tbuckley/cabot-search huggingface dataset:
Abstract 4134754: Trends and Disparities in Mortality Due to Abdominal Aortic Aneurysm: Who Is at Risk?
Authors: Aman Goyal, Humza Saeed, Surabhi Maheshwari, Abdullah ., Amir Sohail, Mah I Kan Changez, GAURANGA MAHALWAR
Journal: Circulation (2024)

Background: Screening studies have reported a prevalence of 3-8% for abdominal aortic aneurysms (AAA). Despite a positive trend of decline over the past two decades, mortality linked to AAA remains a significant public health concern. In the United States alone, AAA complications resulted in an estimated 13,640 deaths between 2018 and 2021. Thus, understanding trends and disparities in AAA mortality is crucial for evaluating the effectiveness of current approaches and identifying vulnerable populations. Methods: This study analyzed death certificates from 1999 to 2020 within the CDC WONDER Database. Deaths among individuals aged 25 years and older caused by AAA were identified using the International Classification of Diseases, Tenth Revision (ICD-10) codes I71.3 and I71.4. Age-adjusted mortality rates (AAMRs) per 1,000,000 individuals and annual percent change (APC) were computed and categorized based on year, gender, race/ethnicity, and urbanization status. Results: Between 1999 and 2020, 195,117 deaths were reported in patients with AAA (both ruptured and non-ruptured). Overall, AAMRs for AAA significantly decreased from 69.0 deaths in 1999 to 27.9 deaths in 2020. This decline occurred in two phases: a steeper decrease from 1999 to 2014 (APC: -5.47; 95% CI: -5.68 to -5.29) followed by a further significant decrease from 2014 to 2020 (APC: -1.66; 95% CI: -2.46 to -0.57). Gender-based analysis revealed that men consistently had higher AAMRs than women (men: 65.6; 95% CI: 65.3 to 66.0; women: 24.5; 95% CI: 24.3 to 24.7). Similarly, AAMRs varied by race/ethnicity, with the highest rates observed among non-Hispanic Whites (45.6; 95% CI: 45.3 to 45.8), followed by non-Hispanic American Indian or Alaska Natives (30.3; 95% CI: 27.9 to 32.7), non-Hispanic African Americans (27.2; 95% CI: 26.7 to 27.8), non-Hispanic Asian or Pacific Islanders (20.7; 95% CI: 20.0 to 21.4), and Hispanics (17.5; 95% CI: 17.0 to 18.0). Additionally, individuals residing in non-metropolitan areas had significantly higher AAMRs than those in metropolitan areas (non-metropolitan: 50.7; 95% CI: 50.2 to 51.1; vs. metropolitan: 39.2; 95% CI: 39.0 to 39.4) (Figure 1). Conclusions: This analysis revealed a significant decline in mortality from AAA. However, disparities persist, with higher AAMRs observed among men, non-Hispanic Whites, and residents of non-metropolitan areas.
Abstract 4134641: Door-in to door-out time and in-hospital mortality in patients with ST-elevation myocardial infarction
Authors: Takahiro Nakashima, Eri Kiyoshige, Soshiro Ogata, James Cranford, Murtuza Ali, Ingrid Kindipan, Jacqueline Tamis-Holland, Kunihiro Nishimura, Abhinav Goyal, Robert Neumar
Journal: Circulation (2024)

Background: Although current guidelines recommend achieving a door-in to door-out (DIDO) time within 30 minutes for 75% of patients with ST-elevation myocardial infarction (STEMI) who require interhospital transfer for primary percutaneous coronary intervention (PCI), disparities between guidelines and clinical performance persist. Methods: We analyzed the association between the DIDO time and in-hospital mortality using data from the Get With The Guidelines® – Coronary Artery Disease STEMI and NSTEMI Registry covering 232,935 admissions between the fourth quarter of 2019 and the third quarter of 2022. We determined the cut-off value of the DIDO time at which the odds of in-hospital mortality markedly increased by a likelihood ratio (LR) and an area under the curve (AUC) derived by generalized linear regression. Results: Of the 103,838 patients with STEMI, 23,865 (23%) required interhospital transfer. The median DIDO time was 63 (interquartile range 43–105) minutes and was within 30 minutes in 9% of cases. Generalized linear mixed models showed that a DIDO time delay of 5 minutes was significantly associated with higher in-hospital mortality (adjusted odds ratio [OR], 1.88; 95% confidence interval [CI], 1.56–2.27; p&lt;0.001). The LR test and AUC showed that DIDO time cut-offs at 30, 42, 63, and 93 minutes were associated with increased in-hospital mortality. Compared with a reference DIDO time of within 30 minutes, the in-hospital mortality did not significantly differ for a DIDO time from 30 to 42 minutes (adjusted OR, 1.20; 95% CI, 0.83–1.73; p=0.340), but it was significantly higher for DIDO times from 42 to 63 minutes (adjusted OR, 1.48; 95% CI, 1.06–2.06; p=0.020), 63 to 93 minutes (adjusted OR, 1.89; 95% CI, 1.36–2.63; p&lt;0.001), and over 93 minutes (adjusted OR, 2.85; 95% CI, 2.08–3.90; p&lt;0.001). Conclusion: A delayed DIDO time was significantly associated with higher in-hospital mortality, particularly beyond 42 minutes.
Abstract 4134277: Impairment of Vascular Endothelial Function by Inhalation of Smoke or Aerosol from Tobacco and Marijuana Products is Dependent on Vagus Nerve Input from the Airway
Authors: Xiaoyin Wang, Christian Cheung, Natasha Goyal, chaitanya punnati, Shadi Abdelaal, Ronak Derakhshandeh, Matthew Springer
Journal: Circulation (2024)

Background: Smoke or vaporizer aerosol from different tobacco or marijuana products can cause vascular endothelial dysfunction in humans and rodents. Mechanisms of acute smoke-induced endothelial dysfunction are complex and remain ambiguous. We reported that endothelial functional impairment by tobacco smoke is dependent on intact vagus nerves, leading us to hypothesize that endothelial function impaired by smoke/aerosol from tobacco or marijuana relies on vagal input from the airway. Methods: We used Sprague-Dawley rats at 10-12 weeks of age (n=8/group; 4M+4F). Rats were anesthetized by ketamine/xylazine and exposed to one session of exposure to smoke/aerosol of tobacco (Marlboro Red) or marijuana (~10% THC) cigarettes, e-cigarettes (JUUL), or IQOS (American HeatSticks). Exposure was pulsatile (10 cycles of 5s 2x/min for 5 min via nosecone). Endothelial function was assessed as flow-mediated dilation (FMD) in the femoral artery pre- (baseline) and post-exposure. Surgical bilateral cervical vagotomy was performed in the anesthetized rats post-baseline FMD (before exposure). Sham surgical procedures were carried out without severing vagus nerves. We used paired Student t tests to compare FMD values in each group pre- and post-exposure. Significance was P &lt;.05. Results: FMD was decreased from pre- to post-exposure in all exposed sham groups as expected, whereas the impairment of FMD by smoke/aerosol exposure was completely abrogated in all vagotomized groups (Figure), with no apparent effect of sex. The pre- vs. post-exposure FMD values (mean±SD) in exposed sham groups were 16.0±3.0% vs. 6.7±3.1% for tobacco cigarettes, 13.1±2.3% vs. 5.0±2.3% for JUUL, 14.3±3.0% vs. 6.0±2.2% for IQOS, and 16.2±4.9% vs. 7.1±3.6% for marijuana. For exposed vagotomized groups, pre- vs. post-exposure FMD values were 13.3±3.7% vs. 12.6±3.7% for tobacco cigarettes, 12.8±2.6% vs. 13.0±3.2% for JUUL, 13.9±2.2% vs. 13.3±2.7% for IQOS, and 14.4±4.2% vs. 15.1±5.0% for marijuana. Heart rate was increased and respiratory rate was decreased in vagotomized groups as expected. Conclusions: Inhaling smoke or aerosol causes vascular endothelial impairment via a common mechanism involving vagal stimulation from the airway.
Abstract 4134778: Myocardial Recovery and Survival after Weaning of Left Ventricular Assist Device Therapy in Patients with Toxic and non-Toxic Cardiomyopathy, A Canadian Experience
Authors: Jean-Simon Lalancette, David Belzile, Alexandre Cinq-Mars, Sacha-Michelle Dubois-Senechal, Sylvain Lemay, Goran Rimac, Pierre Yves Turgeon, Joelle Morin, Christine Bourgault, Marie-Helene Leblanc, Celine Dupuis, Eric Charbonneau, Maxime Laflamme, mathieu bernier, Alexander Beaulieu-Shearer, Mario Senechal
Journal: Circulation (2024)

Left ventricular assist devices (LVAD) are increasingly used in refractory heart failure, mainly as a bridge to transplant or as destination therapy. LVAD unloading of the left ventricle (LV) can also promote myocardial recovery leading to improvement of the LV systolic function, allowing LVAD explantation. However, parameters associated with LVAD weaning and long-term outcomes are not well documented. The aim of this study was to assess the clinical and echocardiographic characteristics of weaned patients and to evaluate their event-free survival post-explantation. We conducted a single-center retrospective study recruiting patients who underwent a second or third generation LVAD implantation at a Canadian cardiology center between November 2009 and October 2021. A total of 98 patients underwent LVAD implantation during this period. All patients were on guideline-directed medical therapy (GDMT). Fourteen patients (14%) had significant LV recovery and were explanted/decommissioned after a median support time of 309 days (range 55-595 days). Toxic cardiomyopathy, defined as abuse of amphetamines (n=2), energy drinks (n=2) or multiple substances (n=6), was the most likely diagnosis in 10 of the weaned patients (71%). The LVEF was significantly higher and the left ventricular end-diastolic diameter (LVEDD) was significantly lower in weaned patients compared to unweaned patients after 3 months of support. Myocardial recovery manifested as pump thrombosis in 4 of the weaned patients (29%). Prior to explantation, 12 patients had a decrease in GDMT doses to minimize post explantation vasoplegia. After explantation, median follow-up time was 40 months (range 8-109 months) and the majority of patients were anticoagulated for 3 months. At last follow up, the LVEF was 44±6% and no patient had a LVEF below 35%. All patients were NYHA I or II and no death, heart transplant, or mechanical support initiation occurred. LVAD therapy can induce LV reverse remodeling leading to myocardial recovery in a significant proportion of patients, especially young patients with toxic and non-ischemic cardiomyopathies. Early reverse remodeling with decreasing LVEDD and improving LVEF at 3 months following implantation is associated with successful weaning. Pump thrombosis seems to be associated with LV reverse remodeling and weaning of mechanical support in certain patients. Weaned patients maintain satisfactory LVEF recovery after explantation and have good long-term event-free survival.
Abstract 4134267: Effects of GLP-1 Receptor Agonists and SGLT2 Inhibitors on In-Hospital Mortality and 30-Day Readmission in Type 2 Diabetic Patients with Acute Coronary Syndrome
Authors: Abraheim AL-Nasseri, Usman Kazi, Hunter Reed, Huy Ho, Aakash Patel, Nishant Nerella, Suman Pasupuleti
Journal: Circulation (2024)

Background: The effects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium–glucose cotransporter 2 inhibitors (SGLT2is) on reducing cardiovascular events in heart failure patients are well-established; however, less is known about their effects after a myocardial infarction. This study aims to investigate the effects of GLP-1RAs and SGLT2is on in-hospital mortality and 30-day readmission in type 2 diabetic patients with/without heart failure who were hospitalized for acute coronary syndrome (ACS). Methods: We conducted a multicenter retrospective cohort on type 2 diabetic patients who were admitted to the hospital for ACS from 01/01/2020 to 01/31/2024 across 16 West Florida hospitals. Patients receiving a GLP-1RA alone, SGLT2i alone, or both were compared to those taking neither. Chi-square and binary logistic regression were used to predict the clinical outcomes of in-hospital mortality, all-cause readmission within 30 days, and cardiac readmission within 30 days. Results: Among 7,481 type 2 diabetics with ACS, 392 (5.24%) were taking GLP-1RA monotherapy, 577 (7.71%) were taking SGLT2i monotherapy, 144 (1.92%) were taking both, and 6,362 (85.12%) were taking neither. The likelihood of in-hospital mortality was similar among patients on neither medication compared to patients on both (χ 2 = 0.06, p = 0.802), GLP-1RA monotherapy (χ 2 = 0.61, p = 0.435), and SGLT2i monotherapy (χ 2 = 0.002, p = 0.968). The odds of all-cause readmission within 30 days was similar among patients on neither medication compared to patients on both (χ 2 = 0.0004, p = 0.983), GLP-1RAs monotherapy (χ 2 = 0.07, p = 0.791), and SGLT2i monotherapy (χ 2 = 3.10, p = 0.078). The likelihood of cardiac readmission within 30 days was similar among patients on neither medication compared to patients on both medications (χ 2 = 1.63, p = 0.202), GLP-1RA monotherapy (χ 2 = 0.95, p = 0.329), and SGLT2i monotherapy (χ 2 = 0.94, p = 0.332). Conclusion: Our study found no significant differences in the odds of in-hospital mortality or 30-day readmission among type 2 diabetics with ACS who were taking GLP-1RAs, SGLT2is, or both, when compared to those taking neither. These findings further support the outcomes discovered in the EMPACT-MI trial.
Abstract 4134273: Low 5-hydroxytryptamine levels are associated with adverse outcomes in patients with heart failure with preserved ejection fraction
Authors: Ryo Ogawara, Tomofumi Misaka, Satoshi Okochi, Shohei Ichimura, Yu Sato, Tetsuro Yokokawa, Akihiko Sato, Takeshi Shimizu, Masayoshi Oikawa, Atsushi Kobayashi, Akiomi Yoshihisa, Yasuchika Takeishi
Journal: Circulation (2024)

Background: Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome and its pathophysiology is not fully understood. A monoamine, 5-hydroxytryptamine (5-HT), is involved in diverse biological functions and suggested to play a role in cardiovascular diseases. However, the clinical relevance of 5-HT in HFpEF remains unclear. Aims: This study aimed to elucidate the clinical significance and prognostic value of 5- HT in patients with HFpEF. Methods: We conducted a prospective study involving 240 consecutive hospitalized patients with HFpEF (mean age 72 years, 52% male). We measured circulating blood 5-HT levels using the enzyme-linked immunosorbent assay method. Clinical and outcome data were collected. Results: Correlation analysis revealed that 5-HT levels were negatively correlated with blood B-type natriuretic peptide concentration and tricuspid regurgitation pressure gradient. When patients were stratified into two groups based on the median 5-HT levels (90.5 ng/mL), Kaplan-Meier analysis showed that HFpEF patients with low blood 5-HT levels had lower event-free survival rates from the composite event of cardiac death and worsening heart failure over a median follow-up period of 725 days (Figure). In a multivariable Cox proportional hazard model adjusting for confounding variables, low levels of 5-HT were independently associated with increased risks of the composite of cardiac events (hazard ratio, 3.25; P &lt; 0.01). Conclusion: Low 5-HT levels are associated with adverse outcomes in patients with HFpEF and 5-HT may serve as a useful biomarker for predicting prognosis in such patients.
Abstract 4134340: Title: Comorbidities Associated with One Year Mortality and Hospital Readmission After Leadless Pacemaker Implantation
Authors: Peter Brodeur, Enrico Ferro, Timothy Maher, Shu Yang, Jonathan Waks, Patricia Tung, Eduardo Saad, Andre d'Avila, peter zimetbaum, Daniel Kramer, Robert Yeh, Andrew Locke
Journal: Circulation (2024)

Introduction: Previous studies have noted racial and ethnic disparities in access to leadless pacemaker implantation (LPI), but none have evaluated the socioeconomic disadvantaged (SED). Additionally, few studies have evaluated outcomes of LPI beyond thirty days on a large scale. This study aimed to determine which comorbidities are associated with one-year readmissions and mortality after LPI, including SED via the Social Deprivation Index (SDI). Methods: Patients ages ≥18 were identified in the Healthcare Cost and Utilization Project State Inpatient Databases in New York and Florida from 2016-2019 with follow-up into 2020. These states were chosen due to availability for linkage of the 2018 SDI (1-100, higher scores representing more disadvantage). International Classification of Diseases 10 codes for LPI were used. The risk of readmission and mortality was assessed using Cox proportional hazards first in an unadjusted fashion for each comorbidity in the Charlson Comorbidity Index. In addition to demographic variables, only significant variables from the unadjusted analysis were included in the final adjusted multivariable models. Results: 3,094 patients met inclusion criteria. The readmission and mortality rates at one, three, and twelve months were 17.2%, 31.3%, 50.2% and 5.7%, 7.1%, 10.7%, respectively. The most common diagnoses for readmission were dyspnea/chest pain (9.4%), heart failure (4%), and sepsis (3.8%). Federal insurance, heart failure (CHF), pulmonary disease, diabetes without complications, and renal disease (CKD) were associated with increased risk for twelve-month readmissions. African American race, myocardial infarction, CHF, CKD, and higher SDI were associated with increased risk for twelve-month mortality. Conclusion: CHF and CKD put patients at high risk of readmission and mortality. Sepsis was among the most common causes of readmission at twelve months. Patients of higher SED are at increased risk of mortality within one year after LPI.
Abstract 4132909: Hemodynamic Indices of Right Ventricular Function Differentially Predict Adverse Clinical Outcomes in Heart Failure with Preserved vs Reduced Ejection Fraction
Authors: Leah Kosyakovsky, Juhi Parekh, Emily Zern, Jenna McNeill, Eugene Pomerantsev, Michael Picard, David Dudzinski, Emily Lau, Jennifer Ho
Journal: Circulation (2024)

Background: While the critical role of right ventricular dysfunction (RVD) in heart failure (HF) is increasingly recognized, the prevalence and prognostic impact of RVD across HF subtypes is poorly understood. Research Questions/Aims: We aimed to characterize differences in hemodynamic indices of RV function among patients with HF with preserved vs reduced ejection fraction (HFpEF, EF≥50% vs HFrEF, EF&lt;50%) and to examine associations of RVD with longitudinal clinical outcomes by HF subtype. Methods: We identified patients with prevalent HF undergoing clinically indicated right heart catheterization at Massachusetts General Hospital (2005-2016). We examined three RV hemodynamic indices: right atrial to wedge pressure ratio (RA/PCWP), RV stroke work index (RVSWI), and pulmonary artery pulsatility index (PAPi). We used multivariable linear regression to assess differences in RV indices in HFpEF vs HFrEF. We then used Cox models to examine the association of each index with HF hospitalizations (HFH), major adverse cardiac events (MACE), and death, stratified by HF subtype. Models were adjusted for age, sex, BMI, hypertension, diabetes, lung disease, sleep apnea, and prior MI. Results: Of 2,062 patients (age 66 years, 33% women), 1,242 (60%) had HFrEF and 820 (40%) had HFpEF. RVD (RVSWI &lt;450 mm Hg*ml/m 2 ) was present in 27% of HFrEF vs 21% of HFpEF patients. Those with HFpEF had higher RA/PCWP (β 0.12, SE 0.05, p=0.012) and RVSWI (β 0.22, SE 0.05, p&lt;0.001) relative to HFrEF. Over 4.1 median years follow-up, 915 HFH, 1,066 MACE, and 1,116 death events occurred. Among those with HFrEF, lower PAPi was associated with greater risk of HFH (HR 0.84 (0.77, 0.92); p&lt;0.001) and MACE (HR 0.88 (0.81, 0.96); p=0.003), and higher RVSWI was associated with greater risk of death (HR 1.17, (1.07, 1.27); p&lt;0.001, Figure ). In contrast, in those with HFpEF, only higher RA/PCWP was associated with greater risk of death (HR 1.11 (1.00, 1.23); p=0.042). Conclusion: RVD occurs frequently in both HFrEF and HFpEF, and hemodynamic measures of RV function are associated with greater risk of MACE, death, and HFH. Importantly, the prognostic value of RV indices varied by HF subtype, highlighting key differences in the role of RVD in HFrEF vs HFpEF.
Abstract 4126304: A Cardiac Targeting Peptide Linked to miRNA106a Targets and Suppresses Genes Known to Cause Heart Failure: Reversing Heart Failure at the Source
Authors: Ming Lu, Claire Deng, Kaan Taskintuna, Gerard Ahern, Ray Yurko, Kazi Islam, Maliha Zahid, Ian Gallicano
Journal: Circulation (2024)

Background: About one in five adults at age 40 will develop heart failure (HF) during their lifetime. Risk factors for HF (e.g., hypertension, etc.) alter cardiomyocytes structure and function resulting in HF. At the cellular level, these changes consist of mis/over-expression of genes that regulate cardiac identity (e.g., CamK2d, PKC, etc). The current paradigm for treating HF is pharmacological intervention or surgery; however, with few exceptions, the condition worsens with time. We are proposing a paradigm-shift for treating HF from a drug-centric system to a molecular approach that would reverse hypertrophy and adverse remodeling. Methods: A cardiac targeting peptide (CTP) was generated and linked by disulfide bond to miRNA106a, which was then introduced into a HF mouse model to measure its ability to reverse multiple heart failure parameters. CTP-miRNA106a was also introduced into a human cardiac cell line, followed by multiple analyses including Western Blot, qPCR, FACS, immunofluorescence all used to identify mechanism(s) utilized by CTP-miRNA106a to reverse HF characteristics. Results: Bio-distribution studies showed CTP delivered its miRNA106a cargo specifically to the heart within 30 mins, followed by clearance of CTP from the heart to the kidneys and liver by 3-5hrs post systemic drug injection. MiRNA106a persisted in cardiomyocytes until day 7 (latest tested time-point). CTP-miRNA106a reversed Ang2/Iso induced hypertrophy in 90% of the experimental mice ( Fig1 ). We also identified two potential HF intracellular signaling mechanisms (PLCb1/PKC/IP3 and NfkB) targeted by CTP-miRNA106a that could benefit both types of HF, HFrEF and HFpEF. PLCβ1 is a direct target for miRNA106a while the Nfkb pathway is indirectly targeted by decreased Camk2d (an miRNA106a target) signaling to IκBα. NfkB activity is quelled by miRNA106a. Conclusions: Our approach utilizes the function of miRNA106a to downregulate genes involved in cardiac hypertrophy and inflammation through the PLCb1 and CamKIId/Nfkb pathways. Most importantly, using a CTP-miRNA106a, we show delivery of miRNA106a cargo is specific to cardiomyocytes both in vitro and in vivo and that once delivered, many HF parameters including hypertrophy are reversed.