bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 101: Gender Has Differential Effects on Non-Hemorrhagic Stroke Outcomes
Authors: Pieper Justin , Ashamalla Michael , Sedhom Daniel , Yager Neil , Ghate Ketan , Nguyen Veronica , Shkolnik Boris , Torosoff Mikhail 
Published: July 2021

Background:
We sought to examine the relationship between gender, age, co-morbidities, and outcomes in patients with non-hemorrhagic stroke.

Materials and methods:
Retrospective chart review was performed on 517 consecutive non-hemorrhagic stroke patients (48% women, 20% with diabetes, 26.8% with CAD, 38% with dyslipidemia, 62.2% with HTN, 4.2% with peripheral vascular disease, 4.7% with renal insufficiency) treated at a single academic medical center.

Results:
Younger patients were more likely to be men (age<50 55%, 51-60 58.3%, 61-70 59.6%; p<0.05) while older patients were likely to be women (age 71-80 54.9%, >80 56.6; p<0.05). Accordingly, the subsequent analysis stratified the cohort into two groups, <70 and >70 years old.

Regardless of age, men had a higher prevalence of CAD (age <70, 25.2% vs 18.8% in women, and age >70, 43.7% vs. 23.1% in women; p<0.05) and dyslipidemia (age <70, 43.4% vs 32.5% in women and age >70, 44.8% vs. 30.6% in women; p=.05). There were no significant gender based differences in BMI, prevalence of diabetes, hypertension, peripheral vascular disease, or chronic renal insufficiency.
The mean follow up duration was 47.3+/-0.9 months. Gender did not affect mortality in patients younger than 70 years old (15.5% men vs. 15.6% women.) However in patients of age >70 mortality was significantly increased in men (50.5% in men vs. 41.7% in women; chi-squared p<0.001, log-rank p<0.0001, Figure). In logistic regression analysis, when compared to women younger than 70 years old, men of the same age had similar mortality (HR 1.0; 95%CI 0.5-1.9, p=0.980); while age greater than 70 conferred 4-5 fold increased risk of mortality (HR 3.9; 95%CI 2.1-7.0, p<0.0001 in women, and HR 5.5; 95%CI 3.0-10.3, p<0.0001 in men). When gender and age were accounted for, history of coronary artery disease and/or dyslipidemia did not affect the outcomes.

Conclusion:
Men with non-hemorrhagic stroke were more likely to have dyslipidemia and history of coronary artery disease. This, however, did not translate into increased mortality in younger men.

Gender appears to have a differential effect on non-hemorrhagic stroke outcomes which warrants future investigation.
Abstract 108: Racial and Ethnic Disparities in Heart Failure Readmissions and Mortality in a Large Municipal Healthcare System
Authors: Durstenfeld Matthew S , Park Hannah , Katz Stuart D , Blecker Saul B 
Published: July 2021

Background:
Hispanic and black patients with heart failure have been shown to have higher risk of readmission but lower risk of post-discharge mortality than white patients. To determine whether disparities exist among patients with similar access to care, we examined outcomes after heart failure hospitalization within a large municipal healthcare system.

Methods:
This retrospective cohort study included adults hospitalized with a principal diagnosis of heart failure at the 11 hospitals in The New York City Health and Hospitals Corporation in 2007-2010. Clinical data from electronic health records were linked to New York State hospital registry and vital statistics data. The primary exposure was hospital-reported ethnicity/race, which was categorized as Hispanic, non-Hispanic black, and non-Hispanic white; patients of other and unknown races were excluded. Outcomes were 30 and 90-day readmission and 30-day and one-year mortality. Logistic regression models were used to test for association between ethnicity/race and outcomes with adjustment for demographics, comorbidities, lab results, and vital signs.

Results:
Among 9,059 hospitalizations for heart failure (mean age 67±15 years), 2,629 (29%) were for Hispanic patients, 4,785 (53%) were for black patients, and 1,645 (18%) were for white patients. Of these patients, 3,248 (36%) had Medicare, 2,512 (28%) had Medicaid, and 1,489 (16%) had no insurance.

The one-year mortality rate was 24% (625 of 2,629) for Hispanics, 20% (964 of 4,785) for blacks, and 33% (541 of 1,645) for whites. Even after risk-adjustment, Hispanics and blacks had lower one-year mortality than whites, with adjusted odds ratios (aORs) of 0.78 (95% CI 0.67-0.91) and 0.78 (95% CI 0.68-0.90). Hispanics, but not blacks, had lower 30-day mortality compared to whites with aORs of 0.68 (95% CI 0.48-0.97) and 0.76 (95% CI 0.55-1.06).
Hispanics had higher rates of 30-day readmission than whites (aOR 1.25; 95% CI 1.09-1.44), but there was no difference between blacks and whites, (aOR 0.99; 95% CI 0.87-1.13). At 90 days, both Hispanics and blacks were more likely to be readmitted than whites with aORs of 1.39 (95% CI 1.22-1.59) and 1.13 (95% CI 1.00-1.29), respectively.

Conclusions:
Racial and ethnic disparities in outcomes after heart failure hospitalization comparable to prior reports were present within a large municipal healthcare system. Although outcomes were similar for black and white patients for 30 days post-discharge, during longer-term follow-up, black patients had higher readmission rates and lower mortality rates than white patients. Hispanic patients had higher readmission rates and lower mortality rates compared to white patients during all intervals studied. Further research is needed to identify causes for these disparities.
Abstract 168: Impact of Continuing Medical Education on the Treatment of Hypertriglyceridemia with Omega-3 Fatty Acids
Authors: Larkin Amy , LaCouture Michael , Boutsalis George , Bays Harold 
Published: July 2021

Introduction:
The less prominent role of triglycerides in determining cardiovascular risk keeps these lipids from being top-of-mind for practicing clinicians, yet epidemiologic data affirm that hypertriglyceridemia contributes to atherosclerotic disease development and progression. We sought to determine if online continuing medical education (CME) could improve the clinical knowledge and competence of primary care physicians (PCPs) and cardiologists regarding hypertriglyceridemia and the use of omega-3 fatty acids in its treatment.

Methods:
The effects of two educational interventions about advances in hypertriglyceridemia treatment (activity 1) and educating patients about omega-3 fatty acid products (activity 2) were analyzed to determine efficacy of online education presented in the form of online video-based roundtable discussions. The activities launched online in May and June, 2015 respectively, and data were collected through July, 2015. The effects of education were assessed using knowledge- and case-based matched pre-assessment/post-assessments. The effect sizes were calculated with Cohen’s d (> 0.8 is large, 0.8-0.4 is medium, and < 0.4 is small).

Results:
In total, 842 PCPs and 75 cardiologists who completed all pre/post assessment questions in any of the two activities during the study period were included in analyses. Significant overall improvements were seen for PCPs (activity 1: n = 452,
P
<.05, effect d= 0.68; activity 2: n = 390,
P
<.05, effect d= 0.96) and cardiologists (activity 1: n = 35,
P
<.05, effect d= 0.77; activity 2: n = 40,
P
<.05, effect d= 0.9). Compared with baseline, specific areas of improvements include:

• 22% more PCPs and 31% more cardiologists identified weight loss as a nonpharmacological intervention that can effectively lower triglyceride levels for overweight/obese patients with hypertriglyceridemia, (both
P
< .05)

• 35% more PCPs and 32% more cardiologists identified the appropriate dosing of prescription omega-3 fatty acids (both
P
<.05)

• 23% more PCPs (
P
< .05) and 20% more cardiologists (
P
=.068 ) recognized that reducing the risk for pancreatitis is a primary medical objective in patients with severe elevations in triglyceride levels Areas identified as needing additional education include:

• 57% of all physicians remain unaware that omega-3 fatty acids reduce apolipoprotein C3
• 61% of PCPs and 60% of cardiologists did not demonstrate a thorough understanding of the differences between prescription omega-3 fatty acids and omega-3 supplements

Conclusion:
This study demonstrates the success of a targeted educational intervention with two educational components on improving knowledge, competence, and clinical decision-making of PCPs and cardiologists regarding hypertriglyceridemia treatment and the role of omega-3 fatty acid products in its treatment.
Abstract 2: Comparative Effectiveness and Safety of Anticoagulant Therapy With Warfarin, Dabigatran, Apixaban, or Rivaroxaban in Patients With Nonvalvular Atrial Fibrillation
Authors: Adeboyeje Gboyega , Sylwestrzak Gosia , White Jeff , Rosenberg Alan , Abarca Jacob , Crawford Geoffrey , Barron John 
Published: July 2021

Background:
The efficacy and safety of novel oral anticoagulants (NOACs) as alternatives to warfarin therapy in nonvalvular atrial fibrillation (NVAF) patients have been studied in randomized trials. Given the increasing use of NOACs, additional data is required to assess the relative effectiveness and safety of anticoagulation with warfarin, dabigatran, apixaban, or rivaroxaban therapy in real-world settings in the United States (U.S).

Methods:
A retrospective cohort study design was used to analyze data from a U.S. commercial claims database of > 38 million members. Study population included new users of warfarin, dabigatran, apixaban, or rivaroxaban aged ≥ 18 years with ≥ 2 diagnoses of NVAF from November 2010 to February 2015. The primary effectiveness outcome was a composite of thromboembolic event or stroke; the primary safety outcome was major bleeding event requiring hospitalization. Cox proportional hazards models with inverse probability of treatment weighting (IPTW) were used to compare event rates between NOAC and warfarin users, and among NOAC users.

Results:
In the final NVAF cohort studied, there were 23,431 warfarin, 8,539 dabigatran, 3,689 apixaban, and 8,398 rivaroxaban users. A total of 7,022 primary outcome events and 3,264 safety events were identified. Warfarin users were older than dabigatran, apixaban, or rivaroxaban users (mean: 73 vs 66 vs 69 vs 67 years). After IPTW, all treatment groups were balanced on all baseline risk factors including stroke and bleeding risk.

Compared to warfarin, NOAC users had fewer thromboembolic events or strokes: dabigatran (hazard ratio HR, 0.77 [95% CI: 0.72 - 0.82]), apixaban (HR, 0.73 [CI: 0.65 - 0.82]), and rivaroxaban (HR, 0.80 [CI: 0.75 - 0.86]). Additionally, dabigatran ([HR], 0.67 [CI: 0.60 - 0.76]), and apixaban users (HR, 0.52 [CI: 0.41 - 0.67) experienced fewer major bleeding events compared to warfarin users. No significant difference was found in major bleeding risk between rivaroxaban (HR, 1.00 [CI: 0.89 - 1.12]) and warfarin users.
All three NOAC groups had similar risks for thromboembolic event or stroke: dabigatran vs rivaroxaban (HR, 0.96 [CI: 0.88 - 1.05]); apixaban vs rivaroxaban (HR, 0.91 [CI: 0.80 - 1.04]); dabigatran vs apixaban (HR, 1.05 [CI: 0.93 - 1.19]). However, compared to rivaroxaban users, major bleeding risk was 33% and 48% lower in dabigatran and apixaban users respectively (HR, 0.67[CI: 0.58 - 0.78]) and HR, 0.52 [CI: 0.40 - 0.68]).

Conclusions:
Our results demonstrated a lower risk of a thromboembolic event or stroke among dabigatran, apixaban, or rivaroxaban users compared to warfarin users. Among NOACs, risks of a thromboembolic event or stroke were similar. Further studies are needed to clarify the finding of a higher major bleeding risk in warfarin and rivaroxaban users.
Abstract 184: Novel Vasoactive Intestinal Peptide-ELP Fusion Protein VPAC-Agonists Trigger Sustained Pulmonary Artery Vaso-Relaxation in Rats with Acute Hypoxia-Induced Pulmonary Hypertension
Authors: Yeh Steve T , Youngblood Bradley L , Georgopoulos Lynne , Arnold Sue , Hamlin Robert L , del Rio Carlos L 
Published: July 2021

The natural vasoactive intestinal peptide (VIP) triggers potent pulmonary vasodilatation by activating the G-protein-coupled VAPC receptors, and has been suggested as a therapeutic target in pulmonary artery hypertension (PAH); however, VIP’s clinical utility is limited due to its short half-life. A novel ELP fusion technology (PhaseBio’s) permits the creation of long-acting protein-fusion biopolymer-based VPAC-receptor agonists. Here, the pulmonary/systemic hemodynamic effects of two novel ELP-enhanced VIP analogues (ELP-VIP) were evaluated in anesthetized rats with hypoxia-induced PAH.
Sprague-Dawley rats (259 ± 5 g, n = 25) were anesthetized (propofol), intubated, mechanically-ventilated (95% FiO2), and instrumented for systemic (arterial) and mean pulmonary-artery pressure monitoring. Following instrumentation PAH was induced by acutely decreasing the inspired FiO2 (to ∼10-11%). Subsequently, the animals were assigned to receive either a novel VPAC agonist (VIP-ELP, n = 18: 3-6 mg/kg) or placebo (VEH, n = 11: 0.9% NaCl). Treatments were delivered as acute single-dose boluses given either intravenously (IV) or intratracheally (IT) at a fixed volume.
Reductions in the inspired FiO2 resulted in sustained pulmonary artery pressure increases (+45 ± 3%, 28 ± 1 to 41 ± 1 mmHg; P < 0.05), consistent with hypoxic PAH. Induced-PAH was preserved in the absence of active treatment, as pulmonary pressures remained elevated following placebo administration (VEH: -1 ± 2%, from 40 ± 2 to 40 ± 2 mmHg; n = 11, N.S.). Acute administration of the VIP-ELP analogues resulted in rapid pulmonary artery pressure reductions (-24 ± 3%, from 41 ± 1 to 31 ± 1 mmHg, P < 0.05) with moderate/negligible changes in systemic pressures (MAP: -12 ± 6%) and heart rate (-4 ± 3%). Notably, the pulmonary vaso-relaxation triggered by VIP-ELP agonists was sustained and independent of the route of administration (IV: -17 ± 4%, n = 8; IT: -28 ± 4%, n = 10).
The novel ELP-enhanced VIP analogues triggered rapid and sustained reductions in pulmonary-artery pressures in the setting of induced (hypoxic) pulmonary hypertension (PAH). These effects were independent of the route of administration, as both intravenous/intra-tracheal administrations were efficacious.
Abstract 603: Silencing Of PKG1 Gene Mimics Effect Of Aging And Sensitizes Vascular Smooth Muscle Cells To Pro-fibrotic Effect Of Cardiotonic Steroids
Authors: Fedorova Olga V , Shilova Victoria , Lakatta Edward G , Bagrov Alexei Y 
Published: July 2021

Marinobufagenin (MBG), an endogenous Na/K-ATPase inhibitor and a vasoconstrictor, induces vascular fibrosis via PKC-dependent inhibition of Fli-1, a nuclear transcription factor and a negative regulator of collagen synthesis. In vascular smooth muscle cells (VSMC), ANP, via cGMP/PKG1 dependent mechanism, reduces sensitivity of Na/K-ATPase to MBG. Because vascular fibrosis is a hallmark of cardiovascular aging, we hypothesized that VSMC from aged rats, in which cGMP/PKG-dependent signaling is down-regulated, would exhibit heightened sensitivity to the pro-fibrotic effect of MBG.
In primary culture of VSMC from thoracic aorta from young (3 month old) rats, 1 nmol/L MBG inhibited Na/K-ATPase by 15%, and induced a 60% down-regulation of Fli-1 and a concomitant 50% increase in the levels of collagen-1. Alpha-ANP (1 nmol/L) blocked these effects.
In VSMC from aged (24 months old) rats levels of PKG1 and Fli-1 in VSMC were markedly reduced, while PDE-5 was markedly upregulated. MBG (1 nmol/L) inhibited Na/K-ATPase by 26%, suppressed Fli-1 two-fold, and increased level of collagen-1 more than two-fold (P<0.01). Unlike that in young rats, alpha-ANP failed to oppose these effects of MBG in aged animals.
Silencing of the PKG1 gene in VSMC from young rats produced a marked increase in the sensitivity of VSMC to the pro-fibrotic effect of MBG; 1 nmol/L MBG increased levels of collagen-1 2.5-fold (P<0.01).
These results demonstrate that age-associated reduction in vascular PKG1 levels and resultant decline in cGMP signaling sensitize VSMC to pro-fibrotic effect of MBG. Silencing of PKG1 in VSMC from young rats mimics these effects of aging.
Abstract 665: Endothelial Nitric Oxide Negatively Modulates Phenylephrine-induced Contraction In Matrix Metalloproteinase 2 (mmp-2)-filled Rabbit Aortic Rings
Authors: Prado Alejandro F , Pernomian Laena , Bendhack Lusiane M , Gerlach Raquel F 
Published: July 2021

Endothelial nitric oxide negatively modulates Phenylephrine-induced contraction in Matrix metalloproteinase 2 (MMP-2)-filled rabbit aortic rings
The present study aimed to evaluate the vascular function of aortic rings after intraluminal injection of matrix metalloproteinase 2 (MMP-2) and contribution of endothelial nitric oxide (NO) in this response.

METHODS:
thoracic aorta isolated from
New Zealand
rabbits (3.0 Kg) was isolated and were performed in situ gelatinolytic assay (intraluminal exposure with Krebs solution or MMP-2 1.2 μg/mL, at 37° C for 30 minutes, with measure of fluorescence intensity - FI) or vascular reactivity. Cumulative concentration-effect curves for phenylephrine (PE, 0.1 nM - 10 μM/L) were performed in endothelium-intact (E+) or denuded (E-) aortic rings, in the absence or presence of L-NAME (non-selective inhibitor of NOS, 100 μM) or Hydroxycobalamine (scavenger of intracellular NO), 30 min before the PE curves on E+ rings. The vascular contraction was normalized by grams of tension by dry tissue (g/g) and were analyzed the agonist maximum effect (Emax) and potency (pD2). Data represent mean ± S.E.M and the results were statistically analyzed using Student t test, one-way or two-way ANOVA with Bonferroni pos-hoc (p<0,05).

Results:
In situ
gelatinolytic activity was increased in the vessels filled with MMP-2 (19.19+0.93U,n=5) compared to vehicle (10.75+0.45U,n=5). In the vascular reactivity, E- aortic rings filled with MMP-2 increased Emax of PE (1893,28+122,40g/g,n=9) versus vehicle E- (1485.73+76.82g/g,n=9), but no differences were observed on Emax of E+ aortic rings (vehicle: 1416.13+120.87g/g,n=7; MMP-2: 1893.28+122.40g/g,n=9). The presence of L-NAME induced an increase in Emax of E+ aortic rings filled with vehicle (1817.60+76.37g/g,n=7) or MMP-2 (2340.50+130.43g/g,n=5). Hydroxycobalamine also increased the Emax of E+ aortic rings with vehicle (1889,81+129,17,n=6) or MMP-2 (2480,12+192,57,n=5). No difference of pD2 value was observed in this study.

Conclusion:
Data suggest this protease cross the aorta layers from the lumen. An increased vasoconstriction in E- vessels suggests a vascular smooth muscle activity of MMP-2. In the presence of L-NAME and Hydroxycobalamine, vessels filled with MMP-2 shows a greater maximum effect suggesting that NO exerts a negative modulation of the PE-induced vasoconstriction on MMP-2 aortic rings.
Abstract 258: Azilsartan Ameliorates Hypertension and Kidney Damage in Zucker Diabetic Fatty (ZDF) Rat
Authors: Khan Md Abdul H , Haines Jasmine , Imig John D 
Published: July 2021

Azilsartan, an angiotensin II receptor blocker, demonstrated anti-hypertensive and organ protective effects in hypertension. We investigated if azilsartan can be utilized in ameliorating kidney damage associated with cardiometabolic syndrome using Zucker Diabetic Fatty (ZDF) rats. Two groups of 6-8 week-old male ZDF rats were treated with vehicle or azilsartan (10 mg/kg/d, p.o.) for 8 weeks. A set of male Zucker Diabetic Lean (ZDL) rats were used as the control group. At the end of the treatment period, urine and plasma samples were collected for biochemical analysis while kidney tissues were collected for histopathological examination (n=6/group). ZDF rats were diabetic with fasting blood glucose levels averaging 287±45 mg/dL compared to 107±6 mg/dL in ZDL rats. Azilsartan treatment ameliorated hyperglycemia in ZDF rats (167±46 mg/dL). ZDF rats were also hypertensive compared to ZDL rats (181±4 vs 126±4 mmHg), and azilsartan treatment attenuated blood pressure in ZDF rats (109±4 mmHg). ZDF rats demonstrated marked renal damage compared to ZDL with elevated urinary excretion of albumin (ZDF vs ZDL, 92±47 vs 4±2 mg/d) and nephrin (842±364 vs 16±4 μg/d). ZDF rats also had 2-4-fold higher tubular cast formation and glomerular injury compared to ZDL rats. In ZDF rats, azilsartan treatment markedly reduced renal injury by attenuating elevated urinary albumin (7±2 mg/d) and nephrin (73±28 ug/d) along with a reduction in renal tubular cast formation and glomerular injury index. ZDF rats demonstrated increased inflammation and oxidative stress with elevated urinary monocyte chemoattaractant protein-1 (MCP-1) excretion (ZDF vs ZDL, 645±373 vs 319±76 ng/d) and kidney malondialdehyde (MDA) content (5±1 vs 10±1 μmol/mg). Azilsartan treatment reduced inflammation and oxidative stress in ZDF rats by reducing MCP-1 (335±80 ng/d) and kidney MDA content (6±1 ug/d). In summary, we demonstrate marked kidney protective, anti-inflammatory, and anti-oxidative effects of azilsartan in cardiometabolic syndrome ZDF rats.
Support provided by Takeda Pharmaceuticals Inc., USA
Abstract 302: Aerobic Exercise Effects on Endothelial Health Status in Pre- and Post Menopausal African American Women
Authors: Grimm Heather , Jan Kretzschmar Jan , Thakkar Sunny , Ling Chenyi , Diaz Keith M , Sturgeon Kathleen , Feairheller Deborah L , Perkins Amanda , Lee Hojun , Williamson Sheara , Babitt Dianne , Brown Michael D 
Published: July 2021

Background:
When compared to other racial groups, African American women (AAW) reach menopause at an earlier age and are at an increase risk for CVD and endothelial health complications. A known intervention for the treatment of both CVD and menopausal changes is aerobic exercise training (AEXT). The purpose of this study was to compare the effects of AEXT on endothelial function between pre- and post- menopausal AAW.

Methods:
Sedentary, non-smoking pre- and post- menopausal AAW not on hormone replacement therapy and free of CVD completed AEXT. Participants exercised at 65% of their VO2max for 40 min, 3 days/wk, for 6 months. Participants completed flow-mediated dilation (FMD) testing and blood sample collection. Endothelial microparticles from plasma samples were analyzed by labeling with late stage apoptotic antibodies CD31+/CD42b- and early phase endothelial dysfunction and endothelial activation CD62E+ and quantified using flow cytometry.

Results:
No difference in FMD was found between groups before (7.11±1.2 vs. 7.73±0.8 %) or after (10.38±0.2 vs. 9.88±0.6 %) AEXT. Both pre- (7.11±1.2 vs. 10.38±0.2 %, p≤0.005) and post- (7.73±0.8 vs. 9.88±0.6 %, p≤0.043) menopausal women significantly increased FMD after AEXT.

CD31+/CD42b- EMPs did not differ between pre- and post-menopausal AAW before (4.52±0.9 vs. 2.9±0.4 events/μL) or after (2.1±0.4 vs. 2.31±0.5e vents/μL) AEXT. CD31+/CD42b- levels significantly decreased in pre-menopausal AAW (4.52±0.9 vs. 2.1±0.4 events/μL, p≤0.015) after AEXT.
CD62E+ EMPS were not different between pre- and post-menopausal groups before (44±8.5 vs. 42.5±9 events/μL) or after (26.64±8.4 vs. 19.79±3.2 events/μL) AEXT. Both pre- (44±8.5 vs. 26.6±8.4 events/μL, p≤0.034) and post-menopausal (42.5±9 vs. 19.8±3.2 events/μL, p≤0.008) groups had lower levels of CD62E+ EMPs after AEXT.

Discussion:
No difference was found in terms of vascular function or health between pre- and post-menopausal AAW. Both groups showed improvements in vascular function and health after AEXT. Our findings suggest AEXT has significant improvements in terms of endothelial function and vascular health in AAW regardless of being a pre- or post-menopausal.