acid phosphatase staining in DOCA-salt hypertension (27.4 ± 2.3) vs. sham (12.09 ± 1.7, p=0.0002). Using microCT analysis of femoral bone, we found that Ang II-induced hypertension caused striking bone loss as reflected by decreases in cortical bone area, cortical thickness and trabecular number (see Table). We also examined bone strength using a three-point biomechanical testing. In keeping with the micro-CT data, both forms of hypertension were associated with increased bone fragility, reflected by several parameters including maximum force to failure and rigidity (see Table). Recent studies have implicated T cells in the genesis of osteoporosis, and in keeping with this, we found almost two-fold increase in both CD4
+
and CD8
+
T cells in the marrow of mice with DOCA-salt hypertension. Thus, in two models of experimental hypertension there is marked bone loss and the development of bone fragility, potentially related to T cell accumulation and cytokine release. These findings might explain the association between osteoporosis and hypertension.
Abstract P143: Salt-sensitivity And Salt-resistance Differentially Modulate Renal And Colonic T Regulatory Cells
Authors: Molina Patrick A , Edell Claudia J , Muir Rachel Q , Colson Jackson C , Maynard Craig L , Pollock Jennifer S
Published: September 2020

High salt diets (HSD) promote both inflammation and immunosuppression as shown in numerous studies utilizing salt-sensitive or hypertensive models. However, mechanisms involved in the homeostatic immune response to HSD, alone, have not been fully elucidated. Regulatory T cells (FOXP3
+
CD4
+
T cells) play a role in host protection against disease or environmental stressors. Further, recent studies show that RORt
+
expression by Tregs may represent a functional adaptation by Tregs in response to alterations to the diet. Thus, we hypothesized that these Treg populations may expand in response to HSD alone, and a hypertensive insult prior to the HSD blunts this response. We designed experiments to determine whether Tregs and RORt
+
Tregs expand in response to HSD or with LNAME hypertension followed by HSD. We evaluated the following groups in male C57BL/6J mice: NSD (normal salt diet, 0.4% NaCl), LNAME/NSD (0.5mg/ml for 3-wks in drinking water, followed by 3-wks NSD), HSD (4% NaCl+1% NaCl in drinking water, 2-wks), or LNAME/HSD (0.5mg/mL for 3-wks in drinking water, with 1-wk NSD followed by 2-wks HSD). Following immune cell isolation, we utilized flow cytometry to phenotype renal and colonic T cells. Data are expressed as frequency of means (% of CD4
+
TCRbeta
+
T cells)±SEM (n=3-8/group) compared to NSD. In kidneys, HSD significantly expanded Tregs and RORt
+
Tregs, while LNAME/HSD group was unchanged compared to controls (% Treg: NSD: 5.7±0.5; L-NAME: 6.5±0.5; HSD: 9.2±1.0**; LNAME/HSD: 6.2±0.3; % RORt
+
Treg: NSD: 0.4±0.07; L-NAME: 0.6±0.13; HSD: 1.8±0.41***; LNAME/HSD: 0.6±0.14; **p<0.01, ***p<0.001). In the colon, HSD significantly expanded Tregs and RORt
+
Tregs, whereas the LNAME/HSD group had no change in these T cell populations (% Treg: NSD: 36±2; LNAME: 42±1; HSD: 46±2*; LNAME/HSD: 43±2; % RORt
+
Tregs: NSD: 16±1; LNAME: 19±1; HSD: 23±1*; LNAME/HSD: 20±2; *p<0.05). These data suggest that Tregs and RORt
+
Tregs expand in response to HSD in the kidney and colon, with a greater magnitude of expansion by RORt
+
Tregs. However, this expansion of T cell populations is not evident in mice pre-exposed to a hypertensive insult. We propose that HSD stimulates pathways that promote Treg expansion, which may be associated with salt-resistance and protective mechanisms.
Abstract P146: Testicular Inflammation Is Associated With Immune Cell Infiltration And Lymphangiogenesis In L-NAME-induced Hypertension
Authors: Navaneethabalakrishnan Shobana , Goodlett Bethany L , Mitchell Brett M
Published: September 2020

Hypertension (HTN) is associated with reduced fertility in men. Although numerous studies report that HTN disrupts hormonal balance in men, less is known about the direct effect of HTN on testes and how HTN influences testicular inflammation and lymphatics. We hypothesized that HTN increases testicular lymphatic vessel density and this is associated with immune cell infiltration and inflammation. Male mice (8 weeks old) were made hypertensive by providing them with L-arginine methyl ester hydrochloride (L-NAME) (0.5 mg/mL) in the drinking water for 3 weeks and control mice received tap water. Testes of hypertensive mice had a significant increase in gene expression of the lymphatic vessel markers Lyve-1 (17.7 ± 2.1 fold; p<0.05), Podoplanin (6.7 ± 1.2 fold; p<0.05), and Prox-1 (68.1 ± 10.6 fold; p<0.05), the lymphangiogenic growth factors VEGF-C (5.7 ± 1.1 fold; p<0.05), VEGF-D (2.2 ± 0.7 fold; p<0.05), and VEGF-A (5.8 ± 1.1 fold; p<0.05) and their receptors VEGFR-2 (8.0 ± 2.0 fold; p<0.05) and VEGFR-3 (25.4 ± 3.5 fold; p<0.05). There was also a significant increase in the expression of the pro-inflammatory cytokines TNF-a (24.0 ± 6.8 fold; p<0.05), IFN-g (17.5 ± 3.0 fold; p<0.05), IL-1b (4.2 ± 1.2 fold; p<0.05), IL-6 (24.8 ± 13.0 fold; p<0.05), and IL-17 (4.4 ± 0.4 fold; p<0.05). There were also increases in the lymphatic endothelial cell-derived immune cell trafficking chemokines CCL21 (7.8 ± 1.7 fold; p<0.05) and CCL19 (9.0 ± 4.1 fold; p<0.05) and their receptor CCR7 (9.6 ± 3.2 fold; p<0.05), as well as the cell adhesion molecule ICAM (6.2 ± 1.0 fold; p<0.05) in testes of hypertensive mice. Flow cytometry analysis revealed an increased accumulation of F4/80+ macrophages in the testes from hypertensive mice. Together, these data demonstrate that HTN induces inflammation-associated lymphangiogenesis in testes, in association with immune cell infiltration. It is possible that increasing testicular lymphatics may reduce inflammation and improve reproductive function in hypertensive men.
Abstract P152: Impact Of New Hypertension Guidelines On The Prevalence And Control Of Hypertension In A Clinical Hiv Cohort
Authors: Mallipeddi Vishnu Priya , Levy Matthew , Monroe Anne , Moeng Letumile , Powers Happ Lindsey , Wilcox Ronald
Published: September 2020

Introduction:
People living with HIV (PLWH) with hypertension (HTN) have a higher risk of cardiovascular events and all-cause mortality compared with PLWH with normal blood pressure (BP) and HIV-uninfected adults with HTN. The prevalence and control of HTN among PLWH have not been widely studied since the release of newer 2017 ACC/AHA guidelines (new guidelines). To address this research gap, we evaluated and compared the prevalence and control of HTN using both 2003 JNC 7 (old guidelines) and new guidelines in a large clinical cohort of PLWH.

Methods:
We identified 3206 PLWH with HTN from the DC Cohort study in Washington, D.C, from 01/2018 to 06/2019. We defined HTN using International Classification of Diseases (ICD) -9/-10 diagnosis codes for HTN or ≥ 2 BP measurements obtained at least one month apart (>139/89 mm Hg per old or >129/79 mm Hg per new guidelines). We defined HTN control based on recent BP (≤139/≤89 mm Hg per old or ≤129/≤79 mm Hg per new guidelines). We identified socio-demographics, cardiovascular risk factors and co-morbidities associated with HTN control (per new guidelines) using multivariable logistic regression (adjusted Odds Ratio; 95% CI).

Results:
The prevalence of HTN was 50.9% per old versus 62.2% per new guidelines. Of the 3,206 PLWH with HTN based on 2017 ACC/AHA guidelines, 887 (27.7%) had a recent BP ≤129/≤79 mm Hg, 1,196 (37.3%) had a BP between 130-139/80-89 mm Hg and 1,123 (35.0%) had a BP ≥140/≥90mm Hg. After adjusting for socio-demographics, cardiovascular risk factor and co-morbidities, factors associated with HTN control included age 60-69 (vs. <40) years (1.42; 1.03-1.98), Hispanic (vs. non-Hispanic Black) race/ethnicity (1.49;1.04-2.15), receipt of HIV care at a hospital-based (vs. community-based) clinic (1.21; 1.00-1.47), being unemployed (1.42; 1.11-1.83), and diabetes (1.35; 1.13-1.63).

Conclusion:
In a large urban cohort of PLWH, nearly two-thirds had HTN and less than one-third of those met new guideline criteria. Older PLWH were more likely to have their HTN controlled compared to the younger PLWH. Our data suggests that more aggressive HTN control is warranted among PLWH, with attention to younger patients.
Abstract P160: Long-term Blood Pressure Variability And Cognitive Decline And Dementia Among Community-dwelling Elderly
Authors: Ernst Michael E , Ryan Joanne , Chowdhury Enayet K , Murray Anne M , Woods Robyn L , Orchard Suzanne G , Wolfe Rory , Storey Elsdon , Shah Raj C , Tonkin Andrew , Reid Christopher M
Published: September 2020

Greater blood pressure variability (BPV) in midlife increases the risk of dementia, but the impact of BPV in cognitively intact older adults is unknown. We examined the risk of incident dementia and cognitive decline associated with long-term, visit-to-visit BPV in participants of the ASPirin in Reducing Events in the Elderly (ASPREE) study, a randomized primary prevention trial of daily low-dose aspirin in community-dwelling adults in Australia and the US aged 70 and older (65 if US minority), who were free of dementia or evidence of cognitive impairment at enrollment. The mean of three BPs using an automated cuff was recorded at baseline and annually; participants also underwent baseline and biennial standardized assessments of global cognition, delayed episodic memory, verbal fluency, processing speed and attention. Cognitive decline was pre-specified as a >1.5 standard deviation (SD) decline in score from baseline on any of the cognitive tests, while incident dementia was a pre-specified secondary endpoint of ASPREE which was adjudicated using DSM-IV criteria. BPV was estimated using within-individual SD of mean systolic BP across baseline and the first two annual visits, and participants with cognitive decline or incident dementia during this period were excluded from the analysis to avoid immortal time bias. After adjustment for key covariates, Cox proportional hazards regression revealed increased risks for dementia and cognitive decline during follow-up for individuals in the highest SD tertile of BPV (Table). Our findings suggest that high BPV in older ages should be considered a potential therapeutic target to preserve cognitive function.
Abstract P172: Orthostatic Hypotension And 24-hr Ambulatory Blood Pressure Monitoring In The Sprint Trial
Authors: Ghazi Lama , Drawz Paul , Pajewski Nicholas , Juraschek Stephen P
Published: September 2020

Background:
Clinic blood pressure (BP) is measured in the seated position, which can miss important home BP phenotypes such as low ambulatory BP (white coat effects) or high supine BP (nocturnal non-dippers). Orthostatic hypotension (OH) is determined based on BP measurements in both seated (or supine) and standing positions, and thus could theoretically identify these important phenotypes in clinic.

Objective:
To determine the association of OH with white coat effects or night-to-daytime systolic BP (SBP)

Methods:
SPRINT was a randomized trial testing the effects of intensive (<120 mmHg) or standard (<140 mmHg) SBP treatment strategies in adults at higher risk of cardiovascular disease. OH was assessed at 6, 12, or 24-mths and defined as a decrease in standing and mean seated SBP ≥20 or DBP ≥10 mmHg after 1 min of standing. White coat effects, based on 24-hr ambulatory BP monitoring performed at the 27-mth visit (every 30-minutes), were defined as the difference between 27-mth seated clinic and ambulatory BP ≥ 20/≥10 mmHg. SBP dipping ratio was defined as the ratio of night-to-daytime SBP >0.9.

Results:
Of 897 adults (mean age 71.5 [SD, 9.5] yrs, 28.7% female, 28.0% black), 128 had OH at least once. Among those with OH, 14.8% had white coat effects versus 7.2% among those without OH. Moreover, 68.8% of those with OH demonstrated non-dipping patterns versus only 52.0% of those without OH. OH was positively associated with both white coat effects (OR=2.24; 95% CI: 1.28, 4.27) and higher night-to-daytime SBP (β=0.04; 95% CI: 0.02, 0.06) (
Table
).

Conclusions:
Clinic-based assessments of OH may be a useful tool for identifying BP phenotypes often missed with traditional seated BP assessments.
Abstract P178: Sentinel Platform Reduces Blood Pressure And Crisis Hypertension (2020 Update)
Authors: Shah Nirav H
Published: September 2020

Introduction:
We assessed the efficacy of mobile healthhypertension monitoring for patients enrolled inMedicare’s Remote Physiologic Monitoring (RPM)program.

Hypothesis:
Uncontrolled hypertension is an increasingepidemic associated with cardiovascular disease.Despite many available treatments, the averagetime to blood pressure control is slow. Lack ofaccess to patient information including bloodpressure data outside of the clinic setting meansthat clinicians cannot easily titrate medications. Wehypothesized that mobile health monitoring andcommunication with clinicians in a Medicare cohortwould decrease the hypertension burden andmitigate crisis blood pressure in patients.

Methods:
1,544 patients who had contributed ≥ 20 bloodpressure readings in a remote monitoring programwere included in the study population, spanningclinics in Florida, Tennessee, Arizona, Ohio, Texas,New York, and California. Eligible patients carried adiagnosis of hypertension and had been seen bytheir doctor within the year they were referred. Themobile health platform was utilized to aggregateblood pressure data, which was analyzed by aremote care team and provided to clinicians on amonthly basis. Patients’ doctors and their teamsreviewed and managed the patients based on thedata provided by the mobile-cloud platform. Theremote monitoring program provided alerts to clinicstaff for patients who had blood pressures greaterthan 180mm Hg systolic (crisis hypertension) forexpedited decision making.

Results:
1,544 patients who provided >20 BP readingsfrom January 2018 to January 2020 wereincluded in the study. A total of 297,731 bloodpressure readings were included in thisanalysis. Patient readings were stratified byepoch chronologically. The first epoch (E1),represented the first 25% of readings in theremote monitoring system, and the fourth epoch(E4) represented the final 25% of readings.From E1 to E4, patients saw an averagedecrease of 3.8 mmHg in systolic bloodpressure (132.9 vs. 129.1; p<0.001). Theproportion of readings in crisis hypertensionrange decreased from 2.3% to 1.1%; p=0.03).

Conclusions:
RPM offers a scalable solution to resistant hypertension.
Abstract P187: Testing Of A Long-term Implantable Blood Pressure Waveform Monitoring System
Authors: Joseph Jeffrey I , Verkiak Josiah , Torjman Marc , Loeum Channy , Liu Ji-Bin , Devine Denise , Dicciani Nance K
Published: September 2020

The long-term Implantable Blood Pressure Waveform Monitoring System consists of a miniature applanation tonometer sensor head connected to a battery powered electronics module via a flexible lead. The BP Sensor continuously monitors the arterial BP waveform with data transmitted to a smart phone for real-time data analysis and display. Key data can be transmitted via the cellular network to a central monitoring station for advanced analysis by a computer and clinician. The BP Sensor has been evaluated for safety, accuracy, stability, and reliability for up to 10 months surrounding the external carotid arteries of large canine. Serial ultrasound studies of the artery-sensor interface shows normal artery shape, diameter, and blood flow velocity. BP Sensor performance remained stable for ~ 60 days between calibrations and correlated with reference BP waveform measurement (± 2.5 mm Hg). The BP Sensor head has a novel design that securely couples the diaphragm to the outside wall of a peripheral artery in optimal alignment with minimal flattening (~ 15 %). The Figure below shows the BP Sensor output signal’s detailed BP waveform four months after implantation. The waveform shows subtle and consistent fluctuations in the peaks and valleys of the BP waveform due to positive pressure mechanical ventilation with a respiratory rate of 14 breaths per minute. This is a significant observation which indicates that the BP Sensor has very good sensitivity (± 1 mm Hg) in the normal hemodynamic range (reference BP ~100/60). The real-time and recorded BP Sensor waveform data will be used to make a diagnosis and adjust medication in a more timely and effective manor, leading to improved clinical outcomes.
Abstract P196: Chymase Inhibition: Is It An Ideal Target For Controlling Salt-Induced Hypertension?
Authors: Devarajan Sankar , Urata Hidenori , Yahiro Eiji
Published: September 2020

Chymase, a serine protease, has been extensively studied with respect to its role in the pathogenesis of salt-induced hypertension and is noteworthy for the generation of Angiotensin II. Studies to decipher the pathophysiological role of chymase in cardiac disease have gained momentum in recent times, and ACE-independent Angiotensin II synthesis by chymase has been implicated in the structural remodeling associated with cardiovascular disease. Chymase upregulation in alimentary tract, skin and skeletal muscle upon high salt consumption caused hypertension and altered the renin-angiotensin system. Chymase is the novel therapeutic target in salt-dependent hypertension, and as such, inhibitors of chymase from natural foods warrant preclinical investigation. Therefore, we examined the hypothesis that chymase inhibitory dried young leaves of Polygonum hydropiper (PPH) or young leaves extract of Polygonum hydropiper (PHE) could reduce salt-induced hypertension. In this study, 8-wk old wild-type mice were allocated into three experiments and experiment I included groups, I- normal water drinking, II- high salt (2% NaCl) water (HSW) drinking, and III- HSW plus PPH (500 mg kg
-1
, orally) for 12-wk. Blood pressure (BP) and heart rate (HR) were measured at baseline and weekly up to wk-12. In experiment II, mice were given HSW for 12-wk followed by 8-wk treatment with PPH plus HSW (62.5, 125, 250 and 500 mg kg
-1
for groups I, II, III and IV, respectively). BP and HR were measured at baseline and monthly until wk-12, following weekly for 8-wk. Experiment III comprised of four groups of mice placed on 12-wk HSW and 8-wk treatment with PHE plus HSW (2.5, 5, 10 and 20 mg kg
-1
for groups I-IV, respectively). BP and HR were measured at baseline and monthly up to wk-12, following weekly for 8-wk. Significant reduction in BP (SBP123.72±1.9; DBP 85.2±3.2) and HR were observed in mice treated with PPH (500 mg kg
-1
) compared to HSW control. PPH reduced BP and HR dose dependently in hypertensive mice and the higher dose showed maximum reduction. PHE at its maximum dose (20 mg kg
-1
) significantly suppressed BP (SBP 121.47±2.6; DBP 81.28±2.4) and HR. Overall, we found that the young leaves of Polygonum hydropiper oral treatment suppressed salt-induced hypertension.
Abstract P204: Home Blood Pressure Monitoring: A Missed Opportunity?
Authors: Chang Gin Den William , Shamuilova Berta , Mazurkiewicz Rebecca , Kodra Arber
Published: September 2020

Introduction:
The 2017 American College of Cardiology and American Heart Association hypertension guidelines recommend self-measured and home blood pressure (BP) monitoring to confirm the diagnosis of hypertension, to titrate anti-hypertensives and to assess adherence to treatment. However, it is unclear to what extent is home blood pressure monitoring being optimally utilized in everyday clinical practice.

Hypothesis:
We hypothesized that our Internal Medicine resident clinic underutilizes home BP monitoring as part of the diagnosis and continued management of hypertension.

Methods:
We performed a retrospective chart review of patients with a history of hypertension patients seen for at our Internal Medicine resident clinic in New York City between July 2019 and September 2019. We examined all progress notes in this time frame for documentation of home BP cuff measurements or prescriptions for home BP monitors as well as patient comorbidities such as tobacco use, coronary artery disease, diabetes and hyperlipidemia. The chi-square test was performed to evaluate and compare guideline adherence between groups. Statistical significance was considered at
p
< 0.05.

Results:
A total of 282 patients (mean age: 59) met inclusion criteria, of which, 114 (40.1%) had progress notes discussing home BP monitoring. Of those currently monitoring BP at home, 75/175 female patients (42%) and 68/107 male patients (63%) were not prescribed either a BP cuff or mention of a plan for home BP monitoring (p=0.0007). There was no significant correlation for BP cuff prescriptions or implementation of a BP diary in terms of resident year level, ethnicity, diabetes, coronary artery disease, hyperlipidemia, smoking history.

Conclusion:
There is a discrepancy in our current practice to incorporate home BP monitoring as part of the comprehensive care of hypertension particularly among males and females. There is a possibility that females are being targeted more for home blood pressure due to the preventive emphasis of cardiovascular morbidity in females. Current interventions including physician and patient clinic education as well as utilization of pamphlets to targeted patients are underway to improve this often overlooked component of hypertension management.
Abstract P205: Finger Ring Provides Nocturnal Blood Pressure Dipping Status Based On Analysis Of Oscillatory Photoplethysmography
Authors: Felder Robin A , Schiermeyer Katherine , Akhter Mahabuba , Xu Peng , Yue Wei , Marshall Stephen , Carey Robert M , Gildea John J
Published: September 2020

Ambulatory blood pressure monitoring is more useful for the diagnosis of various forms of hypertension including white coat and morning surge as well as other conditions that are associated with increased morbidity and mortality such as sleep apnea. Nocturnal changes in blood pressure (BP) can also aid in the diagnosis of various manifestations of blood pressure independent of hypertension known as salt sensitivity (SS) and inverse salt sensitivity (ISS) of blood pressure. SS individuals experience an increase in BP on a high salt diet while ISS individuals experience a paradoxical increase in BP on a low salt diet. SS and ISS phenotypes affect approximately 18% and 15% of normotensives, respectively, which may result in significant morbidity and mortality similar to untreated hypertension. Consuming a personally appropriate salt diet can result in a circadian drop in BP during sleep, and failure to “dip” can lead to significant cardiovascular diseases. Nocturnal dipping is usually recorded using an ambulatory blood pressure monitoring (ABPM) device. Arterial pulse wave measurements using oscillatory photoplethysmography (OP) are minimally invasive when compared to an inflatable cuff, which can disturb sleep and raise blood pressure. We measured nocturnal blood pressure using a ring based photoplethysmograph (SensoGram Technologies, Plano Texas). A UVA Salt Study participant wore their device upon going to bed and then uploaded nocturnal data to the internet each morning. Systolic and diastolic BP is capable of being measured 30 times a minute for approximately 9 hours and providing over 5000 data points each night. Three representative dipping profiles for an individual yielded a dipping reduction of 24% ± 3% for systolic and 40% ± 10% for diastolic (1 - mid-sleeping lowest value/start of evening highest value). This additional data afforded by nocturnal BP measurement is anticipated to improve diagnostic opportunities in the measurement of SS and ISS phenotypes and provide the user with reassurance that nocturnal BP dipping is occurring.
Abstract P208: Imaging The Longitudinal Reduction In Placental Ischemia In Response To Therapeutic Intervention For Preeclampsia
Authors: Lawrence Dylan J , Bayer Carolyn
Published: September 2020

Preeclampsia is believed to be induced by abnormal vascular remodeling and the resulting placental ischemia during early development. Sildenafil, a phosphodiesterase-5 inhibitor, reduces the maternal symptoms of preeclampsia by promoting angiogenesis and enhancing NO-mediated vasodilation. However, the effect of sildenafil on
in vivo
placental function has not been demonstrated. We performed longitudinal spectral photoacoustic (sPA) imaging of placental therapeutic response to sildenafil in the reduced uterine perfusion pressure (RUPP) model of preeclampsia. Sprague Dawley rats were administered sildenafil (S) via drinking water beginning on gestational day (GD) 11. Imaging was performed on GD14, 16, and 18 with the RUPP procedure implemented after the first imaging session. sPA images of oxygenation show that the placental ischemia induced by the RUPP surgery (RUPP, n=8, 48%; NP, n=8, 54%), was effectively eliminated by treatment with sildenafil (RUPP+S, n=8, 53%, p<0.05). In addition to improved placental oxygenation, sildenafil was also found to reduce mean arterial pressure in RUPP animals by GD18 (RUPP, 110 mmHg; RUPP+S, 98 mmHg; p<0.05), consistent with prior reports. Our studies demonstrate that sPA imaging can detect changes in placental oxygenation which could be used to indicate
in vivo
placental therapeutic response.

Figure 1:
Placental hypoxia in the RUPP is improved by treatment with sildenafil on GD16. B-mode US images (a, c) of anatomy were used to manually select the placenta (p) and average placental oxygenation was calculated. A custom red-blue oxygenation colormap was then overlaid for visualization (b, d). Scale bars = 3mm.
Abstract P215: Hyperglycemic Rats Have Increased Fetal Demise But Not Hypertension During Pregnancy
Authors: Spradley Frank T , Wilson Barbara , Anderson Christopher
Published: September 2020

While obesity is a major cause for pregnancy complications including preeclampsia and fetal demise, it is not exactly clear the precise obesity-related metabolic factors that promote these adverse outcomes. Epidemiological studies have pointed toward hyperglycemia as one such factor. Therefore, we tested the hypothesis that hyperglycemic rats have hypertension and fetal demise during pregnancy. For this purpose, we utilized the type II diabetic model, the Goto-Kakizaki (GK) rat (N=16), compared to normoglycemic Wistar Hannover (WH) rats (N=9), which were maintained on Envigo 8640 standard chow. The GK rat allows for assessment of hyperglycemia on pregnancy without confounding obesity. Maternal fasting glucose levels were significantly greater (P<0.05) in GK (97±8 mg/dL) vs. WH (72±9 mg/dL) rats by gestational day 19. Body weight was lower (P<0.05) in GK (248±4 g) versus WH (289±4 g) pregnant rats, whereas perirenal fat (1.56±0.07 g vs. 1.38±0.07 g, P>0.05) and circulating levels of the adipokine, leptin (1.6±0.2 ng/mL vs. 2.2±0.3 ng/mL, P>0.05) were similar between GK and WH pregnant groups, respectively. Endothelial-dependent relaxation to acetylcholine (sensitivity as logEC50: -5.2±0.3 M vs -5.2±0.4 M) and endothelial-independent relaxation to the nitric oxide-donor sodium nitroprusside (logEC50: -7.2±0.2 M vs. -7.5±0.1 M) were similar (P>0.05) in uterine arteries isolated from GK and WH rats, respectively. It was then determined if reduced uterine perfusion pressure (RUPP)-induced placental ischemia, a significant contributor to the development of preeclampsia, promoted greater maternal hypertension in GK rats. RUPP was conducted on gestational day 14 and blood pressure assessed on day 19. RUPP produced hypertension to a similar extent (P>0.05) in GK (116±5 mmHg vs. Sham 102±5 mmHg) and WH (124±4 mmHg vs. Sham 100±2 mmHg) groups. Blood pressure was similar under Sham conditions. Fetal demise was already greater in Sham GK vs. Sham WH pregnant rats (% absorptions: 13±2 vs. 2±2, P<0.05) but increased similarly following RUPP in GK (61±11 %) and WH (65±5 %) pregnant rats. In conclusion, these data suggest that high glucose levels promote fetal demise during pregnancy but do not exaggerate the outcomes of placental ischemia-induced hypertension.
Abstract P216: Inhibition Of T Cell Activation In Response To Placental Ischemia During Pregnancy Improves Hypertension And Activation Of Natural Killer Cells
Authors: Campbell Nathan , Deer Evangeline M , Amaral Lorena M , Reeve Kristen , Fitzgerald Sarah , Herrock Owen , Franks Michael , Ibrahim Tarek , Lamarca Babbette B
Published: September 2020

Preeclampsia (PE), new onset hypertension during pregnancy, is the leading cause of death and morbidity world-wide for the mother and fetus during pregnancy. The Reduced Uterine Perfusion Pressure Rat Model of PE (RUPP) exhibits many characteristics of PE including hypertension, suppressed regulatory T cells (T
RegS
) associated with increased CD4+ T cells and B cells secreting agonistic autoantibodies to the AngII receptor (AT1-AA). We have previously shown that blockade of T-helper cells improves blood pressure and lowers AT1-AA secretion. A potential mechanism for the decreased blood pressure is decreased cytolytic natural killer (cNK) cells. Abatacept (Aba) is a fusion molecule designed to inhibit T cell co-stimulation in response to antigens and is used to treat autoimmune diseases. We hypothesize that treatment with Aba will prevent the activation of T-helper cells and therefore lower AT1-AA as a mechanism leading to less cNK cells in response to placental ischemia in RUPP rats. Aba was given on day 13 via the jugular vein. On day 19, blood and tissues were collected, blood pressure (MAP), pup weight, and NK cells were measured by flow cytometry in the blood and placenta. A one-way ANOVA was used for statistical analysis. On GD19, MAP significantly increased in RUPP 119±2 mmHg (n=7, p<0.05) compared to NP controls 102±2 mmHg (n=7) and was normalized with Aba (100±2 mmHg (n=10, p<0.05). Compared to the NP controls (2.2±0.06, n=7), pup weight significantly decreased in RUPP (2±0.08, n=7, p<0.05) but was 2± 0.07, with Aba (n=10). Circulating and placental total NK cells were 32±5, 44±13, % gate in NP rats (n=7), 59±4, 60±16 % gate in RUPP rats (n=7, p<0.05; n=4), which significantly decreased to 40±6, 28±8 % gate with Aba (n=10, p<0.05; n=11). Our findings indicate that prevention of T cell activation lowers total NK cell number and blood pressure in response to placental ischemia of pregnancy.
Abstract P221: Tregs Do Not Expand In Pregnancy After Recovery From Ischemia Reperfusion Injury
Authors: Gillis Ellen E
Published: September 2020

Recent studies in our laboratory report that pregnancy after renal ischemia reperfusion (IR) injury results in adverse maternal and fetal outcomes, including decreased fetal growth, increased fetal demise, and maternal renal insufficiency. In the current study, we examined the effect of IR injury on the immune system during pregnancy. Pregnancy is a unique state of immunosuppression, where regulatory T cells (Tregs) increase to combat the immune response to the allogenic fetus. Tregs are also known to play a critical role in recovery after IR, and may serve as a link between IR and poor pregnancy outcomes. We hypothesized that Tregs would be decreased during pregnancy after recovery from IR. Briefly, female Sprague Dawley rats (12 wks of age, n=4) were randomized to receive either 45 minutes of warm, bilateral renal IR injury or sham surgery. Rats were then allowed 30 days to recover, and renal recovery was confirmed by plasma creatinine and urinary protein excretion. Rats were then randomized to either be mated or serve as an age-matched virgin control. Pregnancy was confirmed by vaginal cytology, with presence of sperm on the slide indicative of day 1 of pregnancy. Pregnancies were terminated on pregnancy day 20, and blood and kidneys were collected for flow cytometric analysis of T cells. Interestingly, Tregs only increased during pregnancy in control rats in the kidney (4.7±0.7 to 12.6±0.3 FoxP3
+
T cells as % CD3
+
CD4
+
, 2-Way ANOVA interaction p<0.01) and blood (5.7±0.3 to 13.4±1.2 % FoxP3
+
T cells as % CD3
+
CD4
+
, 2-Way ANVOA interaction p<0.01) Tregs did not increase during pregnancy in the IR rats in the kidney (5.0±0.3 to 5.2±0.7 FoxP3
+
T cells as %CD3
+
CD4
+
) or in the blood (6.6±0.4 to 6.8±0.5 % FoxP3
+
T cells as %CD3
+
CD4
+
in the blood). Tregs in IR dams and virgin IR were similar to the virgin surgical sham controls. These data suggest that Tregs fail to expand during pregnancy after IR, potentially contributing to the increased rate of fetal demise and poor pregnancy outcomes observed in this model.
Abstract P224: Cyclooxygenase-dependent Mechanisms Mediate In Part The Anti-dilatory Effects Of Uterine Perivascular Adipose Tissue In Rat Pregnancy
Authors: OSIKOYA Oluwatobiloba , Cushen Spencer C , Goulopoulou Styliani
Published: September 2020

Introduction:
Uterine perivascular adipose tissue (PVAT) contributes to uterine blood flow regulation in pregnancy, at least in part, due to its effects on uterine artery tone. We hypothesized that the anti-dilatory effects of uterine PVAT are mediated by vascular nitric oxide synthase (NOS)- and cyclooxygenase (COX)-dependent mechanisms.

Methods:
Main uterine arteries from pregnant and non-pregnant rats were mounted onto a wire myograph. Concentration-response curves to acetylcholine (ACh, 10
-9
- 3x10
-5
M) were performed on arteries exposed to physiological salt solution or PVAT-conditioned media (PVAT
media
) in the presence of the following inhibitors: a) L-NAME (NOS inhibitor, 100 μM), b) indomethacin (COX inhibitor, 10 μM), c) SC560 (COX-1 inhibitor, 1 μM), d) NS398 (COX-2 inhibitor, 1 μM)].

Results:
NOS inhibition abolished ACh-induced relaxation in uterine arteries from pregnant rats and exposure to PVAT
media
did not change this effect [AUC, (-)PVAT
media
: 244.6 ± 18.1 vs. (-)PVAT
media
/(+)L-NAME: 52.64 ± 7.4, p < 0.0001; (+)PVAT
media
: 202.4 ± 15.5 vs. (+)PVAT
media
/(+)L-NAME: 56.17 ± 11.3, p < 0.0001]. Indomethacin suppressed ACh-induced relaxation in uterine arteries from pregnant rats [AUC, (-)PVAT
media
: 243.6 ± 6.6 vs. (-)PVAT
media
/(+)Indomethacin: 123.6 ± 12.3, p < 0.0001] but not in non-pregnant rats (p>1.0). In arteries incubated with PVAT
media
, the presence of indomethacin increased ACh-induced relaxation [AUC, (+)PVAT
media
: 125.2 ± 11.4 vs. (+)PVAT
media
/(+)Indomethacin: 179.1 ± 14.7, p = 0.01]. COX-1 but not COX-2 inhibition suppressed relaxation responses to ACh [AUC, COX-1 inhibition, (-)PVAT
media
: 244.6 ± 12.0 vs. (-)PVAT
media
/(+)SC560: 142.4 ± 15.4, p = 0.02; COX-2 inhibition, (-)PVAT
media
vs. (-)PVAT
media
/(+)NS398, p=0.1). The anti-dilatory effects of PVAT were not observed in the presence of SC560 or NS398 (p>0.05). Exposure to PVAT
media
increased the protein content of COX-1 (p=0.05) and COX-2 (p=0.03) and the production of thromboxane B
2
(p=0.01) in uterine arteries from pregnant rats.

Conclusion:
The anti-dilatory effects of PVAT-derived factors on uterine arteries are mediated in part by COX-derived products and this mechanism is specific to pregnancy.
Abstract P232: Dilated Cardiomyopathy With Electrocardiographic Changes And Coronary-Pulmonary Fistula: An Uncommon Presentation Of Primary Aldosteronism In The Covid-19 Era
Authors: Marzano Luigi , Scanelli Giovanni
Published: September 2020

Primary aldosteronism is the most frequent forms of curable hypertension and elevated aldosterone levels have been associated with endothelial proliferation and pathological remodeling of the heart and arteries; however, coronary arterial abnormalities have never been reported in patients with primary aldosteronism. We report the case of a 53-year-old Caucasian obese man (BMI 37 Kg/m
2
) with recent history of hypertension, fatigue and subjective dyspnea who was admitted to our hospital after performing an outpatient echocardiography that showed hypertensive and ischemic heart disease in dilated phase (LVEDVI 95 mL/m
2
; LVEF 43%). His laboratory results showed hypokalemia (3 mmol/L) and an elevated aldosterone-renin ratio [(294 ng/L)/(1μU/mL)]. After case confirmation with saline infusion test, the abdominal CT scan showed a subcentimeter adenoma in the right adrenal gland. Surprisingly we noticed that, after oral potassium correction, the electrocardiogram revealed a symmetrical T-wave inversion and subsequently a coronary angiography detected a coronary artery fistula between the left anterior descending artery and the pulmonary artery in the absence of significant stenosis. In the Italy's CoViD-19 pandemic full spread, we preferred to postpone the diagnosis of the lateralization of aldosterone hypersecretion by adrenal vein sampling and we started a mineralocorticoid receptor antagonist with a clinical follow-up of cardiovascular symptoms for the optimal treatment of coronary artery fistula. After about two months of follow-up, the patient remains asymptomatic with good blood pressure control, normal potassium levels and significant echocardiographic improvement (LVEDVI 67 mL/m
2
; LVEF 51%). Our case highlights a possible association between hypertensive patients with coronary artery fistulas and primary aldosteronism. We recommend cardiologists and clinicians to maintain a high level of suspicion of primary aldosteronism in these patients.