tbuckley/cabot-search huggingface dataset:
Abstract 4145543: ChatGPT-4 Improves Readability of Institutional Heart Failure Patient Education Materials
Authors: Ryan King, Jamil Samaan, Joseph Haquang, Vishnu Bharani, Roxana Ghashghaei
Journal: Circulation (2024)

Introduction: Heart failure consists of complex management involving lifestyle modifications such as daily weights, fluid and sodium restriction, and blood pressure monitoring placing additional responsibility on patients and caregivers. Successful adherence requires comprehensive counseling and understandable patient education materials (PEMs). Prior research has shown that many PEMs related to cardiovascular disease exceed the American Medical Association’s 5 th -6 th grade recommended reading level. The large language model (LLM) Chat Generative Pre-trained Transformer (ChatGPT) may be a useful adjunct resource for patients with heart failure to bridge this gap. Research Question: Can ChatGPT-4 improve heart failure institutional PEMs to meet the AMA’s recommended 5 th -6 th grade reading level while maintaining accuracy and comprehensiveness? Methods: There were 143 heart failure PEMs collected from the websites of the top 10 institutions listed on the 2022-2023 US News&amp;World Report for “Best Hospitals for Cardiology, Heart&amp;Vascular Surgery”. The PEMs of each institution were entered into ChatGPT-4 (Version updated 20 July 2023) preceded by the prompt “please explain the following in simpler terms”. The readability of the institutional PEM and ChatGPT prompted response were both assessed using Textstat library in Python and the Textstat readability package in R software. The accuracy and comprehensiveness of each response were also assessed by a board-certified cardiologist. Results: The average Flesch-Kincaid grade reading level was 10.3 (IQR: 7.9, 13.1) vs 7.3 (IQR: 6.1, 8.5) for institutional PEMs and ChatGPT responses (p&lt; 0.001), respectively. There were 13/143 (9.1%) institutional PEMs meeting a 6 th grade reading level which improved to 33/143 (23.1%) after prompting by ChatGPT-4. There was also a significant difference found for each readability metric assessed when comparing institutional PEMs with ChatGPT-4 responses (p&lt;0.001). While improving readability, ChatGPT-4 maintained accuracy and comprehensiveness with no responses graded as less accurate or less comprehensive and 33/143 (23.1%) deemed more comprehensive than institutional PEMs. Conclusion: ChatGPT-4 significantly improved the readability metrics of heart failure PEMs. The model may be a promising adjunct resource in addition to care provided by a licensed healthcare professional for patients with heart failure leading to improved health literacy and potentially improved outcomes.
Abstract 4146464: The Clinical and Electrocardiographic Phenotype of Genotype Negative Long QT Syndrome
Authors: Vanessa Karlinski Vizentin, Raquel Neves, Sahej Bains, Iuri Ferreira Felix, Johan Bos, David Tester, John Giudicessi, Michael Ackerman
Journal: Circulation (2024)

Background: LQTS is a genetic heart disease associated with an increased risk of sudden death. Despite advances in genetic testing, a small subset of patients still lacks identifiable genetic markers. Consequently, the true prevalence and clinical phenotype of genotype negative remains to be determined. Objective: To determine the prevalence and clinical characteristics of patients with a clinical diagnosis of LQTS but a negative genetic test. Methods: A retrospective review was conducted on patients evaluated and treated at a tertiary hospital between 2000 and 2024, focusing on those with a clinical diagnosis of LQTS, but a negative genetic test for all LQTS-associated genes, with available follow-up of at least 1 year. Results: After exclusion for follow-up and lack of genetic testing, the study cohort consisted of 1834 patients with LQTS including 1708 (93%) with a (likely) pathogenic (LP/P), LQTS-causative variant. Also, in 95 patients (5%), their variant of uncertain significance was clinically upgraded to a LP/P-variant, leaving only 31 patients classified as phenotype positive but genotype negative (1.6%). Of these, 16/31 underwent next-generation genetic sequencing, revealing the genetic cause in 6/16 cases (37%; 0.3% of all patients). For the remaining 25 genotype negative LQTS patients (1.3%), the mean age at diagnosis was 26 ± 15 years, with 19 (76%) being female, and an average initial QTc of 497 ± 41 ms. In total, 11 patients (44%) experienced a cardiac event before diagnosis [1 sudden cardiac arrest (SCA), 1 Torsades, 1 VT, 8 syncopes] and 1 patient had his first cardiac event during follow-up; 7/12 patients had more than one subsequent event. Twenty patients were proband (80%) and 6 had a family history of SCA. Eleven patients received an ICD (44%), left cardiac sympathetic denervation was performed in 4 (16%), and 2 patients experienced arrhythmia-related deaths (8%). The mean follow-up since diagnosis was 7 ± 5 years. Conclusion: With a prevalence of genotype-negative LQTS of 2%, the number of these patients is much lower than previously suggested, underscoring the advancements in identifying new genetic markers and the role of phenotype-enhanced variant adjudication and next-generation sequencing. Additionally, significant disease severity was observed in the remaining patients, emphasizing the pivotal role of genotype-phenotype correlations and risk stratification in managing and counseling patients lacking identified LQTS-causing mutations.
Abstract 4145538: Components of the Environmental Justice Index are Associated with Hypertension in Adolescents: Analysis of PEDSnet Data
Authors: Carissa Baker-Smith, Zugui Zhang, Bonita Falkner, Robert Akins
Journal: Circulation (2024)

Introduction: The Environmental Justice Index (EJI) uses data from the U.S. Census Bureau, the U.S. Environmental Protection Agency, and the U.S. Centers for Disease Control and Prevention to rank the cumulative impact of environmental injustice on health for every Census tract. Cross-sectional studies in adults identify an association between cumulative environmental burden and hypertension (HTN) in adults. The aim of this study is to examine the relationship between environmental injustice exposure, using the EJI, and HTN in youth. Hypothesis: Greater cumulative exposure to environmental toxins is significantly associated with HTN status in adolescents, adjusting for other demographic and socioeconomic factors. Methods: Using PEDSnet (a PCORI-funded aggregate of pediatric health data) data from 2009 to 2019 and geocoded EJI, we modeled the relationship between HTN and components of the EJI, adjusted for area deprivation index (ADI; scaled 1-100) terciles (ADI &lt; 25 = best/low, 25-52, &gt; 52 = worst/high); where ADI of 52 represents the upper quartile ADI for the state of Delaware. The HTN status of each youth, 13 to 17 years of age, was classified into three levels: Normal: SBP ≤ 120 + DBP &lt; 80; Elevated: SBP 120-129 + DBP &lt; 80; and HTN: SBP ≥ 130 or DBP ≥ 80. Multinomial logistic regression was used to analyze HTN status as the outcome and EJI index components and other covariables as predictors. Results: Among the 122,177 youth, 51% were female, 58% were non-Hispanic white, and 22% were non-Hispanic Black. Twenty-four percent lived in neighborhoods with ADI &lt; 25, and 35% lived in neighborhoods with ADI &gt; 52. Female sex and private/other insurance were associated with lower odds of HTN and elevated BP (ref= normal BP). Compared to ADI &lt; 25, ADI &gt; 52 was associated with 35% and 21% greater odds of having HTN or elevated BP, respectively. For each unit increase in the Air Toxins Respiratory Hazard Index, the odds of having HTN vs. normal BP was 2.83 times higher, and the odds of having elevated BP vs. normal BP was 1.81 times higher. For each unit increase in the Air Toxics Cancer Risk or Lead Paint Index, the odds of having HTN vs. normal BP was significantly higher (Table). Conclusions: Environmental toxin exposure is associated with greater odds of HTN in adolescents. Analysis of HTN and environmental injustice is an important step toward reducing HTN burden, beginning in youth.
Abstract 4146439: Predictors of Cardiovascular-Kidney-Metabolic (CKM) Syndrome Progression Among Atherosclerosis Risk in Communities (ARIC) Study Participants
Authors: Matthew Belanger, Bige Ozkan, Sui Zhang, Vijay Nambi, Janani Rangaswami, Justin Echouffo, Roger Blumenthal, Christie Ballantyne, Sadiya Khan, Joseph Coresh, Chiadi Ndumele
Journal: Circulation (2024)

Background: Progression along Cardiovascular-Kidney-Metabolic (CKM) stages confers greater cardiovascular disease (CVD) risk. However, the factors associated with CKM stage progression over time are not yet defined. Methods: We evaluated ARIC Visit 4 (1996-98) participants without CVD at Visit 1 (1987-89) and with available data to define CKM stages at both Visits 1 and 4. CKM stages were defined as: stage 0, no CKM risk factors; stage 1, excess/dysfunctional adiposity; stage 2, metabolic risk factors (hypertriglyceridemia, hypertension, metabolic syndrome, or diabetes) and/or moderate- to high-risk chronic kidney disease (CKD); stage 3, ≥20% predicted CVD risk per the PREVENT calculator or very high-risk CKD; and stage 4, clinical CVD. Among those in CKM stages 0-3 at Visit 1, we used logistic regression to concurrently assess the association of age, sex, race, area deprivation index (ADI, a measure of neighborhood deprivation), education, household income, physical activity (categorized as consistently ideal, intermediate, or consistently poor per AHA recommendations), and diet (per Life’s Essential 8 healthy diet score) with progression to a higher CKM stage from Visit 1 to Visit 4. Results: Among 8,376 participants, the mean age at Visit 1 was 55 years, with 52% female and 21% Black adults. Older individuals had higher odds of CKM progression (OR: 1.49 [95% CI 1.42-1.56] per 5-years of age), whereas females had lower odds (OR: 0.72 [0.64-0.80]) and Black race did not have an independent association ( Figure ). More adverse social determinants of health were associated with higher odds of CKM progression, including higher ADI (deciles 7-10 vs deciles 1-3 OR: 1.39 [1.23-1.57]), lower income (&lt;$12,000 vs ≥$50,000 OR: 1.40 [1.12-1.75]) and less education (grade school vs graduate school OR: 1.36 [1.10-1.67]). Higher physical activity levels were associated with lower odds of CKM progression (ideal vs poor OR: 0.82 [0.70-0.96]), while healthy diet score was not significantly associated with CKM stage progression. Conclusion: Several sociodemographic and behavioral factors are associated with CKM stage progression. This understanding can help to guide population strategies to preserve and improve CKM health.
Abstract 4146438: IgA-Deficiency Attenuates Angiotensin II-Induced Hypertension in Mice
Authors: Jasmeen Kaur Monga, Annie Zhou, Tao Wang, Abdul Momen, M. Ahsan Siraj, Mansoor Husain
Journal: Circulation (2024)

Background: Hypertension [HTN] has been associated with B cell-derived immunoglobulins, particularly IgA. In spontaneously hypertensive rat and humans, IgA has been implicated in HTN pathophysiology, but the mechanisms are not known. Here we explore effects of angiotensin-II [Ang-II]-induced HTN in IgA knockout [ -/- ] mice. Methods&amp;Results: Invasive hemodynamic assessments during anesthesia showed male 10-12 wk old IgA -/- mice to have lower baseline systolic blood pressure [SBP] vs. non -littermate IgA +/+ controls housed separately (86.8±2.1 vs. 104.0±2.7 mmHg; N=18-19/group; p&lt;0.0001). Metabolic studies revealed increased 24-h urine (0.082±0.003 vs. 0.055±0.003 mL/g body weight; N=22-23/group; p&lt;0.0001) and Na + (0.24±0.02 vs. 0.17±0.02 mg/d/g; N=11-12/group; p&lt;0.05) excretion as compared to non -littermate IgA +/+ controls. Next, male 10-12 wk old IgA -/- and IgA +/+ littermate controls received Ang-II (500 ng/kg/min) via osmotic minipumps for 28d. Surprisingly, IgA -/- and littermate IgA +/+ controls showed no differences in SBP in response to Ang-II (150±18 vs. 135±22 mmHg; N=5/group; p=0.75). As mice engage in coprophagy, allowing passive IgA transfer between co-housed littermates, we separately crossed IgA -/- and IgA +/+ females with IgA -/- and IgA +/+ males to yield separately housed IgA -/- and IgA +/+ offspring. In this setting, IgA -/- offspring showed blunted SBP response to Ang-II vs. IgA +/+ offspring (103±18 vs. 152±14 mmHg; N=5/group; p&lt;0.0001), demonstrating how passive IgA transfer via breastmilk or coprophagy permits Ang-II-induced HTN. Finally, we crossed IgA -/- females with heterozygous IgA +/- males and separated offspring by genotype at weaning. In this experiment as well, IgA -/- mice showed an attenuated SBP response to Ang-II vs . co-housed (until weaning) IgA +/+ littermates (106±22 vs. 137±27 mmHg; N=6-9/group; p&lt;0.05), indicating that IgA +/+ mice become hypertensive despite not receiving IgA from breast milk. Conclusion: IgA -/- mice exhibit reduced baseline SBP and increased 24-h Na + and water excretion as compared to separately housed IgA +/+ controls. Co-housing influences SBP responses in mice, likely due to passive IgA transfer. Separating animals by genotype at weaning confirmed loss of the SBP response to Ang-II in IgA -/- mice, highlighting the importance of IgA in Ang-II-induced HTN. Further studies are underway to understand if this effect is mediated by changes in mucosal immunity and microbiome.
Abstract 4146428: Molecular Imaging of Atherosclerotic Plaque Erosion Using Hyaluronan-Targeted Near-Infrared Fluorescence
Authors: Alessandro Maino, Khanh Ha, Yoshiko Iwamoto, Adam Mauskapf, Ashvita Ramesh, Jason McCarthy, Farouc Jaffer
Journal: Circulation (2024)

Introduction: Plaque erosion (PE) has a distinct pathogenesis, clinical presentation, and prognosis than other acute coronary syndrome (ACS) causes such as plaque rupture (PR). At present the ability to distinguish between PE and PR using in vivo imaging is limited. A critical feature of PE is the enrichment of hyaluronic acid (HA) at the luminal interface, which is poorly present in the other types of plaque. To better resolve mechanisms of ACS in vivo, we designed and investigated a new hyaluronan-targeted near-infrared fluorescence (NIRF) molecular imaging agent and tested the agent in vitro, in mouse PE in vivo, and in resected human carotid specimens. NIRF has emerged as a translational intravascular imaging modality that allows visualization of plaque pathobiology in vivo. Methods: The NIRF agent was generated via microwave-assisted solid phase peptide synthesis and was conjugated to the NIR fluorophore CyAl5 (ex/em 643/661 nm), to yield the hyaluronan-targeted NIRF agent (HAT-CyAl5). In vitro binding of HAT-CyAl5 to HA was assessed by fluorescence reflectance imaging (FRI). HAT-CyAl5 or a scramble control peptide-CyAl5 (scrambled-CyAl5) were intravenously injected in an established electrical injury-based mouse model of carotid artery PE; intravital microscopy (IVM, n=7) was performed in mice injected with HAT-CyAl5 (n=4) or scrambled-CyAl5 (n=3). Next, freshly resected human carotid specimens were incubated with HAT-CyAl5 (n=4) or PBS (n=4). Histological analyses then assessed specific binding of HAT-CyAl5 in murine PE and human atheroma. Results: The blood half-life of HAT-CyAl5 was 5.7 minutes (95% CI, 3.4-9.8min). In vitro HA binding analyses showed a significant higher target-to-background ratio (TBR) in the HAT-CyAl5 group (P &lt; 0.03 vs. Scrambled-CyAl5). In carotid PE undergoing IVM, HAT-CyAl5 double the TBR in vivo (4.7 ±1.36 vs. 2.38 ± 0.17 Scrambled-CyAl5, P&lt; 0.05). In human carotid plaques, HAT-CyAl5 markedly increased plaque NIRF signal (TBR post-incubation - pre-incubation 4.95 ±3.36 vs. 0.00 ± 0.15 PBS, P&lt; 0.03). Histology of human plaques showed that HAT-CyAl5 localized well with HA immunohistochemical expression. Conclusion: HAT-CyAl5 is a new NIRF probe that avidly and specifically binds HA in murine PE in vivo and in human plaques. HAT-CyAl5 coupled with intravascular NIRF imaging has the potential to specifically diagnose PE and provide new insights into the pathogenesis of PE.
Abstract 4146466: Targeting Gut Microbiota-Derived Kynurenine to Predict and Protect the Remodeling of the Pressure Overloaded Young Heart
Authors: Xiaomin He
Journal: Circulation (2024)

Background: Without timely intervention, pressure-overloading left ventricular (poLV) remodeling may become progressive and readily degenerate into heart failure. The relative risk is especially high in children with congenital heart disease who are awaiting surgical correction. Aims: The aims of this study were to identify a plasma metabolite that is clinically and mechanically linked to poLV remodeling and heart failure in children and investigate a safe, efficacious treatment that blocks its action. Methods: We used multi-omics including untargeted metabolomics on the plasma of poLV children and neonatal ascending aorta constriction (nAAC) mice, whole-transcriptome resequencing and single-nucleus RNA sequencing of mouse and human LV samples, and metagenomics analysis of mouse gut microbiota to disclose the gut microbiota-kynurenine (Kyn)-remodeling axis. Aryl hydrocarbon receptor (AHR) knockout mice and germ-free (GF) mice as well as fecal microbiota transplantation were used to clarify its mechanism. Results: Abnormally elevated plasma kynurenine (Kyn) was detected in both the patient cohort and the mouse model. Plasma Kyn levels were clinically associated with the cardiac functions and the degree of remodeling. Excessive Kyn induced the hypertrophy and fibrosis phenotypes both in vitro and in vivo, which was blocked by AHR inhibitors and by AHR knockout, respectively. It was demonstrated that Kyn affected both cardiomyocytes and cardiac fibroblasts by promoting AHR nuclear translocation, initiating ADAMTS2 transcription which accelerates hypertrophy, and inducing FN1 and COL1A1 which exacerbate fibrosis. There were significant alterations in the gut microbiota of nAAC mice.Transplantation of nAAC mouse feces to GF mice augmented their Kyn level, indicating the existence of a gut microbiota-Kyn relationship. Oral probiotic supplementation reconstructed the gut microbiota in the nAAC mice, modulated the Kyn-AHR axis, and alleviated poLV remodeling. Conclusions: Plasma Kyn levels were strongly correlated with cardiac remodeling and function in pediatric patients and mice with poLV. Kyn is a pathological signal from an altered gut microbiota to activates AHR and its gene targets in poLV remodeling heart, promoting hypertrophy and fibrosis in respective cells. Oral probiotics reshaped the gut microbiota, lowered Kyn levels, and showed great potential at delaying cardiac remodeling and preventing heart failure.
Abstract 4146264: A Meta-analysis of the Right Ventricle Changes in Cancer Therapy-Induced Cardiotoxicity - The Forgotten Ventricle in Cardio-Oncology
Authors: Caroline De Oliveira Fischer Bacca, RAMON HUNTERMANN, Rodrigo Gomes, Francisco Alexandrino, MARIANE YOSHIE SATO, Edielle de Sant Anna Melo
Journal: Circulation (2024)

Introduction: Cancer therapy-induced cardiotoxicity (CTRCD) is one of the most significant adverse effects of oncologic treatment, responsible for considerable morbidity and mortality. Heart failure stands out due to its higher frequency and severity with the focus of most studies being left ventricular dysfunction and remodeling. The right ventricle (RV) may also be damaged by CTRCD, however the effects on RV function have not been elucidated. Research Question: What are the echocardiographic changes in RV due chemotherapy treatment? Objective: To conduct a systematic review and meta-analysis evaluating the RV echocardiographic parameters in patients undergoing chemotherapy treatment. Methods: Pubmed, Embase and Cochrane were systematically searched for studies that assessed RV echocardiographic changes in patients due to chemotherapy treatment. Statistical analysis was performed using the R statistical environment, with a summary estimate using Mean Differences (MD), adopting a random-effects model to account for variability among studies and a two-tailed significance level of 5%. A correlation coefficient of 0.5 was assumed for the paired measurements. Heterogeneity was assessed using the I2 statistic. Results: We included 641 patients from 11 studies, 75.5% of whom were women and with a mean age of 50.2±6.1 years. RV function was significantly lower after cancer treatment, with reduction in the fractional area change (MD -3.53%; CI -5.25, -1.41; p&lt;0.0011 - Figure 1A), RV global longitudinal strain (MD 2.27%; CI 1.24, 3.29; p&lt;0.0011 - Figure 1B) and in RV free wall strain (MD 3.22%; CI 1.76, 4.67; p&lt;0.0001 - figure 1C). Additionally, the pulmonary artery systolic pressure was significantly higher (MD 1.36mmHg; CI 0.32, 2.4; p=0.01 - Figure 1D) and the tricuspid annular plane systolic excursion was significantly reduced (MD -1.98mm; CI -3.27, -0.68; p=0.0027 - Figure 1E) after chemotherapy. Conclusion: RV dysfunction is common in CTRCD and its echocardiographic quantification should be included in clinical practice follow-up during cancer treatment. Further research is needed to elucidate the underlying factors contributing to RV dysfunction in CTRCD and to develop methods for its early detection.
Abstract 4146268: Apolipoprotein A1 infusion in patients with Acute Myocardial Infarction: A Systematic Review and Meta-analysis of randomized trials
Authors: Alonzo Prata, Christian Fukunaga, Eric Katsuyama, Ana Carolina Coan, Pedro Gabriel Scardini, Rafael Petri Santos Pinheiro, Wilson Falco Neto, Julia Fernandes, Naieli Andrade, Luciana Gioli-Pereira
Journal: Circulation (2024)

Background: Low cholesterol efflux is associated with increased cardiovascular (CV) event risk. CSL112 is a reconstituted, infusible human plasma-derived apolipoprotein A-I that enhances cholesterol efflux, but its efficacy in reducing CV events is unclear. We aim to conduct a systematic review and meta-analysis comparing CSL112 infusions with placebo in acute myocardial infarction patients. Methods: We searched Cochrane, Embase and Pubmed databases for randomized controlled trials (RCT). The outcomes of interest were: (1) all-cause mortality; (2) emergent serious adverse events (SAE); and (3) major adverse cardiovascular events (MACE). Heterogeneity was examined with I2 statistics.We pooled risk ratios (RR) with 95% confidence intervals (CI) using a random effects model. Statistical analysis was done using R Studio 4.3.2. Results: Three RCTs were included, encompassing 19,557 patients, of whom 10,004 (51%) were in the CSL112 group. Most of the participants were male (74.5%), with a mean age of 65.1 years and a mean follow-up of 11.6 months. In the pooled analysis, there was no significant statistical difference in all-cause mortality (RR 1.06; 95% CI 0.57, 1.97; p=0.86; I2=19%; Fig 1), SAE (RR 1.01; 95% CI 0.84, 1.22; p=0.90; I2=48%; Fig 2A), and MACE (RR 0.94; 95% CI 0.83, 1.06; p=0.32; I2=0%; Fig 2B). Conclusion: Our findings suggest that the administration of CSL112 was not associated with a reduction in mortality, SAE or MACE in patients with acute myocardial infarction.