bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract P066: Case Report on IV Albumin in Postural Orthostatic Tachycardia Syndrome with Meniere’s Disease
Authors: Ashangari Chandralekha , Hamid Stacy E , Suleman Amer 
Published: July 2021

Postural orthostatic tachycardia syndrome (POTS) is characterized by an increase in a patient’s heart rate when they move from a supine to an upright position. This syndrome is often treated with a high sodium diet. Meniere’s disease is a disorder of the inner ear generally treated with diuretics and a low sodium diet. This poses a challenge when treating a patient suffering from both Meniere’s and POTS because by treating the Meniere’s with diuretics and a low salt diet it will exacerbate the symptoms of POTS. We hypothesize that the administration of IV albumin will result in an increase in the plasma oncotic pressure thus intravascular volume while simultaneously decreasing extra cellular fluid pressure therefore leading to an improvement in the patient’s symptoms.
This case involves a 35-year-old female suffering from low blood pressure, debilitating dizziness with fainting, shortness of breath with exercise intolerance, and chest pain that was sent to us for further evaluation and treatment of her symptoms. Growing up she had several recurring ear infections, and by the age of 30, she started developing symptoms of vertigo and dizziness that had no relationship to posture. She was diagnosed with Meniere's disease. The patient appeared to have primarily vestibular-type symptoms. Her tilt table was indicative of POTS. Her clinical symptoms were partly reproduced during the tilt table test. We were not able to completely alleviate the patient’s symptoms by the administration of Midodrine. Intravenous treatment with Albumin and saline was started which was changed to treatment with IV Albumin alone. The patient reports improvement of her symptoms.
We hereby suggest the use of IV albumin in the treatment of POTS in a patient with Meniere’s disease.
Abstract P070: Exercise Prevents Cardiac Diastolic Dysfunction in a Female Model of Over-Nutrition Induced Obesity by Reducing Oxidant Stress and Fibrosis without Lowering Bodyweight
Authors: Bostick Brian , Habibi Javad , Ma Lixin , Garro Mona , DeMarco Vincent , Jia Guanghong , Aroor Annayya , Sowers James 
Published: July 2021

Obesity is being classified as a global epidemic by both the WHO and the CDC. Sedentary lifestyle and consumption of a high-fat/high-fructose Western diet (WD) are implicated in this epidemic. Women are particularly vulnerable to obesity related cardiovascular disease. Obese women suffer higher rates of hypertension, insulin resistance and heart failure, especially diastolic heart failure early in their lives. There are no evidence based treatments for diastolic heart failure. We hypothesized that voluntary daily exercise would prevent WD induced diastolic dysfunction by reducing oxidant stress, fibrosis and inflammation.
To test this hypothesis, we developed a diastolic heart failure model by subjecting C57BL6/J female mice to a solely WD fed regimen for 16 weeks. We treated a parallel cohort with daily exercise, via voluntary wheel running, for the entire 16 weeks of WD feeding alongside control diet (CD) groups (n=7 for each group). We monitored food consumption, running activity and body weight. After 16 weeks, we assessed diastolic function by cardiac MRI and echocardiography. Detailed myocardial staining and Western blotting were done for cardiac oxidant stress, fibrosis and inflammatory markers.
Both imaging modalities revealed diastolic dysfunction with WD feeding that was normalized by voluntary exercise. Mice ran similarly high intensities on both CD (6.5 km/d) and WD (7.1km/d). While WD feeding increased bodyweight, there was no reduction in weight with exercise. Body composition analysis showed WD fed mice treated with voluntary exercise had increases in visceral fat weight similar to sedentary WD fed mice. There was a notable increase in lean body mass with exercise. WD feeding resulted in insulin resistance that was prevented by exercise. Finally, while WD feeding markedly increased oxidant stress and fibrosis in sedentary mice, exercise prevented myocardial oxidant stress and fibrosis.
Our work provides seminal evidence that diastolic dysfunction of over-nutrition induced obesity can be prevented by exercise. Surprisingly, our study suggests that the mechanisms behind the amelioration of diastolic dysfunction are predominantly through reductions in oxidant stress and fibrosis without reductions in body weight or visceral fat.
Abstract P141: Cardiac TRH Partly Mediates Angiotensin II-induced Fibrotic and Hypertrophy Effects in "in vivo" and "in vitro" Models
Authors: García Silvia I , Peres Diaz Ludmila S , Aisicovich Maia , Schuman Mariano L , Landa María S 
Published: July 2021

Cardiac TRH (cTRH) is overexpressed in the hypertrophied ventricle (LV) of the SHR. Additionally in vivo siRNA-TRH treatment induced downregulation of LV-TRH preventing cardiac hypertrophy and fibrosis demonstrating that TRH is involved in hypertrophic and fibrotic processes. Moreover, in a normal heart, the increase of LV TRH expression alone could induce structural changes where fibrosis and hypertrophy could be involved, independently of any other system alterations.
Is well-known the cardiac hypertrophy/ fibrotic effects induced by AII, raising the question of whether specific LV cTRH inhibition might attenuates AII induced cardiac hypertrophy and fibrosis in mice.
We challenged C57 mice with AII (osmotic pumps,14 days; 2 mg/kg) to induce cardiac hypertrophy vs saline. Groups were divided and , simultaneously to pump surgery, injected intracardiac with siRNA-TRH and siRNA-Con as its control. Body weight, water consume and SABP were measured daily.
As expected, AII significantly increased SABP (p<0.05) in both groups treated , although cardiac hypertrophy (heart weight/body weight) was only evident in the group with the cardiac TRH system undamaged, suggesting that the cardiac TRH system function as a necessary mediator of the AII-induced hypertrophic effect.
As hypothesized, we found an AII-induced increase of TRH (p<0.05) gene expression (real-t PCR) confirmed by immunofluorescence that was not observed in the group AII+siRNA-TRH demonstrating the specific siRNA treatment efficiency.
Furthermore, AII significantly increase (p<0.05) BNP (hypertrophic marker), III collagen and TGFB (fibrosis markers) expressions only in the group with AII with the cardiac TRH system intact. On the contrary, the group with AII and the cTRH system inhibited, shows genes expressions similar to the saline control group. We confirmed these results by immunofluorescence.
Similar fibrotic results were observed with NIH3T3 cell culture where we demonstrated that AII induced TRH gene expression (p<0.05) and its inhibition impedes AII-induced increase of TGFB and III/I collagens expressions telling us about the role of the cTRH in the AII fibrosis effects.
Our results point out that the cardiac TRH is involved in the AII-induced hypertrophic and fibrotic effects.
Abstract P177: The Myotrophoblast of the Rat Placenta Ex Vivo Study of Nitric Oxide Synthase Inhibition
Authors: Ariel Ilana , Skarzinski Galina , Belzer Vitali , Abu Ahmad Wiessam , Abassi Zaid , Bursztyn Michael 
Published: July 2021

In pregnancy spiral arteries, are invaded by endovascular trophoblasts (EVT) and remodeled. Previously, NOS, and of smooth muscle proteins expression in EVT, and endothelin-1 (ET1) ex-vivo contraction of the remodeled artery were demonstrated, mediated by ET1 receptors A and B (ETA, ETB)
Placentas on gestational day 21, were dissected, spiral artery rings devoid of smooth muscle were fixed to a silicon-coated 8-well chamber slide in oxygenated solution.
Rings cut surface area (CSA) was observed under laser scanning confocal microscope. Following baseline, L-NAME and 10- 5 M, ET-1 10-7 M were added to some chambers. In other wells, also with ETA antagonist at 10-6 M (BQ-123).
CSA was measured using ImageJ software.
L-NAME alone, reduced CSA by 2.5% p=0.002. Addition of ET-1 to L-NAME, reduced CSA area immediately, compared with a plateau at 60min by ET1 p=0.001 .L-NAME, followed by ET-1 and ETA antagonist, the isolated constrictive effect of ET-1 via ETB, 7.2%, was earlier and stronger n than via ETA, 6.1% p< 0.001 (figure).
L-NAME + ET-1 causes contraction of the arterial ring via ETA and ETB, without the dilatory effect of NO.
ET-1 alone shows an earlier, immediate CSA reduction, compared to that of ET-1 without L-NAME, achieved at 40-60 minutes. This is in accordance with the instantaneous NO effect through ETB, compared with the gradual ET-1 induced CSA reduction .To isolate the contracting effect via ETB, we added L-NAME + ETA+ ET-1. The ETB contraction is earlier and stronger than that via ETA.
Thus, EVT of the rat remodeled spiral artery react to ET-1 like vascular smooth muscle of non-modified arteries: contraction via receptors A and B and relaxation via receptor B through NOS.
Abstract P637: Pigment Epithelium Derived Factor (PEDF) Deficiency Increases Blood Pressure And Accentuates Glomerular Pathology In Diabetic Mice
Authors: Ye Minghao , Volpert Olga , Wysocki Jan , Batlle Daniel 
Published: July 2021

Pigment Epithelium Derived Factor (PEDF) encoded by SERPINF1 gene has potent anti-angiogenic and cytoprotective activities. It has been reported that PEDF protein levels are reduced in the kidneys of rodents with experimentally induced diabetes. However the effect of PEDF on blood pressure has not been elucidated. Here, we used SERPINF1 KO mice to examine the impact of PEDF deficiency on kidney pathology and blood pressure in the STZ-induced mouse model of diabetes.
Twelve weeks after diabetes induction by STZ, SERPINF1 KO mice showed exacerbated glomerular damage with ~ 2-fold increase in mesangial matrix (2.8±0.14 vs. 1.2±0.14 arbitrary units, p<0.01) and ~ 20% decrease in podocyte counts (8.2±0.0.4 vs. 9.7±0.2 podocytes/glomerulus, p<0.01) compared to the wild type controls. Of note, STZ-treated SERPINF1-/- mice displayed elevated systolic blood pressure (SBP) (127±4 vs. 109±4 mmHg, p<0.01, n=11).
Our data indicate that global PEDF deficiency intensifies glomerular injury in STZ-induced mouse model of diabetes. An important drawback of most murine models of diabetic kidney disease is the lack of hypertension, a known key factor that accelerates progression to CKD in humans. In contrast, we found that STZ-treated SERPINF1-/- mice become hypertensive. Together, our findings point to SERPINF1-/- mice as an attractive model to study diabetic kidney disease and hypertension in mice and suggest an important causative role of PEDF downregulation in glomerular pathology in diabetes.
Abstract 041: New Evidence for G Protein-coupled Estrogen Receptor as a Natriuretic Factor
Authors: Gohar Eman Y , Obi Ijeoma E , De Miguel Carmen , Pollock Jennifer S , Pollock David M 
Published: July 2021

Premenopausal women have a lower risk of cardiovascular and renal diseases compared to age-matched men. This protection includes fewer salt-dependent complications. We have shown that female rats have a more robust natriuretic capacity compared to males in response to increased dietary salt. The novel estrogen receptor, G protein-coupled estrogen receptor (GPER), is a membrane-bound receptor linked to acute signaling pathways. GPER activation elicits protective effects throughout the cardiovascular system. However, its role in sodium handling is not defined. We hypothesized that activation of GPER in the renal medulla stimulates sodium excretion. In female Sprague Dawley (SD) rats, isosmotic saline was infused into the renal medullary interstitium (500 μl/h) during a 60-80 min equilibration period and 20 min baseline urine collection period. This was followed by infusion of the GPER agonist G1 (50 pmol/kg/min) or vehicle into the renal medulla for two further 20 min periods. Compared with vehicle, G1 significantly increased urinary sodium excretion and urine flow (from 0.5 ± 0.1 to 0.9 ± 0.2 μmol/min and from 5.3±1.1 to 8.3±1.6 μl/min, respectively, n=6, p<0.05). Urinary potassium excretion and mean arterial pressure remained unchanged during the experiments (0.5 ± 0.1 vs. 0.4 ± 0.1 μmol/min and 108.6 ± 3.4 vs. 107.2 ± 5.1 mmHg, respectively, n=6). Immunohistochemical analysis of GPER revealed more predominant staining in both inner and outer renal medulla in female SD rats, compared to males. GPER appears to be predominantly expressed in interstitial cells. These data reveal that renal medullary GPER plays an important role in renal sodium handling and may account for the enhanced ability to handle increased dietary salt in females.
Funded by AHA 15POST25090329 to EYG and P01 HL136267 to DMP
Abstract P100: Bioavailability of Arginine versus Erbumine Formulations of Perindopril in Healthy Subjects
Authors: Bishop Andrew 
Published: July 2021

Perindopril is an angiotensin converting-enzyme inhibitor with a proven track record in cardiovascular clinical trials. Traditionally formulated as the
t
-butyl amine (“erbumine”) salt, perindopril’s arginine salt has been FDA-approved in combination with amlodipine besylate. The arginine salt has the advantage of being more stable at higher temperatures or humidity.

To demonstrate bioequivalence (using the standard FDA definition of 90% confidence intervals that are within 80-125% of the values seen with the reference product), the bioavailability of the two perindopril formulations was compared. After screening 121 healthy subjects, 30 (73% male, 38.9±9.5 years of age, 67% African American, BMI of 26.6±2.7 kg/m
2
) signed informed consent, and were studied in a randomized, single-center, single-dose, open-label, 2-period, 2-way cross-over design with a 14-day washout period. After an overnight fast, perindopril was administered orally with 240 mL of water, and blood samples taken at defined time points.

After dose-normalization (the arginine salt has a molecular weight 1.43-fold greater than that of the erbumine salt), all pharmacokinetic parameters for perindopril plasma concentrations were similar between treatments. Mixed model analysis of these parameters demonstrated bioequivalence (e.g., area under the time-plasma concentration curve: 10.2 vs. 10.5 hr•ng/mL/mg, P = 0.54). Very similar results with non-significant differences were also seen for the pharmacokinetics of perindoprilat (perindopril’s active metabolite): 33.3 vs. 38.3 hr•ng/mL/mg, P = 0.17. Two subjects did not complete the perindopril arginine arm of the study: one withdrew consent, and the other experienced a protocol deviation. No subjects experienced a serious adverse event or withdrew due to a treatment-emergent adverse event. Four subjects reported adverse events after perindopril arginine, and two subjects reported neck pain or presyncope after perindopril erbumine.
After dose-normalization, these two formulations of perindopril meet all traditional criteria for AB rating and interchangeability.
Abstract P259: Characterization of Hyperandrogenemic Female Rats With History of Pregnancy
Authors: Patil Chetan N , Dalmasso Carolina , Maranon Rodrigo O , Reckelhoff Jane F 
Published: July 2021

Women with polycystic ovarian syndrome (PCOS) experience hyperandrogenemia, elevated MAP, irregular menses, and difficulty becoming pregnant. As a result many PCOS women undergo assisted fertilization. The long-term cardiovascular consequences of pregnancy in PCOS women are not clear. We tested the hypothesis that a single pregnancy attenuates cardio-renal parameters in hyperandrogenemic female rats, a model of PCOS. Female SD rats were implanted with Dihydrotestosterone (DHT, 7.5mg/90d; replaced every 85 d) or placebo pellets, beginning at 6 wks of age. At 3 months females were paired with SD males. After delivery and lactation, females were divided into placebo (PL) or DHT rats with (P) or without pregnancy (NP) and allowed to age to 10 mos (still estrous cycling) or 16 mos (post cycling) (n=5-8/grp). At 10 mos, body weight (BW), proteinuria (UPrV), and MAP were higher in DHT than PL rats, and pregnancy history had little effect. At 16 mos, BW was higher in DHT than PL rats, and was similar in NP and P groups. UPrV and MAP were also higher in DHT groups than PL, but were significantly attenuated in DHT-P vs DHT-NP. These data suggest that pregnancy in women with PCOS may be cardiovascular protective with aging. The mechanisms remain to be determined.

a, p<0.05 vs PL-NP; b, p<0.05 vs PL-P; c, p<0.05 vs DHT-NP, mean ± SEM, two-way ANOVA.
Supported by NIH-R01HL66072, PO1HL51971 (JFR).
Abstract P354: Left Ventricular Mass and Exagerated Hypertensive Blood Pressure Response to Bruce Exercise Stress Test in Diabetics and Nondiabetics
Authors: Balderas Michael , Cigarroa Joaquin , Lozano Daniel , Hecht Joan , Oliveros Rene A 
Published: July 2021

The aim of or study was to see if an exaggerated BP response during the Bruce exercise test could differentiated target organ damage (TOD) in a population of diabetics v/s nondiabetic pts . We studied 105 pts for the performance of a stress test because of chest pain whose systolic BP rose 50mmHg or more at their peak exercise compared to their resting BP. There were 45 diabetics pts (DM) and 60 nondiabetic pts (NDM) pts. All pts were hypertensive on medication but their beta blocker medication was on hold for the performance of the stress test. The echocardiograms were performed using a Phillips IE 33 echo machine and the LV mass was calculated using the Deveraux formula using single plane views.
The was no statistical difference between both groups with respect to age, BMI and systolic and diastolic BP’s during rest and exercise. The HR at rest was not different between both groups but the HR at peak exercise was significantly higher for NDM compared to DM (p < 0.016). The LVMI was significantly higher in DM compared to NDM pts ( p = 0.04).
In conclusion, an elevated LVMI which is evidence for hypertensive target organ damage should be suspected in hypertensive pts who have an exaggerated BP response to the exercise Bruce stress test.
The reason for a significantly higher HR at peak exercise for NDM patients compared to DM pts may be related to better physical performance and therefore longer duration of exercise. Other possibilities will be discussed.
Abstract P367: Masked Hypertension is Not Associated With Orthostatic Hypertension
Authors: Cigarroa Joaquin , Balderas Michael , Baez Christopher , Garza Benjamin , Hecht Joan , Oliveros Rene A , Chilton Robert 
Published: July 2021

The aim of this study was to see if there is any association between masked hypertension (MHTN) and orthostatic HTN (OHTN). In addition, we evaluated if MHTN was associated with diabetes (DM). Lastly we compared BP and HR changes between DM and non-diabetics (NDM)pts.
We performed ambulatory BP monitoring (ABPM) in 70 consecutive pts referred to us for evaluation of hypertension. From this number of pts there were 20 pts with OHTN for an incidence of 28%. There were 8 pts with MHTN for an incidence of 11.4%. There were 26 pts with DM and 44 pts were NDM
The studies were performed after 5 minutes of rest. We obtained BP’s in the dominant arm. We subsequently performed the 24hs ABPM using Space Lab On Trak 90227 monitors.
Out of 8pts with MHTN, none had OHTN and only 2 were pts with DM. In addition, we compared age, weight, BP sitting and standing as well as HR sitting and standing in our 70 patients that were divided in 2 groups, DM v/s NDM. The following table depicted our results:
In summary, we found a higher sitting diastolic BP in nondiabetic pts. There was no significant difference between both groups in the remaining parameters.
In conclusion, in our small population of pts there was no association between MHTN and OHTN. The association between MHTN and DM was very low. When comparing 8 different parameters depicted in the table the only significant difference between DM and NDM was on the sitting diastolic BP.
Abstract P399: The Association of Serum Aldosterone with Sex, Age, and Sodium Status
Authors: Rao Ajay D , Zhao Huaqing , Vasan Ramachandran S , Adlin E V 
Published: July 2021

Primary aldosteronism (PA) is now recognized as the most common cause of secondary hypertension. Although the aldosterone-to-renin ratio is recommended for case detection, screening rates for PA remain low. Based on our prior study in low-renin hypertension, we hypothesized that a statistical adjustment for age, sex, and sodium status would improve the diagnostic accuracy of aldosterone measurements.
Data from the cohort of 3,345 individuals in the sixth examination cycle of the Framingham Offspring Study was analyzed. In addition to the standard study protocol, blood was drawn for later measurement of aldosterone. After exclusions, the final analysis consisted of 1,468 normotensives (652 men and 834 women), aged 29 to 85. To compare levels of continuous variables in two groups, we used independent samples t tests. We regressed natural-log-transformed values of aldosterone on age, sex, and the urine sodium/creatinine ratio. Unimodality of aldosterone (adjusted and unadjusted) was tested utilizing dotplots and the dip test.

The mean aldosterone levels were 10.4 ± 5.89 ng/dL in women and 11.3 ± 6.14 ng/dL in men (p < 0.005). Age, sex, and urine sodium/creatinine ratio were each significantly associated with aldosterone (p < 0.005). The proportion of variability explained by age, sex, and urine sodium/creatinine was 0.91%,1.3%, and 8%, respectively. The fully adjusted model r
2
= 0.0948. When adjusted for age, sex, and urine sodium/creatinine ratio, the distribution of aldosterone was unimodal (dip test: 2.26 ± 0.17 ng/dL, p = 0.9973); when unadjusted, the distribution of aldosterone was not unimodal (dip test, p ≤ 0.005). The dotplot and Q-Q plot showed a normal distribution of aldosterone after adjustment.

In this large, community-based population, adjustment for age, sex, and sodium status resulted in a more normal distribution of aldosterone. PA has been described as a condition “in which aldosterone production is inappropriately high for sodium status.” Our study suggests that appropriate adjustment of the measured serum aldosterone concentration may provide a more accurate approximation of the renin-angiotensin aldosterone system. Studies in populations of PA are needed to test for improved diagnostic accuracy that may result from this adjustment.