bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract P200: Post-transplant Weight Control and Hypertension After Kidney Transplantation
Authors: Tantisattamo Ekamol , Vutthikraivit Possawat , Mopuru Haritha
Published: July 2021

Background:
Pre-transplant obesity is associated with post-transplant hypertension (HTN). The contribution of weight change after kidney transplantation and BP is unclear.

Methods:
A retrospective cohort study during a 24-month follow-up was conducted in 70 kidney transplantation recipients whose BMI either <30 and ≥30 kg/m
2
. The association between pre-transplant BMI as well as change of post-transplant BMI in each group and post-transplant HTN (SBP ≥140 mmHg), was determined.

Results:
Of 70 patients (48 (69%) non-obese and 22 (31%) obese), mean age±SEM was 52.66±1.43 years. Mean pre-transplant SBP in non-obese group was not significantly different from SBP in obese group (141.6±21.5 VS. 139.59±22.41; p=0.726, CI -9.2036 to 13.1468). Post-transplant HTN occurred earlier in obese than non-obese groups (mean time to develop post-transplant HTN was 29.4±6.1 VS. 50.6±5.7 weeks; Log Rank 6.068, P=0.014; Figure 1.1). During 24-month follow-up period, followed-up mean BMI appears to increase compared with pre-transplant BMI and only non-obese group had a significant increase in BMI; whereas, BMI decreased in obese group. After controlling for age, gender, type of kidney transplantation, and type of induction immunosuppression, the hazard of post-transplant HTN is 2.152 times greater in obese group than that of non-obese groups (p=0.024, CI 1.108 to 4.178; Figure 1.2).

Conclusion:
Although post-transplant weight gain occurred only in non-obese patients, the risk to develop post-transplant HTN in obese patients appears greater than in non-obese patient transplant. Therefore, pre-transplant weight loss remains important to minimize the risk of post-transplant HTN.
Abstract P221: Rural Living May Mean “Pressure Up”: Investigating the Negative Impact of Rurality on Hypertension Control
Authors: Zachary Rice J , Rouf Emran
Published: July 2021

Objectives:
To identify the impact of social determinants of health on adequate blood pressure (BP) control in a Medicare population.

Methods:
The population studied included 8308 adults aged 27 to 85 enrolled in a Medicare Cost Plan in Central Texas in 2016. We included Medicare members with at least one outpatient visit with a diagnosis of hypertension in the first six months of 2016 and at least one outpatient visit with a diagnosis of hypertension in 2015. As part of a program evaluation, we combined clinical and socio-demographic data from claims, enrollment, and electronic medical records to estimate a multivariate logistic regression model and identify the clinical and non-clinical factors associated with poor BP control.

Results:
In 2016, over 74% (6172 of 8308) of Plan members were compliant with NCQA HEDIS age- and diabetes-adjusted BP control standards, a rate above the 2015 national average. Similarly, around 65% (5363 of 8308) of Plan members obtained an end-year target BP <140/90. After controlling for several clinical and demographic factors, a member living in a rural zip code was found to be 6.2% less likely (at
p
<0.01) to achieve a target BP <140/90 than if that member lived in an urban zip code. This negative association was strongest among members living in the most rural zip codes and was limited to Whites: on average, a White member living in a rural zip code was 6.9% less likely (at
p
<0.01) to have a target BP <140/90 than if he or she lived in an urban zip code.

Conclusion:
The medical community has a limited understanding about how socio-geographic factors, such as rural living, impact BP control. Our analyses found that rural Whites were less likely than urban Whites to have BP <140/90, after controlling for comorbidities, hypertension severity, poverty, education, and other demographic factors. Even in our well-controlled Medicare population, system-wide hypertension control remains challenging due to cultural and geographic disparities. In such populations, in-depth qualitative analysis and creative patient outreach strategies may be necessary to improve hypertension control among the hardest to reach patients.
Abstract P226: Aggressive Blood Pressure Control Status Post-acute Aortic Dissection May be Associated With Acute Kidney Injury: A Pilot Study
Authors: Hopley Charles , Reece T. Brett , Hiatt Willaim
Published: July 2021

Management of acute aortic dissection includes appropriate blood pressure control (120/80 mmHg per AHA guidelines) but this is not based on evidence. Excessive lowering of blood pressure may contribute to organ malperfusion. The kidneys are the most commonly affected organs, causing refractory hypertension and acute kidney injury (AKI). Recent landmark blood pressure trials with intensive pressure goals have a significant incidence of AKI. This pilot study tested the hypothesis that achieved systolic blood pressure less than 120 mmHg has a higher incidence of AKI than those treated systolic pressures > 120 mmHg.

Methods:
Patients were identified via surgical log. Retrospective chart review was performed on patients in the acute setting following dissection. Daily average blood pressures were calculated. Patients were included if they underwent surgical repair of aortic dissection and survived the first 24 hours. Patients were excluded if they demonstrated shock physiology or required renal replacement therapy in the first 24 hours. Serum creatinine and clinical course (including anti-hypertensive regimen) were recorded. The primary endpoint was in-hospital occurrence of AKI (defined per KDIGO criteria) in the acute setting status post aortic dissection in patients receiving anti-hypertensive therapy. An unadjusted odds ratio was calculated. Data on potential confounders and covariates (baseline sCR, contrast exposure etc) were also collected.

Results:
From 2013-2017, 37 cases of surgically repaired aortic dissection were identified and 16 cases met inclusion/exclusion criteria. The incidence of AKI in patients treated to an average systolic blood pressure less than 120mmHg was 75% compared with 50% in those with pressure greater than 120 mmhg. OR =3.0 [95% CI 0.3612-24.9];p=0.3019. Covariates and potential confounders were balanced between groups but given the small numbers additional statistical adjustments were not performed.

Conclusion:
The incidence of AKI was numerically higher in the group of patients achieving more intensive blood pressure targets. Our study was limited by small sample size and selection bias. Both of these issues can be addressed if we apply similar methodologies to address the same question on a lager sample size.
Abstract P233: Mas Receptor Deficiency Does Not Impair Cognitive Funcion of Vascular Dementia Model in the Presence of Angiotensin II Type 2 Receptor
Authors: Higaki Akinori , Mogi Masaki , Iwanami Jun , Min Li-Juan , Kan-no Harumi , Bai Hui-Yu , Shan Bao-shuai , Kukida Masayoshi , Yamauchi Toshihiro , Okura Takafumi , Higaki Jitsuo , Horiuchi Masatsugu
Published: July 2021

Objective:
Angiotensin (Ang) converting enzyme (ACE) 2/ Ang-(1-7)/Mas receptor axis has been considered as protective arm in the renin-angiotensin system and Ang-(1-7) is thought to interact with Ang II type 2 (AT
2
) receptor according. Mas receptor is expressed highly in hippocampus and blood vessels in brain, but its actual function is still unclear. Thus, we examined the possible roles of Mas receptor in relation to the vascular cognitive impairment focusing on the interaction with AT
2
receptor.

Design and Methods:
Male 10-week-old C57BL6 mice (wild-type, WT), Mas1 receptor knockout mice (MasKO) and AT
2
/Mas1 receptor double knockout mice (DKO) were subjected to bilateral carotid artery stenosis (BCAS) surgery. After six weeks from the treatment, we evaluated their cognitive function with Y-maze test and the Morris water maze test.

Results:
The cerebral blood flow (CBF) in each BCAS group was significantly reduced compared to its sham-operated counterparts (WT; 31.5±0.6 vs 28.0±0.8, MasKO; 31.7±0.8 vs 27.7±0.8, DKO; 33.0±0.5 vs 29.1±0.7). The alternation behavior (%) was significantly reduced in WT mice with BCAS compared to sham mice (69.6±3.5 vs 57.9±2.1), but there was no significant difference in MasKO and DKO mice (MasKO; 64.1±2.5 vs 63.1±2.5, DKO; 67.6±2.1 vs 61.1±4.0) in Y maze test. In the Morris water maze test, the mean arrival time at platform at day 5 (sec) was significantly higher in WT-BCAS mice than WT-sham mice (Sham; 20.9±4.6 vs BCAS; 47.3±6.5). In contrast to the results in WT, there was no significant difference in MasKO mice (Sham; 32.8±8.5 vs BCAS; 34.5±7.3). DKO-sham mice showed significantly lower spatial learning ability compared with WT-sham mice (DKO; 77.4±11.9 vs WT; 20.9±4.6). The total cell count in dentate gyrus area was significantly lower in WT-BCAS compared to WT-sham (sham; 255.7±7.0 vs BCAS; 209.4±5.4), but there was no significant change in MasKO mice(sham; 256.5±2.5 vs BCAS; 233.2±16.4). We could not see significant difference in the number of DCX-positive cells and the expressions of proinflammatory cytokines such as IL-6, TNF-α and MCP-1in all mouse groups.

Conclusion:
Mas receptor deficiency seems to be beneficial in vascular dementia on condition that AT
2
receptor exists.
Abstract P234: 2-Methoxyestradiol Attenuates Angiotensin II Induced Hypertension: A Novel Paradigm
Authors: Zhang Yong , Ogola Benard , Iyer Laxmi , Karamyan Vardan , Thekkumkara Thomas
Published: July 2021

Estrogen metabolite 2-methoxyestradiol (2ME2) has therapeutic potential in a number of cardiovascular disorders, including hypertension. However, specific or potential targets remains to be determined. In this study, animals were surgically implanted with PA-C40 telemetry in the intra-aortic vessel and 2ME2 (20 mg/kg/day,
i.p.
injection) effects in AngII infused Wistar-Koyoto (WKY) rats and spontaneously hypertensive rats (SHRs) were determined. In WKY rats 2ME2 treatment resulted in significant reduction in AngII induced blood pressure (BP) compared to vehicle control (systolic; 143.69 ± 2.68 vs. 169.75 ± 1.93 mm Hg, diastolic; 99.91 ± 2.49 vs. 120.16 ± 1.25 mm Hg, and mean arterial pressure; 118.94 ± 2.52 vs. 142.73 ± 1.47 mm Hg). We observed a decrease in heart rate in 2ME2 exposed animals compared to control group (272.67 ± 9.88 vs. 329.12 ± 6.14 BPM). In addition, 2ME2 mediated reduction in workload of the heart when we calculated the rate pressure product or pressure rate index by 13.46 ± 2.32 indicating that 2ME2 can reduce AngII induced hemodynamic stress of the heart. [
3
H]AngII binding studies showed that in kidney cortex AT1R expression was inhibited by 2ME2 treatment compared to control (2112 ± 71 vs. 3341 ± 248 DPM/mg protein). In a separate 5-week study, 2ME2-treated SHRs displayed significant reduction in diastolic BP (114.31 ± 0.66 vs. 123.28 ± 0.70 mm Hg) and mean arterial pressure (146.35 ± 0.67 vs. 151.54 ± 0.89 mm Hg) without significant change in systolic BP compare to the vehicle treated animals. Moreover, we found significant decrease in heart rate in 2ME2-treated animals (290.03 ± 2.69 vs. 312.92 ± 1.50 BPM). Analyses of kidney cortical tissue revealed downregulation of AT1R expression after 2ME2 treatments (20227 ± 2211 vs. 9515 ± 2115 DPM/mg protein). Consistent with the reduction in BP, the indicators of cardiac hypertrophy including heart weight (1.28 ± 0.08 vs. 0.99 ± 0.02 gram), cardiac collagen deposit and α-smooth muscle actin (α-SMC) positive myofibroblasts were decreased. The data demonstrate for the first time that 2ME2 control BP through downregulation of AT1R in kidney and heart rate, which may provide an insight to the mechanism(s) of cardioprotective effects of 2ME2 through the blockade of AngII induced hypertension.
Abstract P241: Autophagic Flux is Diminished in Mesenteric Resistance Arteries of Spontaneously Hypertensive Rats
Authors: McCarthy Cameron G , Wenceslau Camilla F , Webb R. Clinton
Published: July 2021

Autophagy is the constitutively active catabolic process regulating protein quality control and energy homeostasis. However, dysregulation of this process can have detrimental effects on cellular function. In particular, insufficient autophagy has been proposed as a mechanism of cellular aging, as this leads to the accumulation of damaged macromolecules and organelles. Hypertension is a condition of vascular aging. In fact, many factors that contribute to the deterioration of vascular function as we age are exacerbated in clinical and experimental hypertension. Nonetheless, whether high blood pressure per se is the cause or effect of diminished autophagy remains to be clarified. We hypothesized that mesenteric resistance arteries (MRA) from spontaneously hypertensive rats (SHR) would have decreased autophagic flux as measured by conversion of microtubule-associated protein light chain 3 (LC3-I to LC3-II) compared to normotensive Wistar Kyoto rats (WKY). We observed that MRA from male 12-15 week old SHR have decreased basal expression both cytosolic LC3 (LC3-I) and phosphatidylethanolamine conjugated LC3 (LC3-II), and expression of these proteins are similarly decreased in SHR chronically treated with hydrochlorothiazide and reserpine (SHR+HCTZ/Res) [Arbitrary units (AU), LC3-1: WKY: 1.4±0.1, SHR: 1.1±0.1*, and SHR+HCTZ/Res: 0.7±0.1*; LC3-II: WKY: 1.4±0.1, SHR: 1.1±0.1*, and SHR+HCTZ/Res: 0.7±0.1*, *p<0.05 vs. WKY]. To understand autophagic flux, some MRA were incubated with lysosomal inhibitor chloroquine (CQ; 30 μM) for 2 hours. CQ incubation significantly increased LC3-II expression to a similar magnitude in WKY, SHR, and SHR+HCTZ/Res MRA (all *p<0.05 vs. basal). However, the percent increase in LC3-II expression after CQ incubation was significantly less in SHR compared to WKY, and SHR+HCTZ/Res was not different from either WKY or SHR (% increase from basal LC3-II, WKY: 546±187, SHR: 156±38*, and SHR+HCTZ/Res: 273±106, *p<0.05 vs. WKY). Overall, these data suggest that SHR have impaired autophagosome-lysosomal fusion, and this is not solely attributable to high blood pressure. Therefore, reconstituting autophagic activity could be a novel prophylactic or therapeutic measure against vascular aging in hypertension.
Abstract P254: Apolipoprotein Expression Changes in the Dahl Salt Sensitive Rat Model of Spontaneous Superimposed Preeclampsia
Authors: Maeda Kenji J , Johnson Ashley C , Garrett Michael R , Sasser Jennifer M
Published: July 2021

Preeclampsia (PE) is a multifactorial pregnancy-specific syndrome with the main characteristic feature of the mother developing hypertension and systemic organ dysfunction after 20 weeks of gestation. Worldwide, PE accounts for up to 8% of pregnancy complications and is considered to be a leading cause of maternal and fetal morbidity and mortality. Currently, there is little progress in developing treatments for PE, nor are there robust biomarkers for early detection. Using the Dahl salt sensitive (S) rat, a model of spontaneous superimposed preeclampsia, and the Sprague Dawley (SD) rat, normal pregnancy control, we previously performed a microarray study (Affymetrix Rat 2.0ST GeneChip) on gestational day 14 placental samples which identified several genes in the apolipoprotein family to be temporarily dysregulated between the Dahl S and SD rats. The goal of the current study was to validate these microarray findings and determine if these changes persist through late pregnancy. We performed quantitative real-time-PCR analysis (BioRad PrimePCR Custom Array) and confirmed significant increases in expression of various isoforms of apolipoproteins in the Dahl S rat compared to that of the SD on gestational day 14 (Table). However, there were no significant differences between the two strains on gestational day 20, indicating a potential role of these apolipoproteins earlier in PE development. Our data are consistent with patient studies suggesting apolipoproteins may be involved in PE, serve as potential biomarkers for early detection, and be a target for therapeutic interventions.
Abstract P267: Placental Ischemia Causes Cardiac Structural and Functional Abnormalities in the Reduced Uterine Perfusion Pressure Rat Model
Authors: Bakrania Bhavisha , Granger Joey P
Published: July 2021

Preeclampsia (PE) is a disorder prevalent in 5-7% of pregnancies. It is characterized by maternal hypertension and endothelial dysfunction. While it has been shown that systolic and diastolic function is impaired in women with PE, the exact mechanisms responsible for the cardiac dysfunction in PE have yet to be fully elucidated. PE is thought to develop in response to placental ischemia and ultimately the release of anti-angiogenic and pro-inflammatory factors into the maternal circulation. However, the impact of placental ischemia on cardiac function is unclear. Therefore the aim of this study was to assess cardiac structure and function in response to placental ischemia utilizing the Reduced Uterine Perfusion Pressure (RUPP) rat model. Briefly in this model, silver clips are placed on the abdominal aorta and branches of the ovarian arteries on gestational day (GD) 14 to induce placental ischemia. For this study, the RUPP (
n
=8) group underwent surgery on GD 14, and both normal pregnant (NP,
n
=8) and RUPP rats had carotid catheters placed on GD 18. Blood pressure and echocardiography measurements, and tissue harvest were performed on GD 19. The RUPP group had significantly increased mean arterial pressure compared to the NP group on GD 19 (123±3 vs. 97±2 mmHg, P<0.01). RUPP rats had lower mean left ventricular ejection fraction (60±2 vs. 78±2 %, P<0.01) and fractional shortening (46±3 vs. 56±1 %, P=0.05), in addition to cardiac hypertrophy (0.97±0.04 vs. 0.91±0.02 g, P=0.02). These data were accompanied by increased cardiomyocyte surface area (348±36 vs. 289±23 μm
2
, P=0.03). In conclusion, this study shows that the RUPP rat develops cardiac structural and functional abnormalities after only five days of placental ischemia. Furthermore, these data suggest that the RUPP model could be useful in investigating and understanding the mechanisms which underpin these cardiac changes in PE patients.
Abstract P289: Cardio-protective Peptide Ac-SDKP is Highly Concentrated in Lymph Nodes
Authors: Romero Cesar A , Vaid Sonal , Kumar Nitin , Liao Tang-Dong , Carretero Oscar A
Published: July 2021

N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a natural peptide released from its precursor Thymosin β4 (Tβ4) by meprin-α and the prolyl oligopeptidase enzymes (POP) in sequential steps. Ac-SDKP is hydrolyzed by the angiotensin converting enzyme (ACE). Ac-SDKP has anti-inflammatory and anti-fibrotic effects in heart, aorta and kidney and part of the beneficial effects of ACE inhibitors has been ascribed to the increased levels of Ac-SDKP. Ac-SDKP is present in spleen and thymus, however, the presence of Ac-SDKP in the lymph node has not been studied. We hypothesized that Tβ4, Ac-SDKP and its releasing enzymes are present in lymph node. Ac-SDKP concentration was evaluated in Sprague-Dawley (SD) rat tissues. Tβ4 as well as Meprin-α and POP enzymes were measured in the lymph node, thymus, spleen and other tissues obtained from SD rats. Additionally, Ac-SDKP content was measured in different cell populations of lymph node obtained through cell sorting. Lymph node showed the highest Ac-SDKP concentration (181±18.3 ng/mg of protein), followed by the testis (104.3±6.5, thymus (54.2±1.8) and spleen (44.9±4.7) in SD rats (P<0.001 lymph node vs. testis, thymus and spleen). Meprin-α and POP activity were present in lymph node, spleen and thymus. Tβ4 and Meprin-α immunostaining were found to be positive in multinucleated giant cells in the cortical region of lymph node and along the septums; it was also found in the follicular region and germinal center. POP staining was found positive in the cortical region. In the lymph node, Ac-SDKP concentration was higher in Macrophages (CD45+CD68+) in comparison with T lymphocytes (CD45+CD3+) (150±110 pmol/100,000 cell vs. 0.3±0.1pmol/100,000cell, respectively). We conclude that in lymph node, Ac-SDKP is highly concentrated and that all the components of Tβ4/Ac-SDKP system are present. Macrophages could be the main source of Ac-SDKP in lymph node. The presence of Ac-SDKP in lymph node may have important implications in understanding inflammation and target organ damage in cardiovascular diseases.
Abstract P307: pNaKtide Attenuates Dyslipidemia and Atherosclerosis by Blocking Na/K- ATPase/Reactive Oxygen Species Amplification in ApoE -/- Mice
Authors: Chaudhry Hibba , Nichols Alexandra , Nawab Athar , Sharma Dana , Sodhi Komal
Published: July 2021

Background:
We have previously reported that the α1 subunit of the sodium potassium adenosine triphosphatase (Na/K-ATPase) acts as an amplifier for reactive oxygen species (ROS) in addition to its ion pumping function. We have also shown that blockade of this amplification with a novel peptide, pNaKtide, ameliorates oxidative stress and obesity in mice subjected to a high-fat diet.

Hypothesis:
Given the importance of oxidative stress in the pathophysiology of atherosclerosis, we chose to examine whether pNaKtide might be effective in ameliorating dyslipidemia and atherosclerosis in ApoE -/- mice.

Methods:
pNaKtide was administered in ApoE -/- mouse fed western diet. 25 mg/Kg pNaKtide was administered intraperitoneally once every 7 days. Lipid profile, glucose insulin levels, and ROS levels were measured. Aortas were dissected and quantification of aortic lesions was done.

Results:
Our results show that pNaKtide improved glucose tolerance and HOMA-IR scores in ApoE-/- mice fed a western diet (p<0.05). Also, pNaKtide administered to these mice significantly decreased plasma ALT, triglycerides, FFA, and LDL levels. Further, our results show that ApoE -/- mice fed a western diet had decreased plasma HDL levels and this decrease was reversed by pNaKtide. Plasma ROS levels were significantly attenuated by pNaKtide treatment. Mice fed a western diet had increased plaque size. Plaque size was significantly decreased by pNaKtide treatment.

Conclusion:
This study suggests that the Na/K-ATPase/ROS signaling cascade is a possible mechanism for the development of dyslipidemia and atherosclerosis associated with the metabolic syndrome phenotype and pNaKtide presents a potential novel treatment for these pathologies.
Abstract P308: Rgs2 Promotes Uterine Blood Flow During Pregnancy
Authors: Koch Jennifer N , Owens Elizabeth A , Dahlen Shelby , Li Jie , Osei Owusu Patrick
Published: July 2021

Regulators of G protein signaling (RGS) proteins are crucial in mediating vascular smooth muscle contraction via the regulation of heterotrimeric G proteins, affecting blood pressure and arterial blood flow. Previous studies by others and us showed that RGS2 deficiency augments vascular tone and impairs uterine blood flow (UBF) in non-pregnant mice, and that an
Rgs2
loss-of-function mutation is linked to preeclampsia in humans; however, the mechanisms are unclear. Here, we tested the hypothesis that increased RGS2 expression and/or function facilitates placental perfusion by promoting vasodilation and UBF. We determined gene expression throughout pregnancy and post-partum period by real-time qPCR, while uterine blood flow and blood pressure were examined by ultrasound and carotid artery catheterization, respectively, under anesthesia. RGS2 expression decreased markedly by pregnancy day 10 (0.049 ± 0.013 vs. 0.023 ± 0.017) but returned to non-pregnancy level by day 15 (0.049 ± 0.013 vs. 0.041 ± 0.008,) in wild type mice. The pattern of changes in impedance to UBF mimicked gene expression profile in WT mice; in contrast, impedance remained elevated in
Rgs2-/-
mice at pregnancy day 15 (RI; WT: 0.516 ± 0.027, vs. RGS2-/-: 0.714 ± 0.020). Systemic blood pressure was similar between WT and Rgst2-/- mice at all stages of pregnancy. The results together indicate that RGS2 promotes uterine perfusion during pregnancy independently of its blood pressure effects. These findings are clinically relevant as selective targeting of G protein signaling could improve utero-placental hypoperfusion during pregnancy and prevent the development of pregnancy complications such as preeclampsia.
Abstract P350: Abnormal VCG and Hi-Res Parameters of P and QRS Complex in Hypertensive Patients Without/with Paroxysmal Atrial Fibrillation
Authors: Filipova Slavomira , Vachulova Anna , Skultetyova Dana , Hlivak Peter , Gaspar Ludovit
Published: July 2021

AIM Today we have not the established and single clinical mode to identifying hypertensive (HT) patients in risk for paroxysmal atrial fibrillation (pAF). Some non-invasive VCG and high-resolution VCG (Hi-Res) for P and QRS loops are available for ECG/VCG measurements in clinical practice via routinely used ECG/VCG equipment (General Electric). It is possible, that especially P wave and P loop values can reflect the abnormal status in atrial myocardium prior the pAF onset. MATERIAL AND METHOD We studied 276 HT patients in sinus rhythm: group I (n=133, without documented pAF), group II (n=129, with well-documented pAF) and group III (n=14, patients after successful radiofrequency ablation for AF or atrial flutter). ECG parameters were evaluated: (1) heart rate in SR; (2) VCG P loop and QRS loop non-filtered/filtered duration: nPd, fPd, nQRSd, fQRSd; (3) other Hi-Res P and QRS parameters: HFLAd, RMS(40)v; (4) angle between axes P-QRS and QRS-T loops; (5) echoCG parameters: LA dimension, LV ejection fraction, width of IVS ad posterior wall. RESULTS In group II a III the non-filtered parameters (nPd, nQRSd) and filtered parameters (fPd, fQRSd) were significantly longer than in group I (for nPd : 135.9 ms, 145.1 ms vs. 129.0 ms, p<0.05; for nQRsd : 104.2 ms, 110.0 ms vs. 99.0 ms, p<0.01; for fPd: 143.0 ms, 154.9 ms vs. 133.0 ms, p<0.005; for fQRSd 119.7 ms, 125.9 ms vs. 113.0 ms, p<0.005). P loop axis analysis is significantly higher in loop II and III vs. group I (+48.2 gr., +53.4 gr. Vs. 48 gr., p<0.01). Angle P-QRS is significantly wider in group II and III vs. group I (38.7 gr., 42.1 gr. Vs. 25.0 gr, p= 0.005. EchoCG parameters were not significantly different (LA dimensions for groups I,II,III: 39.8, 42.7 and 42.0 mm, n.s.; LVEF for groups I,II,III> 59.7, 57.8 and 58.1, ns.). CONCLUSIONS HT patients with verified pAF in documentation have more abnormal P and QRS wave/loop parameters than HT patients without history of pAF. According to our results, the most informative ECG and VCG factors for possible future pAF are: fPd, fQRSd, angle between loop axes P-QRS. ECG/VCG parameters (non-filtered and especially after filtration via to Hi-Res analysis) have potential to improve the risk stratification for possible future pAF.
Abstract P366: Blood Pressure Checks for Diagnosing Hypertension (BP-CHECK)
Authors: Green Beverly B , Anderson Melissa L , Cook Andrea J , Campbell Jerry , Hall Yoshio N , Hsu Clarissa , Joseph Dwayne , Klasnja Pedja , Margolis Karen L , McClure Jennifer B , Munson Sean A , Thompson Matthew J
Published: July 2021

Importance:
The US Preventive Services Task Force recommends screening adults for high blood pressure (BP). If BP is high, out-of-office BPs are recommended before making a new diagnosis of hypertension, preferably using 24 hour ambulatory BP monitoring (ABPM), because over 30% have normal BPs outside of clinic or “White coat” hypertension with risk of cardiovascular events and death similar to those without hypertension. Currently few physicians use and few patients have heard of ABPM, which may be less convenient than clinic, home, or kiosk-based monitoring.

Objective:
The BP Check randomized controlled diagnostic study will compare the accuracy and acceptability of clinic, home, and kiosk-based BP monitoring compared to ABPM for diagnosing hypertension. The study aims, design, protocols, materials, and evaluation described below are informed by patient, health care, policy, and expert stakeholders.

Methods:
Adults ages 18-85 will be recruited and randomized to routine screening via clinic screening, home BP monitoring over 5 days, or kiosk-based monitoring on 3 separate days. After completion all participants will complete ABPM. Mean BP assessed via each screening method (clinic, home, and kiosk) will be compared with 24 hour APBM to assess the accuracy of each method. We will also assess the acceptability of each method from the patients’ perspective and the impact of the tests longer-term. Finally, a mixed method analysis is planned to explore physician knowledge and beliefs about BP measurement, diagnosing hypertension, and the perceived feasibility of using each of the tested BP strategies in routine clinical practice.

Results:
Enrollment began in May of 2017 with a target of randomizing 510 participants.

Conclusion and Public Health Impact:
BP-CHECK will inform which hypertension diagnostic methods are most accurate, acceptable to patients, and feasible to implement in primary care. This evidence-base is critical to compare alternate methods of diagnosing hypertension to ABPM
Abstract P371: Incremental Changes in Systolic Blood Pressure Post-mild Exercise, in Normotensive Subjects, is Associated With Significant Structural and Functional Cardiovascular Abnormalities
Authors: Tucker Susan , Byju Arjun , El Shahawy Mahfouz
Published: July 2021

Background:
Abnormal rise in systolic blood pressure (SBP) post-mild exercise (PME) has been associated with early structural and functional cardiovascular abnormalities.

Purpose:
To determine if the differential amount of rise in SBP PME, in normotensive subjects, effected the risk of early structural and functional cardiovascular abnormalities.

Methods:
1416 untreated, asymptomatic subjects were screened for early indicators of cardiovascular disease using the Early CVD Risk Score (ECVDRS), also known as Rasmussen Risk Score (RRS), which consists of a panel of 10 tests; large (C1) and small (C2) artery stiffness, resting BP and post mild exercise (PME), CIMT, abdominal aorta and left ventricle ultrasounds, retinal photography, microalbumuria, ECG, and pro-BNP. 996 subjects were normotensive. Of those subjects, 30 subjects had an abnormal rise in SBP PME between 30-40mmHg and 14 had an abnormal rise in SBP PME >40 mmHg. Focus was placed on the three tests recommended for early CVD assessment; C1, C2 and CIMT.

Results:
As seen in Figure 1.0, an abnormal rise in SBP PME greater than 40mmHg is associated with a statistically significant increase in risk of early structural and functional cardiovascular abnormalities in untreated, asymptomatic, normotensive subjects opposed to those who only had an increase between 30-40mmHg.

Conclusion:
Assessment of SBP PME is an easy, noninvasive, inexpensive test that can be performed by any health care practitioner to evaluate the risk of CVD in patients. Based on the severity of the increase in SBP PME should warrant physicians on the urgency to further investigate and treat patients to divert the progression of CVD.
Abstract P397: Living in Ethnic-enclave Neighborhoods May Attenuate the Negative Effect of Acculturation on Blood Pressure in Refugees and Maintain Immigrant Health Effect
Authors: Dalmar Ahmed , Pryce Douglas , Martinson Brian , Faraha Farhiya , Wewerka Sandra , Dubois Diana , Sanka Laura , Ahmed Osman , Westgard Bjorn
Published: July 2021

Background:
Researchers have long hypothesized that acculturation (duration of U.S. residence [DOR]) is associated with increases in blood pressure in immigrant populations. However, little is known about the potential effects of acculturation on hypertension (HTN) in refugees living in ethnic-enclave neighborhoods. We conducted a cross-sectional study of Somali refugees and immigrants (a largely enclaved population) living in Minneapolis-St. Paul, Minnesota.

Method:
We analyzed data from 1155 Somali refugees/immigrants who arrived in United States from 1990 to 2015 and are participating in an ongoing study of Somali refugees in the Twin Cities. Using 10 years as a threshold, the study population was divided into two groups based on DOR: short (< 10 years) or long (>= 10 years). Main outcome was HTN, which was defined using the protocol of international HTN studies. Differences between the two groups were determined by chi-squared test and t-test. Multivariate logistic regression was used to determine association between HTN and DOR.

Results:
Of 1155 subjects, 572 (49.6%) had DOR >= 10 years. Mean DOR was 9.8 ± 6.0 years (median of 10), and 58.1% (559 of 1155) were women. The short DOR group was younger (mean age 44.6 ± 18.0 vs 51.4 ± 18.1 years, P< 0.001. There was no difference in mean systolic blood pressure (SBP) between groups (117 mmHg vs 119 mmHg, P=0.087) and no correlation between SBP and DOR (linear R
2
=0.012). Prevalence of HTN was 29.5% (341 of 1155), with 179 of these 341 (52.5%) having uncontrolled HTN. HTN increased with aging: 4.1% (19 of 457) for age group 18-39, 15.3% (47 of 306) for ages 40-59, and 29.7% (114 of 384) for ages 60
+
. After adjusting for body mass index, marital status, English language (written and spoken), health insurance, income
/
poverty ratio, language spoken at home, employment, education and DOR, age was the only predicator of HTN. Even after matching two groups by age, the distribution of HTN was similar between the two age-matched DOR groups (P=0.1879).

Conclusions:
DOR (acculturation) was not a predictor of HTN in this highly enclaved refugee/immigrant sample. Further studies are needed to identify which cultural and neighborhood environment factors may operate to blunt the effects of acculturation on blood pressure.
Abstract P492: Lower Body Mass Index is Associated With Arterial Stiffening and Severity of Orthostatic Hypotension in Middle-aged and Older Patients With Abdominal Obesity
Authors: Kobayashi Yusuke , Fujikawa Tetsuya , Yatsu Keisuke , Iwamoto Tamio , Hirawa Nobuhito , Kobayashi Hideo , Umemura Satoshi , Tamura Kouichi
Published: July 2021

Background:
Recently, patients with both sarcopenia and abdominal obesity are known to exhibit subclinical atherosclerosis and high mortality risk. Sarcopenic obesity is considered to be latent in those without increase in body mass index (BMI) despite having abdominal obesity. We aimed to investigate whether arterial stiffening and severity of orthostatic hypotension, which is the risk of cardiovascular disease, is associated with lower BMI in patients with abdominal obesity.

Methods:
We studied middle-aged and older patients with normal to high BMI (BMI ≥ 18.5) and being treated with life-style related diseases. The patients were divided into 2 groups (with or without abdominal obesity) according to waist circumference (WC) (abdominal obesity: men; WC ≥ 85 cm, women; WC ≥ 90 cm). We measured cardio-vascular ankle index (CAVI) for an index of arterial stiffness. We assessed sit-to-stand test for measuring orthostatic systolic blood pressure (SBP) change.

Results:
One thousand and forty-six patients were included in the study. Mean age of the patients was 68.0 ± 10.1 years (42.5% were men), hypertension dyslipidemia and diabetes mellitus was observed in 83.3%, 74.3% and 20.2% of the patients respectively. There was a significant negative correlation with BMI and CAVI in patients with abdominal obesity (r=-0.309, p<0.001, n=434), whereas no significant association was observed in patients without abdominal obesity (p=N.S., n=612). There was a significant positive correlation with BMI and orthostatic SBP change in patients with abdominal obesity (r=0.213, p<0.001) and in patients without abdominal obesity (r=0.117, P=0.004). Multivariate regression analysis revealed that BMI was an independent determinant of CAVI and orthostatic SBP change in patients with abdominal obesity (p<0.001, p<0.001, respectively), and was an independent determinant of orthostatic SBP change in patients without abdominal obesity (p=0.004).

Conclusion:
In patients with abdominal obesity, lower BMI was an independent determinant of arterial stiffening and severity of orthostatic hypotension. Further investigation by evaluating body composition is necessary and now ongoing to assess the risk of lower BMI in patients with abdominal obesity.
Abstract P521: Relationship Between Carotid Arterial Elastic Properties and Central Aortic Hemodynamics in Patients with Stroke
Authors: Kim Sung-ai , Jo Sang-Ho , Park Kyung-Ha , Kim Hyun-Sook
Published: July 2021

Objective:
Patients with ischemic stroke have more thickened, dilated and stiffer aorta and carotid arteries than patients without. However, there was few data about the relations between the carotid and central aortic elastic properties in those patients. This study aims to investigate the association between carotid artery parameters and central aortic hemodynamics in patients with ischemic stroke.

Methods:
A total of 101 consecutive patients with ischemic stroke who underwent clinically indicated transesophageal echocardiography (TEE) were performed carotid ultrasonography to assess vascular elastic properties. Using velocity-vector imaging (VVI), instantaneous vessel area (cm
2
) and deformation as fractional area change (FAC, %) and circumferential strain (%) were obtained in both cross-sectional image of common carotid artery (CA) and descending thoracic aorta (DTA) during TEE.

Results:
In correlation analysis, elastic properties of DTA including FAC, circumferential strain and vessel area were significantly correlated with the corresponding values of CA, respectively (all p<0.01). Among the vascular parameters, FAC of CA showed independent association with the circumferential strain of DTA adjusting for age, gender, blood pressure, heart rate, intima-media thickness, pulse wave velocity and vessel area (ß=0.14, p=0.002, 95% CI 0.05-0.24) in linear regression analysis.

Conclusions:
Non-invasively measured elastic properties of CA using VVI showed significant associations with those of DTA and provide valuable information for better understandings of central aortic hemodynamics in patients with ischemic stroke.
Abstract P532: Hypertension and Gender Differences in Acute Ischemic Stroke Patients Treated With Rtpa
Authors: Nathaniel Thomas I , Gainey Jordan , Wormack Leah , Ubah Chibueze , Brechtel Leanne , Frazier Amber
Published: July 2021

Background:
Women and men have a similar incidence for ischemic cerebrovascular disease but women are more frequently hit by stroke later in life than men. It has been shown that women presented with severe stroke symptoms during admission, a poorer prognosis, are likely to have an overall poorer outcome after ischemic stroke when compared with men. However, some studies indicate similarities in outcome for men and women after stroke. Moreover, there is evidence that women treated with tPA benefit at least as much as men. Since a higher diastolic blood pressure increases the risk for a worse prospective functional status in men, but less significance in women, it is not clear whether hypertensive patients with acute ischemic stroke treated will reveal similarity or difference in functional outcome. We investigated this issue in the current study.

Method:
We performed a retrospective analysis of 4500 acute ischemic stroke patients who presented to a health care system between January 2010 and June 2016 and received rt-PA. We develop a new tool to determine the possibility of erasing any gender difference, and identify the most important factor for the poorer outcomes in women or men and whether thrombolysis may counteract this effect.

Results:
Our results reveal that poorer outcomes after stroke and the observed gender differences is due to age, at stroke onset, and that thrombolysis may neutralize this effect.

Conclusion:
The important factor for the poorer outcome and gender differences in hypertensive patients with acute ischemic stroke is mainly due to stroke severity and thrombolysis may play a major role in neutralizing this effect.
Clinical Outcomes of Autologous Stem Cell–Patch Implantation for Patients With Heart Failure With Nonischemic Dilated Cardiomyopathy
Authors: Domae Keitaro , Miyagawa Shigeru , Yoshikawa Yasushi , Fukushima Satsuki , Hata Hiroki , Saito Shunsuke , Kainuma Satoshi , Kashiyama Noriyuki , Iseoka Hiroko , Ito Emiko , Harada Akima , Takeda Maki , Sakata Yasushi , Toda Koichi , Pak Kyongsun , Yamada Tomomi , Sawa Yoshiki
Published: July 2021

Background

Clinical effectiveness of autologous skeletal cell‐patch implantation for nonischemic dilated cardiomyopathy has not been clearly elucidated in clinical settings. This clinical study aimed to determine the feasibility, safety, therapeutic efficacy, and the predictor of responders of this treatment in patients with nonischemic dilated cardiomyopathy.

Methods and Results

Twenty‐four nonischemic dilated cardiomyopathy patients with left ventricular ejection fraction <35% on optimal medical therapy were enrolled. Autologous cell patches were implanted over the surface of the left ventricle through left minithoracotomy without procedure‐related complications and lethal arrhythmia. We identified 13 responders and 11 nonresponders using the combined indicator of a major cardiac adverse event and incidence of heart failure event. In the responders, symptoms, exercise capacity, and cardiac performance were improved postoperatively (New York Heart Association class II 7 [54%] and III 6 [46%] to New York Heart Association class II 12 [92%] and I 1 [8%],
P
<0.05, 6‐minute walk test; 471 m [370–541 m] to 525 m [425–555 m],
P
<0.05, left ventricular stroke work index; 31.1 g·m
2
·beat [22.7–35.5 g·m
2
·beat] to 32.8 g·m
2
·beat [28–38.5 g·m
2
·beat],
P
=0.21). However, such improvement was not observed in the nonresponders. In responders, the actuarial survival rate was 90.9±8.7% at 5 years, which was superior to the estimated survival rate of 70.9±5.4% using the Seattle Heart Failure Model. However, they were similar in nonresponders (47.7±21.6% and 56.3±8.1%, respectively). Multivariate regression model with B‐type natriuretic peptide, pulmonary capillary wedge pressure, and expression of histone H3K4me3 (H3 lysine 4 trimethylation) strongly predicted the responder of this treatment (B‐type natriuretic peptide: odds ratio [OR], 0.96; pulmonary capillary wedge pressure: ​OR, 0.58; H3K4me3: OR, 1.35, receiver operating characteristic–area under the curve, 0.96,
P
<0.001).

Conclusions

This clinical trial demonstrated that autologous skeletal stem cell–patch implantation might promise functional recovery and good clinical outcome in selected patients with nonischemic dilated cardiomyopathy, in addition to safety and feasibility.

Registration

URL:
http://www.umin.ac.jp/english/
. Unique identifiers: UMIN000003273, UMIN0000012906 and UMIN000015892.
Diabetes Mellitus Is Associated With Poor In‐Hospital and Long‐Term Outcomes in Young and Midlife Stroke Survivors
Authors: MacIntosh Bradley J. , Cohen Ellen , Colby‐Milley Jessica , Fang Jiming , Zhou Limei , Ouk Michael , Wu Che‐Yuan , Shah Baiju R. , Lanctôt Krista , Herrmann Nathan , Linkewich Elizabeth , Law Marcus , Black Sandra E. , Swartz Richard H. , Kapral Moira K. , Edwards Jodi D. , Swardfager Walter
Published: July 2021

Background

The incidence of ischemic stroke has increased among adults aged 18 to 64 years, yet little is known about relationships between specific risk factors and outcomes. This study investigates in‐hospital and long‐term outcomes in patients with stroke aged <65 years with preexisting diabetes mellitus.

Methods and Results

Consecutive patients aged <65 years admitted to comprehensive stroke centers for acute ischemic stroke between 2003 and 2013 were identified from the Ontario Stroke Registry. Multinomial logistic regression was used to estimate adjusted odds ratio (OR [95% CI]) of in‐hospital mortality or direct discharge to long‐term or continuing care. Cox proportional hazards regression was used to estimate the adjusted hazards ratio (aHR [95% CI]) of long‐term mortality, readmission for stroke/transient ischemic attack, admission to long‐term care, and incident dementia. Predefined sensitivity analyses examined stroke outcomes among young (aged 18–49 years) and midlife (aged 50–65 years) subgroups. Among 8293 stroke survivors (mean age, 53.6±8.9 years), preexisting diabetes mellitus was associated with a higher likelihood of in‐hospital death (adjusted OR, 1.46 [95% CI, 1.14–1.87]) or direct discharge to long‐term care (adjusted OR, 1.65 [95% CI, 1.07–2.54]). Among stroke survivors discharged (N=7847) and followed up over a median of 6.3 years, preexisting diabetes mellitus was associated with increased hazards of death (aHR, 1.68 [95% CI, 1.50–1.88]), admission to long‐term care (aHR, 1.57 [95% CI, 1.35–1.82]), readmission for stroke/transient ischemic attack (aHR, 1.37 [95% CI, 0.21–1.54]), and incident dementia (aHR, 1.44 [95% CI, 1.17–1.77]). Only incident dementia was not increased for young stroke survivors.

Conclusions

Focused secondary prevention and risk factor management may be needed to address poor long‐term outcomes for patients with stroke aged <65 years with preexisting diabetes mellitus.
Stroke‐Related Mortality in the United States–Mexico Border Area of the United States, 1999 to 2018
Authors: Khan Safi U. , Kalra Ankur , Yedlapati Siva H. , Dani Sourbha S. , Shapiro Michael D. , Nasir Khurram , Virani Salim S. , Michos Erin D. , Alkhouli Mohamad
Published: July 2021

BACKGROUND

The United States (US)‐Mexico border is a socioeconomically underserved area. We sought to investigate whether stroke‐related mortality varies between the US border and nonborder counties.

METHODS AND RESULTS

We used death certificates from the Centers for Disease Control and Prevention Wide‐Ranging Online Data for Epidemiologic Research database to examine stroke‐related mortality in border versus nonborder counties in California, Texas, New Mexico, and Arizona. We measured average annual percent changes (AAPCs) in age‐adjusted mortality rates (AAMRs) per 100 000 between 1999 and 2018. Overall, AAMRs were higher for nonborder counties, older adults, men, and non‐Hispanic Black adults than their counterparts. Between 1999 and 2018, AAMRs reduced from 55.8 per 100 000 to 34.4 per 100 000 in the border counties (AAPC, −2.70) and 64.5 per 100 000 to 37.6 per 100 000 in nonborder counties (AAPC, −2.92). The annual percent change in AAMR initially decreased, followed by stagnation in both border and nonborder counties since 2012. The AAPC in AAMR decreased in all 4 states; however, AAMR increased in California’s border counties since 2012 (annual percent change, 3.9). The annual percent change in AAMR decreased for older adults between 1999 and 2012 for the border (−5.10) and nonborder counties (−5.01), followed by a rise in border counties and stalling in nonborder counties. Although the AAPC in AAMR decreased for both sexes, the AAPC in AAMR differed significantly for non‐Hispanic White adults in border (−2.69) and nonborder counties (−2.86). The mortality decreased consistently for all other ethnicities/races in both border and nonborder counties.

CONCLUSIONS

Stroke‐related mortality varied between the border and nonborder counties. Given the substantial public health implications, targeted interventions aimed at vulnerable populations are required to improve stroke‐related outcomes in the US‐Mexico border area.