tbuckley/cabot-search huggingface dataset:
Abstract 4118338: Predictors and 3-Year Outcomes of Compromised Left Circumflex Coronary Artery After Left Main Crossover Stenting
Authors: HAMEED ULLAH, Ning Guo, Zuyi Yuan, Karim Hamed, Najeeb Ullah, Muhammad Asad Khan, Habib Ullah
Journal: Circulation (2024)

Background : Predictors of decreased fractional flow reserve at left circumflex coronary artery after left main (LM) crossover stenting are still lacking. The objectives of the present study were to provide the predictors for low FFR at LCx and the possible treatment strategies for the compromised LCx-together with their long term outcomes. Methods: Total of 563 included patients out of 1974 patients admitted to our hospital from February 2015 to November 2020 with significant distal LM-bifurcation lesion. The enrolled patients underwent single-stent cross-over PCI under IVUS-guidance with further LCx-intervention as indicated by measured FFR. Results: The included patients showed angiographic significant LCx ostial affection after LM-stenting, but only 116 (20.6%) patients had FFR &lt;0.8. The 3-year composite MACE rates were comparable between the high and low FFR groups (16.8% vs. 15.5%, respectively; P =0.744). In a multivariable analysis, a low FFR in the LCx was associated with post-stenting MLA of the LCx (OR: 0.032, P &lt;0.001), post-stenting LCx-plaque burden (OR: 1.166, P &lt;0.001), post-stenting LM-MLA (OR: 0.821, P =0.038) and and pre-stenting LCx-MLA (OR: 0.371, P =0.044). In patients with low FFR, management of compromised LCx with DEB had the lowest 3-year MACE rate (8.1%) as compared to either KBI (17.5%) or stenting group (20.5%), P =0.299. Conclusion: FFR-guided LCx intervention can avoid unnecessary LCx intervention. The post-stenting predictors of low FFR include post-stenting MLA and plaque burden of the LCx and MV stent length. The 3-year MACE rates were comparable between high FFR patients and patients who had low FFR and adequately managed.
Abstract 4120469: Racial and ethnic disparities in catheter based interventions vs. open heart surgery in congenital heart disease
Authors: Michael Nguyen, Ruey-Kang Chang, Virender Rehan, Rie Sakai Bizmark
Journal: Circulation (2024)

Introduction: Transcatheter cardiac interventions have emerged as a viable alternative to open heart surgery for specific congenital heart disease lesions. There is literature to support racial and ethnic disparities in medicine, indicating that patients from racially and ethnically marginalized populations are less likely to receive advanced less invasive procedures. This study seeks to delve into the existence of such inequities between transcatheter and surgical interventions, shedding light on potential inequalities in access and outcomes. Methods: We analyzed California and Florida's State Inpatient and Ambulatory Surgery Databases from 2005 to 2017 to study patients under 18 admitted with diagnosis of atrial septal defect, pulmonary stenosis, aortic stenosis, and ventricular septal defects. Multivariable logistic regression, adjusted for patient characteristics, assessed race and ethnicity's influence on procedure type and in-hospital mortality. We also used log-transformed linear regression to examine associations with length of stay, hospitalization cost, and cost per day. Results: We identified 13,771 records who had open surgeries, and 2,045 records who had CBI. Compared to non-Hispanic White patients, Black patients were significantly more likely to undergo open surgical procedures (adjusted Odds Ratio [aOR] 1.49, p &lt; .001). Additionally, Black, Hispanic, and other race patients had higher risks of in-hospital death (aOR 1.92, p = 0.016 for Black; aOR 1.93, p &lt; 0.01 for Hispanic; aOR 2.37, p &lt; 0.01 for other races). Black and Hispanic patients also experienced longer lengths of stay (Adjusted Means Ratio [aMR] 1.34, p &lt; 0.01 for Black; aMR 1.16, p &lt; 0.01 for Hispanic), and higher costs (aMR 1.12, p = .01 for Black; aMR 1.11, p = .01 for Hispanic), but Black patients had a lower cost per day (aMR 0.96, p = .02). Conclusion: Racial and ethnic gaps persist in pediatric cardiac care, with Black patients facing reduced access to less invasive procedures, higher mortality rates, longer hospital stays, and increased costs compared to non-Hispanic whites. However, the higher costs are likely attributed to longer hospital stays rather than expensive interventions. It is imperative to tackle these disparities to prioritize patient-centered care and streamline resource allocation in healthcare.
Abstract 4118076: Right Innominate Artery Endovascular Intervention Via Single Radial Access and Use Of Embolic Protection
Authors: Ahmed El-Shaer, Qais Radaideh, McKayla Deisz, Leonel Dakar, Abdullah Shaik, Areez Shafqat, Ali Abdul Jabbar, Muhammad Noraiz Lodhi, Toufik Mahfood Haddad
Journal: Circulation (2024)

Introduction: The occurrence of innominate artery stenosis is less prevalent compared to subclavian artery disease. Small studies suggest up to 8% of individuals initially diagnosed with suspected subclavian steal syndrome may present with innominate artery lesions. Deployment of an embolic protection filter within the internal carotid artery during percutaneous intervention of the innominate artery presents a solution to mitigate embolism. Case: A 70-year-old female with a history of peripheral vascular disease presented with claudication in both arms, manifested as pain in both arms. Her left subclavian was stented months prior to presentation. An aortogram revealed severe stenosis of the innominate artery (Figure 1). Since multiple attempts to cross the lesion antegrade from the femoral access site were unsuccessful, we proceeded with the successful deployment of an embolic protection filter in the right internal carotid artery via our right radial artery access site (Figure 2). Using the right radial artery, we passed a long run-through guidewire into the distal abdominal aorta. Due to severe aortic tortuosity, we were unable to snare the wire from the aorta. Therefore, we upsized the radial sheath to 7 French over both wires (runthrough and bare). Using a support catheter, we exchanged the runthrough wire for a Glidewire Advantage. We advanced an 8 x 29mm balloon expandable stent to the area of innominate stenosis and deployed it (Figure 3). We postdilated the stent with a 14mm balloon. Angiography demonstrated adequate expansion. On follow up, the patient was without claudication and had triphasic flow in the innominate and left subclavian arteries. Discussion: Treating innominate artery stenosis via radial access employing a sole entry point for both embolic protection and treatment administration offers a substitute where additional access is infeasible. Modern embolic protection techniques are superior due to their flexibility and ease of use. In this case, placing the embolic protection device in the carotid artery was mandatory through the sole radial access to prevent trapping the filter behind the innominate artery stent. We were able to perform both the embolic device placement and the stenting with the same radial access. Conclusion: Endovascular intervention of innominate artery stenosis via radial access, utilizing a single radial access for both embolic protection and treatment delivery, presents an alternative when femoral access is not feasible.
Abstract 4113997: Semaglutide Improves Myocardial Perfusion and Performance in a Large Animal Model of Coronary Artery Disease
Authors: Christopher Stone, Dwight Harris, Mark Broadwin, Meghamsh Kanuparthy, Keertana Yalamanchili, Ju-Woo Nho, Ruhul Abid, Frank Sellke
Journal: Circulation (2024)

Background: Coronary artery disease (CAD) is the leading cause of death worldwide. It imposes an enormous symptomatic burden on patients, leaving many with residual disease despite optimal procedural therapy, and up to 1/3 rd with debilitating angina amenable neither to procedures, nor to current pharmacologic options. Semaglutide, a glucagon-like peptide 1 agonist originally approved for management of diabetes, has garnered substantial attention for its capacity to attenuate cardiovascular risk. Although subgroup analyses in patients indicate promise, studies explicitly designed to isolate the impact of semaglutide on the sequelae of CAD are lacking. Methods: Yorkshire swine (n=17) underwent placement of an ameroid constrictor around the left circumflex coronary artery to induce CAD. Oral semaglutide was initiated postoperatively at 1.5 mg and scaled up in 2 weeks to 3 mg in treatment animals (SEM, n=8) for a total of 5 weeks, while control animals (CON, n=9) received no drug. All then underwent myocardial harvest with acquisition of perfusion and functional data using microsphere injection and pressure-volume loop catheterization. Immunoblotting, immunohistochemistry, and immunofluorescence were performed on the most ischemic myocardial segments for mechanistic elucidation. Results: SEM animals exhibited improved left ventricular ejection fraction, both at rest and during rapid myocardial pacing to 150 bpm (both p&lt;0.03), accompanied by increased perfusion to the most ischemic myocardial region at rest and during rapid pacing (both p&lt;0.03); reduced perivascular and interstitial fibrosis (both p &lt;0.03); and apoptosis (p=0.008). These changes were associated with increased activation of the endothelial-protective AMPK pathway (p=0.005), coupled with downstream increases in endothelial nitric oxide synthase (p=0.014). Conclusions: This study is the first to reveal the capacity of oral semaglutide to augment cardiac function in the chronically ischemic heart in a highly translational large animal model, likely through AMPK-mediated improvement in endothelial function and perfusion to the ischemic myocardium.
Abstract 4122507: Fetal Socioeconomic and Environmental Exposures Influence Fetal Brain Growth and Risk of Neonatal Brain Injury in Congenital Heart Disease
Authors: Lesje DeRose, Megan Martin, Karla Luna Silva, Flora Nunez Gallegos, Martina Steurer, Elizabeth George, Duan Xu, Patrick McQuillen, Shabnam Peyvandi
Journal: Circulation (2024)

Introduction: Fetuses with CHD have smaller total brain volume (TBV) and are at risk for acquired brain white matter injury (WMI), both of which are linked to neurodevelopmental impairments. Social determinants of health (SDOH) and other fetal environmental factors have been linked to fetal brain health in other populations. Our aim was to test our hypothesis that these exposures influence fetal brain growth and postnatal WMI risk in severe CHD. Methods: Our prospective longitudinal cohort study enrolled fetuses with severe CHD to undergo fetal brain MRI and postnatal pre-operative brain MRI. Participants completed home environment surveys on individual SDOH and exposures. Community SDOH metrics were determined using Child Opportunity Index (COI) based on home address. An ‘at risk’ fetus composite was created if there was exposure to: personal/household smoking, welfare/food stamps, or poverty. TBV was calculated at both time points. Presence/degree of WMI was determined on postnatal MRI. Repeated measures analysis and logistic regression were performed to determine association between individual and community SDOH metrics with rate of TBV growth and risk of WMI. Results: 55 participants enrolled (54 fetal scans: mean GA 33.9 wks, 95%CI: 33.7,34.1; 47 neonatal scans: mean GA 39.3 wks 95%CI: 38.9,39.6). Fetal sex, smoking exposure, and several individual SDOH were associated with TBV growth. Adjusting for fetal sex and GA at scan, rate of TBV growth was slower with smoking exposure (coeff: -5.2, 95%CI: -10.3, -0.2, p= 0.04) and trended towards significance for those with welfare/food stamps or poverty. ‘At risk’ fetuses had slower rate of TBV growth than those without risk (coeff: -2.5, 95%CI: -5.0, -0.07, p= 0.04) (Figure 1). There were lower odds of pre-operative WMI with high COI compared to low after adjusting for GA at scan (OR= 0.16, 95%CI: 0.03, 0.9, p= 0.04). Conclusion: Smoking exposure and individual-level SDOH influence brain growth, while community COI is associated with risk of postnatal pre-op WMI in CHD. Our findings identify targets for intervention to optimize brain growth and outcomes in the CHD population, including smoking cessation programs, and nutritional and needs assessment during pregnancy.
Abstract 4122486: Multicenter Study of Primary Fetal Cardiomyopathy: Clinical Outcomes And Genetic Etiologies, A Fetal Heart Society Research Collaborative Study
Authors: Astha Burande, Lisa Hornberger, Oana Caluseriu, Shabnam Peyvandi, Elijah Bolin, Tiscar Cavalle-Garrido, Sue Chandra, James Cnota, Jennifer Conway, Sara Creighton, Bettina Cuneo, Marlayna Despres, Tam Doan, J. Scott Doucet, Michelle Grenier, Whitnee Hogan, Michelle Kaplinski, Mahima K Bijji, Ann Kavanaugh-Mchugh, Sam Keller, Elena Kwon, Steven Lipshultz, Amara Majeed, Gitanjali Mansukhani, Amanda McIntosh, Deani McVadon, Erik Michelfelder, Michelle Miller, Caitlin Milligan, Seema Mital, Adriana Montes Gil, Anita Moon-Grady, Neda Mulla, sheetal patel, Cathleen Pruitt, Amna Qasim, Hari Rajagopal, Sanghee Ro, David Schidlow, Kristin Schneider, Ranjini Srinivasan, Jennifer Sutton, carolyn taylor, Angela McBrien
Journal: Circulation (2024)

Background: Fetal cardiomyopathy (FCM) affects 8 per 100,000 live births, often with unknown etiology. Progress in fetal cardiac screening, genetic testing and management may have impacted historically poor outcomes. Aims: We sought to investigate genetic associations and clinical outcomes of FCM in the current era. Methods: This was a retrospective Fetal Heart Society Research Collaborative cohort study of FCM cases diagnosed from January 2017-December 2021 in 39 centers. Cases of fetal myocardial disease attributable to maternal diabetes, structural heart disease, arrhythmia or extra-cardiac conditions were excluded. Data including outcomes to 1 year after birth were collected. Significance of genetic testing results and FCM subtype were classified by each center. Results: There were 138 FCM cases diagnosed at a median gestational age of 27 +4 weeks (range 13-39 weeks). Suspected fetal heart disease (41%, 56/138) was the most common referral indication. There was a known family history of CM in 19% (26/138). FCM phenotypes included 38% (52/138) dilated, 24% (33/138) hypertrophic, 17% (24/138) non-compacted, 10% (14/138) mixed, 5% (7/138) restrictive, 3% (4/138) ventricular aneurysm, 3% (4/138) unspecified. Hydrops was present at diagnosis in 15% (20/138) and by delivery or at fetal demise in 26% (36/138). Of 128 continued pregnancies, 7% (9/128) had a fetal demise, 92% (118/128) a live birth and one was lost to follow-up. Among live births, 10% (12/118) received only palliative care. Of 106 actively treated, 75% (80/106) survived to 1 year; 7% (7/106) required ECMO, and 22% (23/106) were listed for transplant with 18 of these successfully transplanted. Of the cohort, a total of 80% (110/138) had genetic testing (including 30 with invasive prenatal testing), with 38% (52/138) having a confirmed genetic etiology and 28% (38/138) with a variant of uncertain significance (VUS) (Figure 1). Transplant-free survival to 1 year was similar for those with and without a genetic diagnosis (40%,21/52 vs 47%,40/86, p=0.48). Conclusion: Outcomes remain poor in FCM, with &lt;50% 1-year survival overall. Confirmed genetic etiologies are now identified in nearly 40%, highlighting the importance of genetic testing.
Abstract 4114308: Defective in LYPLA1-Mediated Lysophosphatidylcholine Metabolism Contributes to Diabetes-Induced Atherosclerosis and Subsequent Myocardial Dysfunction
Authors: Bin Gao, Xinyu Zhao, Meng Yuan, Lei Zhang, Xiuzhu Chen, Qin Qin, Yuehua Dong, Li Zhong, Rui Guo
Journal: Circulation (2024)

Background and Objective: Diabetes mellitus (DM) is a chronic metabolic condition that can cause serious damage to blood vessels and the heart. While current metabolomics research mainly focused on metabolic profiles during disease onset or at advanced stages, there remains a gap in understanding the molecular mechanisms of metabolites in the progression of diabetic cardiovascular disease. This study aims to explore effective strategies for preventing cardiovascular complications in diabetics by excavating metabolic pathways and mechanisms. Methods: Peripheral blood samples were obtained from 21 healthy individuals, 20 patients diagnosed with DM, 20 patients with coronary heart disease (CHD), and 25 patients with both DM and CHD (DC). Cardiac function, biochemical parameters and serum metabolome were detected. A specialized methodology with rigorous screening criteria was employed to identify differential metabolites associated with diabetes-induced CHD and cardiomyopathy. Mice were injected with LPC16:0 to assess cardiovascular function. Models of diabetes and diabetic atherosclerosis were induced by STZ injection and high-fat diet feeding in WT and ApoE -/- mice. Cardiac function and differential metabolites in aortic and cardiac tissues were assessed. The effect and molecular mechanism of LYPLA1 on vascular function, mitochondrial function, and metabolites-related enzymes were examined in human aortic endothelial cells (HAECs) and AC16 cardiomyocytes. Results: Cardiac function was markedly declined in DM and DC patients, as well as in mice with diabetes and diabetic atherosclerosis. However, CHD patients and atherosclerosis alone did not exhibit evident cardiac dysfunction. Key metabolites associated with diabetic cardiomyopathy and diabetes-induced CHD were identified as LPE18:1 and LPC16:0, respectively. Intraperitoneal administration of LPC16:0 in mice led to decreased LYPLA1, severe myocardial anomalies, and the appearance of plaques in the aortic arch. Either LYPLA1 knockdown or the treatment with high glucose and palmitic acid in HAECs resulted in impaired mitochondrial function, reduced intracellular NO and eNOS activity, which were mitigated by LYPLA1 overexpression. Conclusion: The metabolite LPC16:0 and the regulatory enzyme LYPLA1 are pivotal in driving the advancement of cardiovascular complications triggered by diabetes. Targeting LYPLA1 could represent a promising strategy for preventing diabetes-induced CHD and subsequent cardiomyopathy.
Abstract 4122122: Comparison of Transradial Versus Transfemoral Access for Chronic Total Occlusion Percutaneous Coronary Intervention: A Meta-Analysis
Authors: Hritvik Jain, Ramez Odat, Aman Goyal, Mayank Jha, Jyoti Jain, Eeshal Fatima, Ancy Jenil Franco, Muhammad Idrees, Siddhant Passey, Maryam Saleem
Journal: Circulation (2024)

Background: Chronic total occlusion (CTO) contributes to increased mortality because it is often revascularized by percutaneous coronary intervention (PCI). Traditionally, transfemoral (TF) access has been preferred in CTO-PCI owing to its high procedural complexity and ease of introduction of a large guide catheter. Transradial (TR) access is gaining popularity in PCI, but its efficacy in CTO-PCI has not been well investigated. Methods: We searched major databases to retrieve studies comparing TR and TF access in patients with CTO who underwent PCI. The DerSimonian and Laird random-effects model was used to pool the odds ratios (OR) and mean differences (MD) with 95% confidence intervals. Statistical significance was considered at p&lt;0.05. Results: We included 18 studies with 30,286 CTO PCI cases (TR: 10921 and TF: 19365). For procedural outcomes, TR access was associated with a significantly lower total contrast volume requirement [MD: -19.57; 95% CI: -34.34, -4.81; p=0.009], with comparable procedural success [OR: 1.16; 95% CI: 0.97, 1.40] and total procedural time [MD: -5.30; 95% CI: -21.09, 10.48]. For clinical outcomes, TR was associated with significantly lower risks of in-hospital mortality [OR: 0.46; 95% CI: 0.25, 0.85; p=0.01], major adverse cardiovascular events [OR: 0.73; 95% CI: 0.59, 0.92; p=0.007], vascular complications [OR: 0.35; 95% CI: 0.25, 0.51; p&lt;0.00001], and major bleeding [OR: 0.33; 95% CI: 0.20, 0.56; p&lt;0.0001] compared with TF access. Conclusion: CTO PCI using TR access demonstrated favourable outcomes regarding lower contrast volume requirement, lower risks of in-hospital mortality, major adverse cardiovascular events, vascular complications, and major bleeding compared with TF access. The selection of appropriate arterial access varies on a case-to-case basis and according to operator preferences.
Abstract 4113336: Characteristics and Outcomes of Ventricular Tachycardia Ablation in Patients with the HeartMate 3 Left Ventricular Assist Devices: Results From a Large Single-Center Registry
Authors: Fawzi Zghyer, Chadi Tabaja, Ioan Liuba, Yi-Wen Liao, Arwa Younis, Arshneel Kochar, Justin Lee, Shady Nakhla, John Rickard, Kenneth Mayuga, J. Emanuel Finet, David Martin, Mandeep Bhargava, Mina Chung, Jeff Courson, Jakub Sroubek, Hiroshi Nakagawa, Robert Koeth, Koji Higuchi, Aaron Weiss, Ayman Hussein, Bryan Baranowski, Wai Hong Tang, Thomas Dresing, Thomas Callahan, Tyler Taigen, Mohamed Kanj, Walid Saliba, Edward Soltesz, Oussama Wazni, Randall Starling, Pasquale Santangeli
Journal: Circulation (2024)

HeartMate 3 (HM3) is a fully magnetically levitated continuous flow left ventricular assist device (LVAD). In patients with HM3 and recurrent ventricular tachycardia (VT), data on the outcomes of catheter ablation (CA) are insufficient. We report our institutional experience with CA of VT in patients with the HM3.Consecutive patients with HM3 and recurrent drug-refractory VT undergoing CA were included. Ablation sites were identified using activation/entrainment mapping (stable VTs) and/or late/fractionated potential ablation and pace-mapping (unstable VTs). Between 2016-2023 a total of 431 patients (age 58±13, INTERMACS 3±0.98, 44% ischemic cardiomyopathy) received an HM3 LVAD at our institution. Of these, 15 (3.4%) underwent CA for recurrent VT despite therapy with 1.3±0.8 antiarrhythmic drugs a median of 700 days from the LVAD surgery (2 patients &lt;1 month from the surgery). The LV access was transseptal in 12 (80%) cases, retrograde aortic in 2 (13%) and both in 1 (7%). A total of 23 distinct VTs were targeted. Of these, 21 (91%) were mapped with activation/entrainment mapping, always utilizing an intracardiac RV reference due to excessive surface ECG noise, and 2 (9%) were hemodynamically unstable with reduced LVAD flows and targeted with substrate-based ablation. A total of 3 (13%) VTs were targeted adjacent to the HM3 inflow cannula, and 20 (87%) from substrate remote from the HM3 cannula. At post-procedural programmed ventricular stimulation, non-inducibility of all targeted VTs was achieved in 13 (87%) patients, 1 patient had residual inducible clinical VT, and in 1 patient no post-procedural programmed stimulation was performed. Periprocedural complications occurred in 1 (7%) case (small pericardial effusion not requiring intervention). At 12 months follow-up following the index procedure, no death occurred and one patient received heart transplantation. Of the remaining 14 patients, 6 (42%) remained free from VT (2 with VT ablation &lt;1 month post-LVAD and 12 with VT ablation &gt;=1 month post-LVAD). In this large single-center HM3 registry, a minority of patients underwent CA for recurrent drug-refractory VT (3.4% over a 7-year period). CA of VT in HM3 recipients is feasible and appears safe also when performed soon after LVAD surgery. Myocardial scar from the underlying cardiomyopathic process rather than the apical cannula is the dominant substrate responsible for VT in these patients.