bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract 14529: Management of Acute Myocardial Infarction in a Patient With a Left Ventricular Assist Device
Authors: Friede Kevin A , Blumer Vanessa , Tcheng James , Jones William , Patel Manesh R , Agarwal Richa
Published: November 2020

Introduction:
We present a case of an LVAD patient presenting with nonspecific symptoms found to have type I MI due to critical LAD stenosis.

Case Presentation:
A 65-year-old male patient with a HeartMate II LVAD as destination therapy for ischemic cardiomyopathy presented with chest pain and generalized malaise. Examination demonstrated euvolemia and no stigmata of infection or thromboembolism. Labs were notable for an INR of 1.4 and high-sensitivity troponin values of 792 and 886 ng/L (ULN, 53 ng/L). ECG showed old anterior and inferior infarct; echocardiography revealed an LVEF of 20% with mild RV dysfunction and an immobile aortic valve. Non-atherosclerosis-related causes of MI were initially explored: CT of the chest and abdomen did not show infection or PE, and LVAD interrogation did not show any abnormal power trends or flows. Coronary angiography showed a 99% ostial LAD lesion, clearly progressed compared to 3 years earlier (Figures 1A and 1B). PCI with a drug-eluting stent restored normal flow (Figure 1C) with prompt resolution of symptoms. The patient is doing well over 1 year after PCI.

Discussion:
Acute MI is uncommon in LVAD patients and may present differently from a traditional CAD population due to the impact of the device on myocardial wall stress and oxygen demand through direct and continuous LV unloading. Case series of PCI in durable LVAD patients generally identify right heart failure, VT, or embolized thrombus from an immobile aortic valve, rather than a type I MI, as the primary indication. There is a paucity of data regarding the best approach for anticoagulation and antiplatelet management in LVAD patients after PCI.

Conclusion:
Type I MI should be considered in the right clinical context in LVAD patients presenting with elevated cardiac biomarkers, recognizing the potential for reduced specificity of clinical and ECG data. Future study of the long-term outcomes and appropriate secondary management of LVAD patients undergoing PCI is needed.
Abstract 14548: Coronary and Aortic Calcification Are Common in Men With Recurrent Prostate Cancer Undergoing PET/CT Imaging
Authors: Som Avira , Shaikh Preet Ayoub , Lenihan Daniel , Zhang Kathleen W
Published: November 2020

Background:
Men who receive androgen deprivation therapy for prostate cancer may be at increased risk for cardiovascular events. Vascular calcification is predictive of coronary events in the general population. The prevalence of vascular calcification in men with prostate cancer is not known.

Methods:
211 consecutive patients who underwent 18F-fluciclovine positron emission tomography (PET) /computed tomography (CT) at Washington University School of Medicine for recurrent prostate cancer were retrospectively identified. Clinical, demographic, and cardiac biomarker data were obtained from the medical record. Coronary and aortic calcification were qualitatively assessed on non-gated CT scans using standardized scoring systems.

Results:
Among 211 men with recurrent prostate cancer, median age was 69 (IQR 64, 75) years. Cardiovascular comorbidities were common (70% hypertension, 65% hyperlipidemia, 20% diabetes mellitus, 47% current or former smoking). 21% carried a clinical diagnosis of coronary artery disease while 6% had peripheral vascular disease. On CT imaging, 147 patients (70%) had coronary artery calcification of whom 29 (20%) had severe calcification. Additionally, 189 patients (90%) had aortic calcification on CT imaging of whom 48 (25%) had severe thoracic aortic calcification and 109 (58%) had severe calcification at the aortoiliac bifurcation.

Conclusions:
Coronary and peripheral vascular calcification are common on PET/CT imaging in men with prostate cancer. Vascular calcification on CT imaging may have utility for cardiovascular risk stratification and guiding implementation of cardiovascular therapies in men receiving androgen deprivation therapy.
Abstract 14573: Association of Human Mesenchymal Stem Cell and Lodenafil in Hypoxia-induced Pulmonary Arterial Hypertension
Authors: Silva Grazielle F , Silva Marina , Da Silva Jaqueline S , Alencar Allan K , Montagnoli Tadeu , Rocha Bruna , Montes Guilherme C , Vasques Juliana , Pimentel-Coelho Pedro , Mendez-Otero Rosália , Zapata-Sudo Gisele
Published: November 2020

Introduction:
Right ventricle (RV) remodeling and vascular dysfunction are present in pulmonary arterial hypertension (PAH).

Hypothesis:
This work focuses on the benefits of the association of human umbilical cord mesenchymal stem cell (hMSC) with lodenafil, a PDE5 inhibitor, on PAH in rats.

Methods:
Experiments were in accordance with the Animal Care and Use Committee at the Federal University of Rio de Janeiro. PAH was induced in male Wistar rats by exposure to hypoxia (10% O
2
) during 3 weeks plus
i.p
. injection of an antagonist of VEGF receptor (SU5416; 20 mg/kg/week). Animals were randomly divided (n=6): PAH + vehicle; PAH + lodenafil (gavage, 10 mg/kg); PAH + lodenafil + hMSC (5x10
5
, i.v.) for 14 days.

Results:
PAH induced the reduction of the ratio of pulmonary acceleration time and RV ejection time from 0.42 ± 0.01 to 0.24 ± 0.01, which was recovered to 0.31 ± 0.01 after treatment with lodenafil + hMSC. RV afterload confirmed by increased systolic pressure (mmHg) of 52.1 ± 8.8 (contro: 24.0 ± 3.1) was normalized to 29.6 ± 2.2 with association. Pulmonary arteries wall thickness (%) measured by immunohistochemistry for alpha-SMA was increased by HAP from 44.7 ± 1.4 to 64.2 ± 1.2 and was partial (57.7 ± 1.4) or totally recovered (47.3 ± 0.9) after treatment with lodenafil and association, respectively. Increased RV collagen fraction (%) of 7.4 ± 1.2 was induced by HAP when compared to control group (1.9 ± 0.1) and although lodenafil did not alter this parameter (6.6 ± 0.9) its association with hMSC restored to 2.7 ± 0.4. Increased RV wall thickness (mm) observed in PAH (from 0.60 ± 0.02 to 1.05 ± 0.13) recovered to 0.58 ± 0.04 after treatment with association. ERK1/2 expression evaluated by western blot analysis recovered from 0.79 ± 0.07 to 0.12 ± 0.06, which reinforced the reduction of cellular proliferation by treatment with lodenafil + hMSC. RV expression of p38 mitogen associated protein kinase was measured by stained area quantification using immunohistochemistry (%) was also increased in PAH group (from 9.4 ± 2.5 to 31.4 ± 2.2,
p
< 0.05) and the association of lodenafil + hMSC reduced to 11.4 ± 3.4.

Conclusions:
Therapy of hMSC and lodenafil improved cardiac remodeling and vascular dysfunction in SuHx-PAH rats, representing an important approach for the future treatment of PAH.
Abstract 14574: Assessing Cardiovascular, Thrombotic and Bleeding Outcomes in Patients With Chronic Liver Disease Undergoing Left Ventricular Assist Device Implantation: Analysis of the National Inpatient Sample Database
Authors: Grant Jelani , Vincent Louis , Ebner Bertrand , Maning Jennifer , olarte neal , Olorunfemi Odunayo P , Khakoo Nidah , Aitcheson Gabriella , Colombo Rosario A , Chaparro Sandra V
Published: November 2020

Introduction:
Coagulopathy and hematologic abnormalities are major concerns in patients with chronic liver disease (CLD) and refractory heart failure which combined with the use of anticoagulation or anti-platelet therapy, may affect perioperative outcomes in patients undergoing left ventricular assist device (LVAD) implantation.

Methods:
The National Inpatient Sample Database was queried from 2012 to 2017 for relevant International Classification of Diseases (ICD)-9 and ICD-10 procedural and diagnostic codes. Baseline characteristics and in-hospital outcomes were compared in patients with chronic liver disease and those without, who underwent LVAD implantation.

Results:
A total of 23,435 patients underwent LVAD implantation, 2,200 patients with CLD and 20,755 patients without CLD. See Table 1 for baseline characteristics. All-cause inpatient mortality (14.8% vs. 11.1%, p<0.001), major bleeding (34.3% vs. 30.2%, p<0.001), transfusion of platelets (18.0% vs. 14.0%, p<0.001), and the occurrence of a subarachnoid hemorrhage (1.6% vs. 0.7%, p<0.001) were greater in patients with CLD. LVAD thrombosis (6.6% vs. 9.4%, p<0.001) and post-operative ischemic stroke (3.4% vs. 6.1%, p<0.001) occurred less in patients with CLD. Using a multivariate logistic regression model to adjust for confounding factors, revealed that CLD was predictive of increased mortality in patients undergoing LVAD implantation (odds ratio: 1.29, 95% confidence interval [CI]; 1.06 to 1.56, p=0.010).

Conclusions:
We demonstrated between 2012 to 2017, given the clinical paradox of pro- and anticoagulant risks in patients with CLD and advanced HF, LVAD implantation was associated with increased mortality, major bleeding with increased utilization of platelet products and yet increased thrombotic complications. Further studies are needed to evaluate both thrombotic and bleeding risks in this population, along with mitigating factors without compromising either outcome.
Abstract 14591: Persistent Racial Disparities in Risks of Readmission and Mortality After Percutaneous Coronary Intervention in the Contemporary Era: Insights From the Blue Cross Blue Shield of Michigan Cardiovascular Consortium
Authors: Spehar Stephanie , Seth Milan , Alaswad Khaldoon , Schreiber Theodore , Berman Aaron , Syrjamaki John , Ali Omar , Bader Yousef , Gurm Hitinder S , Sukul Devraj
Published: November 2020

Introduction:
Racial disparities in the management and outcomes following acute myocardial infarction are well-established. However, there remains conflicting data on whether such disparities exist between black and non-black patients (pts) after percutaneous coronary intervention (PCI) in contemporary practice.

Hypothesis:
We hypothesize that compared with non-black race, black race is associated with increased risks of post-PCI readmission and mortality.

Methods:
We linked clinical registry data from PCIs performed between 1/2013 and 3/2018 at 48 Michigan hospitals to Medicare Fee-for-service claims. Patient race as recorded in the registry was dichotomized as black and non-black. The date of death was obtained from the Medicare beneficiary file. We used a logistic regression model to estimate the odds of 90-day readmission and a Cox model to estimate the association between race and post-discharge mortality after adjusting for important clinical characteristics.

Results:
A total of 30,206 pts (10.0% black, 59.9% men) were included. Black pts tended to be younger (68.9 vs 72.2 yrs), were more likely to smoke (27.7% vs. 19.5%), and had a higher burden of cardiovascular comorbidities. Compared with non-black pts, black pts had an increased risk of 90-day readmission (26.5% vs. 18.2%; adjusted OR 1.34; 95% CI 1.22-1.47; p<0.001) and long-term mortality after PCI (HR 1.13; 95% CI 1.05-1.21; p=0.001) (Figure).

Conclusions:
Even after accounting for clinical comorbidities, in contemporary practice black pts are at an increased risk of readmission and long-term mortality after PCI discharge. Future studies investigating differences in care and social determinants of health are needed to elucidate the mechanisms behind these disparate outcomes and identify potential opportunities to reduce these dramatic and persistent health care disparities.
Abstract 14595: The Clinical Impact of Portal Vein Pulsatility on the Prognosis of Hospitalized Acute Heart Failure Patients
Authors: Kuwahara Naoya , Honjo Tomoyuki , Kaihotsu Kenji , Kamemura Kohei , Nakayama Kazuhiko , Onishi Hiroyuki , Imanishi Junichi , Kajiura Akane , Nagano Tomoyuki , Sone Naohiko , Iwahashi Masanori
Published: November 2020

Introduction:
Heart failure (HF) especially right-heart failure causes hepatic portal system congestion. The Portal vein (PV) pulsatility can be influenced by right atrial pressure (RAP). However, the association between PV pulsatility and the condition of HF remains unclear.

Hypothesis:
In this study, we aim to evaluate usefulness of PV pulsatility as a prognostic marker as well as a therapeutic indicator for hospitalized acute HF patients.

Methods:
We enrolled 54 patients with acute HF and 17 patients without HF served as controls. PV flow velocity was measured by ultrasonography at admission and discharge phase. PV pulsatility ratio (PVPR) was calculated by dividing minimal velocity by peak velocity. The primary endpoint for prognostic analysis was cardiac death and unexpected re-hospitalization for recurrent HF. The observation period was one year from first hospitalization for HF.

Results:
On admission, PVPR was significantly higher in controls compared to acute HF patients (0.91±0.08 vs. 0.71±0.04, p<0.01).PVPR did not change during the hospitalization in controls (admission 0.91±0.08 vs discharge 0.93±0.06, p=0.31). However, in acute HF patients, PVPR was significantly elevated after the improvement of HF (admission 0.71±0.04 vs discharge 0.82±0.02, p<0.05) due to the increase in minimal velocity (admission 12.6±4.5 cm/s vs. discharge 14.6±4.6 cm/sec, p<0.05), indicating the decrease in RAP. To elucidate the association between PVPR and primary endpoint, the patients were divided into three groups according to the tertile of PVPR at discharge (PVPR-Q1:0.92<PVPR<1, PVPR-Q2: 0.73<PVPR<0.92, PVPR-Q3:PVPR<0.73). Kaplan-Meier analysis found that the patients with higher PV pulsatility at discharge had significantly higher event rate among the groups (Figure).

Conclusions:
PVPR at discharge would reflect the condition of HF. It also can be a novel prognostic marker for hospitalized acute HF patients.
Abstract 14909: The Sweet Spot - Achieving Less Mitral Regurgitation at the Cost of Increasing Mitral Gradients Improves Short-term Outcomes in Percutaneous Mitral Valve Repair
Authors: Medranda Giorgio A , Brahmbhatt Kunal , Kokotos William , Donohue Daniel , Schwartz Richard K , Green Stephen
Published: November 2020

Background:
In the last year, percutaneous mitral valve repair (PMVR) using the MitraClip system (Evalve Inc., Menlo Park, California) has established itself as a proven treatment option for patients with inoperable mitral regurgitation (MR). However, reduction of MR usually comes at the expense of forward flow and mean mitral gradients (MMG). Finding the ideal balance of reduction of MR grade and acceptable MMG carries significant clinical implications. The purpose of this study was to compare short-term outcomes in patients with less than moderate MR but elevated MMG to patients with at least moderate MR.

Methods:
This was a retrospective, observational study from 2014-2019 of 128 patients who underwent PMVR at our institution. Patients were separated into cohorts depending on their post-PMVR MR grade and MMG. Cohort 1 included patients with the best possible result post-PMVR, less than moderate MR and a MMG <5mmHg. Cohort 2 included patients less than moderate MR but a MMG >5mmHg post-PMVR. Cohort 3 included patients with at least moderate MR post-PMVR. Our primary outcome of interest was a composite of inpatient death and 30-day readmission.

Results:
Cohort 1 included 30 patients who had less than moderate MR and a MMG <5mmHg post-PMVR. This cohort had the primary composite endpoint in 10.0% of patients. Cohort 2 included 33 patients who had less than moderate MR but a MMG >5mmHg. Cohort 3 included 65 patients who had more than moderate MR post-PMVR. We found that our primary composite endpoint occurred more frequently in patients who had at least moderate residual MR (cohort 3) (9.1% vs. 27.7%, p=0.0438). Patients with less than moderate MR post-PMVR despite a MMG >5mmHg were 3.8 times less likely to have inpatient death or a 30-day readmission when compared to patients with at least moderate MR post-PMVR (CI 0.071, 0.963).

Conclusions:
Our study suggests that achieving a goal of less than moderate MR despite modest increases in MMG can result in better short-term outcomes (inpatient death + 30-day readmission) when compared to patients who are left with at least moderate MR post-PMVR.
Abstract 14918: Mitral Valve Replacement With a Melody™ Valve Improves Survival for Young Children Compared to Mechanical Mitral Valve Replacement - A Case-Matched Control Study
Authors: Chetan Devin , Szabo Adrienn , Fan Steve , Morgan Conall , villemain olivier , Chaturvedi Rajiv , Benson Lee , Honjo Osami
Published: November 2020

Introduction:
Melody™ valve in the mitral position has been described for use in infants.

Hypothesis:
Melody™ valve (Medtronic) in the mitral position would improve survival compared to mechanical mitral valves for young children.

Methods:
Charts were retrospectively reviewed for children who had undergone a Melody™ valve insertion (MEL) between 2014 and 2020. MEL were case-matched by age and weight to those with a mechanical mitral valve (MECH). We compared transplant free survival and cumulative incidence of re-intervention. A sub-analysis was performed for children <1 year of age (8 MEL patients and their matches). Data are presented as median (interquartile range) or frequency (percentage).

Results:
Eleven children underwent Melody™ mitral valve replacement (MVR) over the study period. Age was 157 (104-402) days and weight 5.0 (4.2-7.4) kg. Indications for MVR were insufficiency in 6 (55%), stenosis in 3 (27%), and mixed disease in 2 (18%). MEL underwent a total of 13 repairs and 4 replacements (2 mechanical, 2 bioprosthetic) prior to Melody™ valve replacement. Final valve dilation size was 18 (15.5-18.5)mm. Two (18%) children salvaged from ECMO before MEL subsequently died. Three (33%) of the 9 survivors have required subsequent MVR at 9, 17, and 23 months; 1 for severe insufficiency, and 2 for severe mixed disease. The MECH cohort was not different in age, weight, valve size, bypass or cross-clamp times, indications for replacement, or number of prior repairs or replacements (p>0.10). At 1 and 3 years, transplant free survival (MEL: 80%, 80%; MECH: 82%, 64%; p=0.180) and re-intervention (MEL: 11%, 39%; MECH: 0%, 20% p=0.32) were equivalent between groups. For children <1 year of age, survival was higher in MEL (Figure; p=0.046) but rate of re-intervention remained equivalent (MEL: 17%, 34%; MECH: 0%, 29%; p=0.56).

Conclusions:
Melody™ MVR represents a better surgical strategy for infants less than 1 year of age requiring mitral valve replacement.
Abstract 14951: Maresin 1 Induces Cardiomyocyte Hypertrophy Through RORα/IGF-1/PI3K/Akt Pathway
Authors: Wahyuni Tri , Kobayashi Arisa , Tanaka Shota , Miyake Yoshiaki , Yamamoto Ayaha , Bahtiar Anton , Kotaro Matsumoto , Maeda Makiko , Obana Masanori , Fujio Yasushi
Published: November 2020

Myocardial inflammation is a critical event for the onset and progression of the heart failure. Maresin 1 (MaR1) was originally identified as a macrophage lipid mediator that exhibits anti-inflammatory and pro-resolving activities. Though it is widely accepted that macrophages positively and negatively regulate myocardial inflammation through cytokines and growth factors, the biological functions of lipid mediators, such as MaR1, in cardiomyocytes remain to be addressed. This study explored the functional roles of MaR1 in cardiomyocytes. Neonatal rat cardiomyocytes (NRCMs) were stimulated with MaR1 for 48 hours. Immunofluorescent staining with anti-sarcomeric α-actinin antibody revealed that MaR1 (50 nM) induced a significant increase in cardiomyocyte surface area (1760.34±66.86μm
2
vs. 960.83±29.46μm
2
). Quantitative RT-PCR analyses revealed that the treatment with MaR1 upregulated the expression of IGF-1 mRNA (2.9±0.6 folds), accompanied by the enhanced level of total and phosphorylated Akt. Interestingly, MaR1 did not influence the expression of BNP and skeletal actin significantly, suggesting that MaR1 induced physiological hypertrophy. Since MaR1 is a ligand of RORα, we examined the effects of RORα blockade (SR3335) and found that this compound inhibited the increase of cardiomyocyte surface area by abrogating MaR1-mediated activation of IGF-1/PI3K/Akt pathway. Importantly, treatment with wortmannin or NVP-AEW541, inhibitors for PI3K or IGF-1 receptor, respectively, suppressed MaR1-induced cardiomyocyte hypertrophy, indicating that IGF-1/PI3K/Akt pathway is essential for MaR1-induced hypertrophy. In conclusion, MaR1 is a novel lipid mediator that induces physiological cardiomyocyte hypertrophy by activating RORα/IGF-1/PI3K/Akt pathway. Thus, MaR1 could coordinate the resolving process and tissue recovery in myocardial inflammation.
Abstract 14996: Healthcare Resource Utilization and Costs in Congestive Heart Failure 90-day Episodes Within the Bundled Payment for Care Initiative (BPCI) Model 2, 2016-2018
Authors: Shen Xian , Sullivan Gabriel , Adelsberg Mark , Francis Martins , Schwartz Taylor T , Petrilla Allison A
Published: November 2020

Introduction:
Congestive heart failure (HF) is the fourth most commonly selected clinical episode among Model 2 participants of the Medicare Bundled Payments for Care Improvement (BPCI) Initiative. This study describes utilization of pharmacologic therapies, hospital readmission rates, and HF episode costs within the BPCI framework.

Methods:
The 100% sample of Medicare FFS enrollment/claims were used to identify acute hospital stays with a MS-DRG 291/292/293 between 1JAN2016 and 31DEC2018. A HF episode consisted of the initial hospital stay and all Part A & B covered services up to 90-days post-discharge. Prescription fills for angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), or angiotensin receptor-neprilysin inhibitors (ARNI) during the 90 days post-discharge were captured. Rates of all-cause and HF readmissions were reported per 10,000 episodes during the 30-, 60-, and 90-days post-discharge period. Total episode costs were defined as the sum of Medicare payments for the initial hospital stay plus all Part A & B covered medical services in the 90-day post-discharge.

Results:
The sample included 634,307 HF episodes. Patients received ARNIs in 3%, ACEIs/ARBs in 45%, and neither in 52% of the episodes, respectively. All-cause hospital readmission rates were 2,503, 4,465, and 6,368 per 10,000 episodes during the 30-, 60-, and 90-day periods. The 30-, 60-, and 90-day HF readmission rates were 958, 1,696, and 2,394 per 10,000 episodes. Total mean 90-day episode cost was $20,122, of which $8,002 was attributable to hospital readmissions.

Conclusions:
Hospital readmissions are frequent for HF patients and contribute a notable proportion of overall HF BPCI episode costs. BPCI participants may consider improving utilization of guideline directed medical therapies for HF, including ACEIs/ARBs and ARNI, as a strategy for reducing hospital readmissions and associated costs.
Abstract 15002: Socioeconomic Disparities Exist in Access to Accredited Pediatric Care Centers for Infants With Critical Congenital Heart Disease: A Total-Population Analysis Over 30 Years in California
Authors: Nuñez Gallegos Flora , Fernandes Susan M , Saynina Olga , Shin Andrew , Wise Paul , Chamberlain Lisa J
Published: November 2020

Introduction:
Current research endorses regionalizing the care of infants with critical congenital heart disease (CCHD) to facilities with high levels of obstetrical, neonatal, and surgical volumes. California has a regionalization model that designates these facilities as accredited pediatric cardiac centers (PCCs). The impact of this system on the location of birth and cardiac surgeries for CCHD and for different social groups remains unexplored.

Hypothesis:
We hypothesize, there has been a trend toward increased accredited PCC utilization for birth and surgical intervention for CCHD in California with accompanying widening in social inequality.

Methods:
A retrospective, population-based analysis of CCHD hospitalizations between 1984-2018 using the California Office of Statewide Health Planning and Development’s discharge database was conducted. Demographic data and trends in location of birth and surgical procedures for CCHD from delivery to age 1 were evaluated in relation to hospital designation as an accredited PCC.

Results:
There were 15,091 live births with CCHD and 29,466 surgical admissions meeting inclusion criteria. Births at accredited PCCs increased from 17% in 1984 to 41% in 2018 while surgical admissions were largely above 80%. From 2015-2018, infants with CCHD, born outside an accredited PCC were more likely to have private HMO insurance and live 6-20 miles away. Patients with surgical admission to an accredited PCC were more likely to have private HMO insurance and reside in a zip code where the median income is >2x the federal poverty level.

Conclusions:
Significant gains have been made in the regionalization of care for infants with CCHD in California over 30 years. However, a substantial number of infants with CCHD do not receive care in accredited PCCs and social disparities in utilization remain. Increased efforts to reduce barriers to access, particularly those related to payer type and resident distance from PCCs are needed.
Abstract 15061: Essential Hypertension is Linked to Acetylation of Mitochondrial Superoxide Dismutase and Deacetylation Mimetic Mutation of Lysine 68 to Arginine Protects From Oxidative Stress and Hypertension
Authors: Dikalova Anna , Tkachuk Liliya , Lopez Marcos G , Billings Frederic T , Dikalov Sergey
Published: November 2020

Almost one-half of adults have hypertension, and blood pressure is poorly controlled in a third of patients despite use of multiple drugs, likely due to mechanisms contributing to blood pressure elevation that are not affected by current treatments. Hypertension is linked to oxidative stress; however, common antioxidants are ineffective. We found that hypertension is associated with inactivation of key mitochondrial antioxidant, superoxide dismutase 2 (SOD2), due to acetylation of lysine residues at the catalytic center. The role of specific SOD2 lysine residues in hypertension, however, has not been defined.

Hypothesis:
We proposed that inactivation of key intrinsic antioxidant, SOD2, in hypertension is linked to acetylation of Lysine 68, and mutation of K68 to Arginine mimics SOD2 deacetylation, inhibits vascular oxidative stress and attenuates angiotensin II-induced hypertension. To test this hypothesis, we have investigated SOD2 acetylation in arterioles from patients with essential hypertension and developed a new deacetylation mimic SOD2 mutant K68R mice (SOD2-K68R). Western blot of arterioles isolated from human mediastinal fat showed 3-fold increase in SOD2 acetylation in hypertensive patients compared with normotensive subjects while SOD2 levels were not affected. To define the functional significance of K68 acetylation we performed studies in vivo in SOD2-K68R mice using angiotensin II model of vascular dysfunction and hypertension. Angiotensin II infusion in wild-type C57Bl/6J mice induced vascular inflammation and oxidative stress, and increased blood pressure to 160 mm Hg. Mutation of Lysine 68 to Arginine in SOD2-K68R mice completely prevented the increase in mitochondrial superoxide and significantly attenuated the angiotensin II induced hypertension (135 mm Hg). Angiotensin II and TNFα co-operatively induce SOD2 acetylation and hypertension. Treatment of wild-type aortas with angiotensin II and TNFα in organoid culture increased mitochondrial superoxide by 2-fold which was completely prevented in aortas isolated from SOD2-K68R mice.

Conclusions:
These data support an important role of SOD2-K68 acetylation in hypertension and targeting Sirt3-mediated deacetylation of SOD2 may have therapeutic potential.
Abstract 15085: Association Between Bone Mineral Density and Incident Heart Failure in a Biracial Cohort of Older Adults: The Health, Aging, and Body Composition Study
Authors: Gao Hans , Fohtung Raymond B , Patel Sheena , Xu Shuo , Cawthon Peggy M , Newman Anne B , Cauley Jane A , Carbone Laura , STEIN Phyllis K , Civitelli Roberto , Kizer Jorge R
Published: November 2020

Background:
Osteoporosis and heart failure (HF) are age-related disorders that share some pathogenetic features and may influence each other. Previous studies have suggested an association between bone mineral density (BMD) and HF risk, which may be race-dependent. We sought to further investigate race- and sex-specific associations of BMD with HF in a longitudinal study of older adults.

Methods:
We evaluated the relationship between BMD and HF in the Health, Aging, and Body Composition study, a sample of community-dwelling adults aged 70-79. BMD was measured by dual-energy X-ray absorptiometry (DXA) of the total hip and femoral neck, and in half the cohort by computed tomography of the spine. Analyses were stratified a priori by sex and race, and Cox models were used to estimate risk after adjustment for potential confounders.

Results:
Of 2835 participants, 572 (49% women, 42% black) developed HF during a median follow up of 12.2 years. Lower BMD of the total hip by DXA was associated with higher risk of HF in black women (adj. HR 1.84 [95% CI, 1.43 - 2.37] per SD decrement), with suggestion of lower risk in black men that was not significant (adj. HR 0.81 [0.64 - 1.02]). Corresponding analyses failed to reveal significant associations in white women (adj. HR 0.86 [0.71-1.04]) or white men (adj. HR 1.10 [0.93 - 1.30]). There were a significant interaction of total hip BMD by sex among blacks (p=0.002), but not whites (p=0.363), as well as by race among women (p=0.026) and men (p=0.049). Relationships of BMD of the femoral neck were similar in all groups. Likewise, lower volumetric BMD of the spine was associated with higher risk in black women (adj. HR 1.34 [1.02 - 1.77] per SD decrement), but there were no significant associations in black men (adj. HR 0.91 [0.78 - 1.18]), white women (adj. HR 0.83 [0.64 - 1.08]), or white men (adj. HR 1.17 [0.95 - 1.44]).

Conclusions:
Among a biracial cohort of older adults, lower BMD was associated with higher risk of HF in black women, with no clear evidence of an association in white women or in men of either race. Further research is needed to understand the factors that may account for the particular association in black women, and whether these can be leveraged for therapeutic intervention.
Abstract 15089: Specificity for Inflammatory Pathways and Myocardial Injury Associated With Coronary Microvascular Dysfunction in Rheumatoid Arthritis
Authors: Weber Brittany , He Zeling , Huang Sicong , Solomon Daniel H , Massarotti Elena , Golnik Charlotte , Seyok Thany , Brownmiller Seth , Martell Laurel , Barrett Leanne , Bibbo Courtney , Bolster Mary , Plutzky Jorge , DI CARLI Marcelo F , Liao Katherine P
Published: November 2020

Background:
Coronary microvascular disease (CMD) is associated with increased mortality in rheumatoid arthritis (RA). Studies suggest that higher RA disease activity is associated with a higher degree of CMD. However, it is not known whether specific inflammatory pathways implicated in RA play a stronger role than others in the pathogenesis of CMD. The objective of this study was to identify the associations between inflammatory cytokines, CMD, and resultant myocardial injury.

Methods:
We used baseline data from the first 53 subjects enrolled in a study of RA and CV risk (LiiRA, NCT02714881). LiiRA enrolls RA patients, age>35, prior to TNF inhibitor initiation. All subjects underwent a stress myocardial perfusion PET scan to quantify coronary flow reserve (CFR). CFR is the ratio of myocardial blood flow during maximal hyperemia over that at rest. A lower CFR in the absence of obstructive coronary artery disease (CAD) is indicative of CMD. We tested the association between markers of inflammation and myocardial injury with CFR using the Spearman correlation.

Results:
Clinical characteristics of LiiRA subjects are shown in Table 1. Baseline cardiac risk factors were uncommon. IL-6, sTNFR2, NT-proBNP were correlated with lower CFR. However, no significant associations were observed between IL-1β, hsCRP, or hs-cTnT (Table 2).

Conclusions:
Among RA patients with no history of overt CAD, the severity of CMD was correlated with IL-6 and sTNFR2 but not IL-1β or hsCRP. CMD was further associated with increased levels of NT-proBNP but not hs-cTnT. These findings provide potential insight into the mechanisms by which inflammation mediates CMD and resultant myocardial dysfunction.
Abstract 15094: In Patients on Warfarin, Does a History of Depression Impact Time in Therapeutic Range and Subsequent Dementia Risk?
Authors: Knight Stacey , May Heidi T , Woller Scott , Stevens Scott , McCubrey Raymond O , Bair Tami L , Anderson Jeffrey L , Muhlestein Joseph B , Bunch T Jared J
Published: November 2020

Objective:
Both time in therapeutic range (TTR) for anticoagulation and depression are associated with dementia risk. However, it is unknown if depression impacts TTR or their combined effect on dementia risk.

Methods:
We studied 14,953 patients who were chronically anticoagulated with warfarin (target INR 2-3) for atrial fibrillation (AF), venous thromboembolism (VTE), or a mechanical heart valve and managed by the Intermountain Healthcare Clinical Pharmacist Anticoagulation Service from 2003 to 2015. We excluded patients with a diagnosis of dementia before or within the first six months of warfarin management. TTR was evaluated as a continuous variable and by categories: ≤25%, 26-50%, 51-75%, and >75%. We examined the association of depression to TTR using finite mixture modeling and utilized multivariable Cox hazard regression to determine the association of TTR and depression to 3-year dementia incidence.

Results:
Forty percent (n=6055) of patients were diagnosed with depression while on warfarin therapy. Patients with depression were younger, female, taking warfarin for VTE, and had more comorbidities. They also had a lower TTR compared to patients without depression; after adjustment for baseline differences, depressed patients had an average TTR decrease of 4% (p<0.0001), and were 1.3 times more likely to have TTR <50% than non-depressed patients (p<0.0001). During follow-up, 4.83% of patients received the diagnosis of dementia within 3-years. The 3-year risk of dementia was highest for patients with a ≤50% TTR regardless of depression status (Figure). This rate was more than two times the rate of dementia compared to those without depression and with TTR>75%.

Conclusions:
In patients managed for warfarin, depression is very prevalent and is associated with significant decreases in TTR. TTR appears to be the significant driver for increased 3-year dementia risk in these patients. Examining ways to improve TTR for patients with depression is warranted.
Abstract 15423: Hope is Not a Plan: Re-engaging Transition-aged Young Adults With Congenital Heart Disease Actively Missing From Cardiac Care
Authors: Moore Judson A , Sheth Shreya , Lam Wilson W , Espaillat Andre , Alexander Alexander , Shabosky John , LOVICK DONNA , Broussard Nicole , Dyer Karla J , Lopez Keila N
Published: November 2020

Introduction:
Many studies describe gaps in care for youth with congenital heart disease (CHD), but few reach out to patients actively missing from care. Our study goal was to identify young adults with CHD actively missing from cardiac care to: 1) administer a needs assessment and 2) re-engage patients in cardiac care.

Methods:
We performed a retrospective review of outpatient medical records (2012-2019) for patients 15-21 yrs with CHD at Texas Children’s Hospital. ICD 9/10 codes identified CHD patients; those ≥1 year beyond requested clinic follow-up were defined as ‘actively missing’. Sociodemographic data was collected, and a telephone needs assessment conducted to determine CHD knowledge, barriers to care, and health status. Either a patient or parent completed the survey and was offered to re-engage in cardiac care. Descriptive statistics were performed on available data.

Results:
Of 1057 CHD patients, 33% (n=353) were actively missing. Of those missing, 58% were male and median age was 17 yrs (IQR 16-19). Patients were 46% Non-Hispanic White, 9% Non-Hispanic Black, and 33% Hispanic. Moderately complex CHD was noted in 71%. Insurance status was 63% private and 31% public. Ninety-eight patients/parents (28%) participated in our survey. Fifty-two percent reported having no cardiac care, often citing lack of or incompatible hospital insurance (33%; n = 32). Active cardiac symptoms were reported in 25%. Half of patients felt they could explain their cardiac condition well, and 82% could name their medications. Scheduling barriers (26%; n = 25) and being unaware adults could be cared for at our heart center (15%; n = 15) were the most common obstacles to re-engaging in care. Participants felt text messaging and scheduling visits during cardiology clinic would improve care access. More than half of patients/parents (55%) accepted our help to re-engage in cardiac care (scheduling assistance).

Conclusions:
This data suggests patients require assistance beyond CHD knowledge to stay in care. Problems with insurance, scheduling, and perceptions of adult CHD care were key barriers to maintaining cardiac care despite moderate CHD complexity and active symptoms. Future quality initiatives should include scheduling, insurance coverage, and adult CHD services.
Abstract 15430: Comparison of Ventricular Activation Time in Sinus and His Bundle Paced Beats
Authors: Jamal Shakeel , Bailey Beth , Mahmud Rehan
Published: November 2020

Introduction:
The relationship between conduction time of a sinus impulse and a paced impulse from His bundle to peak of left ventricular activation (HVAT) has not been systematically studied.

Hypothesis:
To perform a comparative analysis of HVAT of sinus and paced impulse in non-selective (NS) His bundle pacing (HBP) and selective (S)-HBP. Furthermore, to determine if pacing voltage and presence of His Purkinje system (HPS) disease affects HVAT.

Methods:
In 102 consecutive patients a comparative analysis of native HVAT and paced HVAT at higher (5-volt) and lower voltage (1-volt) was done in all patients and in groups subdivided into NS-HBP, S-HBP, with and without HPS disease.

Results:
Compared to sinus HVAT (105.9 ± 24.0 ms), paced HVAT was shorter at 5-volt (97.2 ± 17.9 ms) (
p<0.01
) and longer at 1-volt (
p<0.01
). This voltage effect was significant only in NS-HBP (-15.8 ± 15.7 ms,
p<0.01
) but not in selective-HBP (-6.2± 13.6 ms
p=0.16
). In NS-HBP, decrease in HVAT caused by 5-volt was the same in normal
vs
diseased HPS (-14.5 ± 12.8 vs-13.2 ±16.3 ms).

Conclusions:
1) Compared to sinus HVAT, NS-HBP HVAT is significantly shorter at 5-volt, however, tends to prolong at 1-volt.2) The 1-volt to 5-volt HVAT decrease appears to be similar both normal and diseased NS-HBP thus not related to correction of HPS delay. 3) The voltage related decrease in HVAT is significant in presence of pre-excitation wave seen in NS-HBP and is not significant in S-HBP.
Abstract 15439: Lesion Complexity and Long-term Outcomes According to Mean Observed Blood Pressure After Percutaneous Coronary Intervention
Authors: Park Jong Il , Kim Byung Jun , Kim Hun Tae , Lee Jung Hee , Kim Ung , Park Jong Seon
Published: November 2020

Background:
The guideline recommended strict blood pressure (BP) control for the patients treated with percutaneous coronary intervention (PCI). We aimed to evaluate the relationship between mean observed BP and long-term outcomes for patients with or without lesion complexity.

Methods:
A total of 1,470 patients who underwent PCI were investigated. We categorized the study population into four groups based on mean observed BP and lesion complexity (left main & three-vessel disease, chronic total occlusion, total stent length ≥60mm, or bifurcation two stenting): Group A (non-complex & systolic BP ≤120mmHg, n=310), Group B (non-complex & systolic BP >120mmHg, n=674), Group C (complex & systolic BP ≤120mmHg, n=131), and Group D (complex & systolic BP >120mmHg, n=355). We evaluated major adverse cardiovascular and cerebrovascular events (MACCEs), defined as cardiac death, myocardial infarction (MI), repeat target vessel revascularization, or stroke.

Results:
Well-controlled BP group (Group A&C) showed significantly lower systolic BP than uncontrolled BP group (Group B&D) (114.3±6.1mmHg vs. 130.7±7.6mmHg, p<0.001). MACCEs occurred less frequently in Group A (18.9%) than Group B (23.6%), Group C (22.7%), and Group D (33.6%) (p=0.001) at 8 years. After multivariate analysis, with Group A as a reference, the adjusted hazard ratio (HR) for MACCEs was 1.382 (95% confidence interval [CI] 0.978-1.954, p=0.067) for Group B, 1.559 (95% CI 0.957-2.540, p=0.075) for Group C, and 1.872 (95% CI 1.296-2.705, p=0.001) for Group D. In Cox regression model, although lesion complexity was not associated with MACCE, systolic BP≤120mmHg was an independent predictor for reduced rate of MACCE (HR 0.667, 95% CI 0.485-0.918, p=0.013).

Conclusions:
Mean observed systolic BP ≤120mmHg after PCI was independent predictor for reduced MACCEs regardless of lesion complexity.
Key Words:
Blood Pressure; Percutaneous Coronary Intervention; Lesion Complexity;

Treatment Outcome
Abstract 15444: Anticoagulation Treatment of Venous Thromboembolism Across the Weight Spectrum: Insights From the Veterans Health Administration
Authors: Perino Alexander C , Fan Jun , Kothari Mitra , MOHAMMAD ATIF , Hlavacek Patrick , Wygant Gail D , Schmitt Susan K , Pundi Krishna , Heidenreich Paul A , Guo Jennifer , Turakhia Mintu
Published: November 2020

Introduction:
In seminal trials of venous thromboembolism (VTE) treatment with direct oral anticoagulants (DOAC), few patients were enrolled at low and high body weights to estimate treatment effects in these subgroups. Consensus statements have recommended against use of DOACs in VTE for patients ≥120 kg. We sought to describe real-world use of DOACs and other anticoagulants for VTE across the weight spectrum.

Methods:
We performed a retrospective cohort study of patients with first-time VTE that were treated with anticoagulants in the VA health care system from 2008 to 2018. We excluded patients with 1) additional indications for anticoagulation (atrial fibrillation and mechanical valves) and 2) no documented weight in the 90 days prior to 90 days after index VTE. We stratified patients by weight (<60, 60 to 119, ≥120 kg) and determined 1) index anticoagulation prescription in the 30 days after index VTE (DOAC, warfarin, and low molecular weight heparin or fondaparinux [LMWH/F] only) and 2) variables associated with DOAC prescription, as compared to warfarin, in those ≥120 kg.

Results:
After excluding 3,676 patients with missing weight, there were 111,774 patients with VTE (64±13 years, 6% female). The most common therapy was warfarin (66%), followed by DOAC (21%), and LMWH/F only (13%). Median weight was 92 kg (interquartile range: 28), with 13,753 patients (12%) with weight ≥120 kg. Across weight categories, proportion of patients receiving DOAC was similar. In patients ≥120 kg, after multivariate adjustment, multiple comorbidities were associated with warfarin prescription while chronic kidney disease was associated with DOAC prescription (
Table
).

Conclusion:
Weight ≥120 kg is common for VTE patients, with DOAC frequently prescribed despite consensus statements recommending DOAC avoidance. For patients ≥120 kg, comorbidities influence VTE treatment selection, and determination of optimal treatment strategies across the spectrum of comorbidities is needed.
Abstract 15450: Colchicine Therapy in Patients With Coronary Artery Disease: A Systematic Review and Meta-analysis of Randomized Controlled Trials
Authors: Al-Abdouh Ahmad , Barbarawi mahmoud , Khan Safi U , Osman Mohammed , Upadhrasta Sireesha , Solipuram Vinod Kumar Reddy , Abusnina Waiel , Radaideh Qais , Zhao Di , Michos Erin D
Published: November 2020

Introduction:
Inflammation is a substantial mediator of atherosclerosis. Colchicine has anti-inflammatory effects and has been investigated in many randomized controlled trials (RCTs) in patients with coronary artery disease (CAD).

Methods:
We searched PubMed/MEDLINE, Cochrane library, and Embase databases (inception through February 28
th
, 2020) for RCTs evaluating colchicine in CAD patients. The outcomes of interest were major adverse cardiovascular events (MACE), myocardial infarction (MI), all-cause mortality, cardiovascular mortality, and stroke. Estimates were pooled using inverse variance random-effects model. We reported effect sizes as risk difference (RD) with 95% confidence interval (CI).

Results:
A total of 6 RCTs with 6,154 patients were included. The mean age ± SD for the patients in the colchicine group was 61.6±10.8 and control group was 61.5±10.7 years. At the median follow-up of 3.5 months, use of colchicine in patients with CAD was not associated with statistically significant reduction of MACE (RD -0.032; 95% CI, -0.083-0.018; p = 0.15; I
2
= 75%; low level of evidence) [
Figure
]; MI (RD -0.011; 95% CI, -0.030-0.007; p = 0.16; I
2
= 11.3%; low level of evidence); all-cause mortality (RD -0.001; 95% CI, -0.009-0.006; p = 0.65; I
2
= 0%; low level of evidence); cardiovascular mortality (RD -0.003; 95% CI, -0.010-0.004; p = 0.34; I
2
= 0%; low level of evidence); and stroke (RD -0.001, 95% CI, -0.005-0.004; p = 0.69; I
2
= 0%; very low level of evidence).

Conclusion:
This meta-analysis suggests that colchicine was not associated with a significant decrease in cardiovascular endpoints and mortality in patients with CAD.
Abstract 15455: Prevalence of Subclinical Myocardial Dysfunction in Hospitalized Patients With Covid-19 and Association With In-hospital Mortality
Authors: Minhas Anum , Gilotra Nisha A , Goerlich Erin , Garibaldi Brian T , Metkus Thomas S , Sharma Garima , Bavaro Nicole , Phillip Susan , Michos Erin D , Hays Allison G
Published: November 2020

Introduction:
Acute cardiac injury has been reported in COVID-19. However, the extent of subclinical myocardial dysfunction on imaging has not been characterized. We determined the prevalence of myocardial dysfunction using speckle tracking echocardiography (STE) in hospitalized COVID-19 patients and its association with cardiovascular risk factors and mortality.

Methods:
We retrospectively studied hospitalized COVID-19 patients undergoing echocardiography with STE (n=83). We investigated the association of global longitudinal strain (GLS) and myocardial work efficiency (MWE), a load independent measure of myocardial function, with clinical parameters. Logistic regression was used to examine associations of GLS and MWE with in-hospital mortality. Abnormal left ventricular ejection fraction (LVEF) was defined as <50%. Abnormal GLS and MWE were defined as >-18% and <95%, respectively.

Results:
Mean age was 66±14 years and 59% were men. There were 16/83 (19%) with reduced LVEF (<50%), while 64% (53/83) had abnormal GLS (>-18%) and 79% (59/75) had abnormal MWE (<95%) (
Figure
). Patients with abnormal GLS had higher body mass index (BMI) (32±8 vs 28±5 kg/m
2
, p=0.016) and more frequent diabetes (47 vs 23%, p=0.03) and patients with abnormal MWE had more frequent diabetes (49 vs 6%, p=0.002), compared to normal. Higher MWE was associated with lower mortality unadjusted (OR 0.92 [95% CI 0.85-0.99]; p=0.048) and after adjusting for age, sex, diabetes, hypertension, and coronary artery disease (OR 0.87 [95% CI 0.78-0.97]; p=0.014). This remained true on sensitivity analysis of only those with normal LVEF, adjusting for age and sex (n=61). GLS and LVEF were not associated with mortality.

Conclusions:
Abnormal myocardial function is prevalent in hospitalized COVID-19 patients undergoing STE. Higher MWE was associated with lower in-hospital mortality. Larger studies are warranted to determine the prognostic role of sensitive markers of LV function in COVID-19.