tbuckley/cabot-search huggingface dataset:
Abstract 4145010: Efficacy of Autologous Stem Cell Therapy in Myocardial Infarction and Ischemic Cardiomyopathy: A Systematic Review and Meta-Analysis
Authors: Soumyadeep Bag, Tumpa Patra, Snigdha Erva, Henok Regassa, Sruthi nandhaa shanmugam, NAMITHA UMA DWARAKANATH, Merilyn Jerry, Vihoale Kpadenou, Sarah Susan Kelangi, srikanth puli, Ritvika Panghal, Rahul Gujarathi, Badal Thakkar, Ya Ching Hsieh, Urvish Patel, Tanja Dudenbostel
Journal: Circulation (2024)

Introduction: Coronary heart disease(CHD) and myocardial infarction(MI) cost American healthcare $99 billion annually. In the US, 20.5 million adults over 20 years of age suffer from CHD, and 9.3 million from MI. MI causes cardiac myocyte death and scarring, leading to ischemic cardiomyopathy (ICMY), heart failure(HF), and arrhythmia. Current treatments improve perfusion and prevent remodeling but cannot reverse scarring. Stem cell therapy(SCT) aims to replace scarred myocardium with viable tissue, preventing complications like ICMY and HF. Aims: Evaluating the efficacy of SCT, in treating MI and preventing ICMY and HF. Efficacy was measured after 6 months, 1 year, and the long term. Methods: We followed the PRISMA protocol and guidelines to identify all human clinical trials on PubMed since 2010 that used SCT in adults with MI. Observational, non-human studies and isolated case reports were excluded. Our population of interest: adults with MI and SCT were compared to the control group of standard therapy alone(ST). Cardio sphere-derived autologous stem cells, Autologous Bone Marrow Stem Cell Therapy, Bone marrow-derived mononuclear cells via anterograde intra-arterial coronary delivery, Intracoronary infusion of autologous CD34 (+) cell, and Mesenchymal Stem/Stromal Cells were utilized in these trials. The primary outcome measured was efficacy: defined as an increase in Left Ventricular Ejection Fraction(LVEF) by &gt;10%. Results: More than 3000 articles were reviewed, and after applying rigorous inclusion and exclusion criteria, we narrowed down to 32 articles with 2613 patients for qualitative and quantitative analysis. We found an increase in LVEF of &gt;10% with optimal treatment after 12 months of management in the SCT (P&lt;0.05). No significant difference in adverse effects was observed comparing SCT to ST. Reduction in scar size and increase in viable myocardium with improved regional function of infarcted myocardium were observed with SCT. Discussion: CHD and MI are both widespread and impose a significant economic burden on our society. Therefore, it is vital to explore novel treatments for enhancing the survival rate and reducing the negative health outcomes linked to CHD. Our study shows that SCT can lower long-term complications such as ICMY and HF in patients with MI, without creating any substantial negative effects. Hence, additional research, such as extensive multi-center clinical trials, is necessary to examine the potential of SCT in treating MI.
Abstract 4145299: Myocarditis leading to cardiogenic shock: COVID-19's Cardiac Crisis
Authors: Mahmoud Abdalla, Mahnoor Anjum, Lidia Sepulveda, Aftab Ahmad
Journal: Circulation (2024)

Background: COVID-19 can present with a wide spectrum of clinical manifestations ranging from asymptomatic to life-threatening. It is often thought of as a primarily pulmonary infection and different systemic presentations are sometimes overlooked. We present a case of COVID-19 induced myocarditis leading to hemodynamic instability and end-organ dysfunction. Case presentation: A 77-year-old male with a history of CKD, paroxysmal atrial fibrillation, and COPD was transferred to our hospital for a higher level of care due to worsening cardiogenic shock. He was cold and wet (Forrester class IV) with a High Sensitivity troponin of 331 and a BNP level of 21,503. EKG showed atrial fibrillation with RVR but no evidence of acute ischemic changes. A TTE was done which revealed an EF of 30-35% and diffuse hypokinesis with regional variation, a significant reduction from an EF of 50-55% just 4 weeks prior. The patient exhibited end-organ dysfunction, as evidenced by deranged liver function tests and a rise in creatinine from a baseline of 2 to 4.6, indicating congestive hepatopathy and cardiorenal syndrome respectively. The patient’s hemodynamics necessitated milrinone and norepinephrine infusions and efforts to wean them off were unsuccessful due to repeated failed fluid bolus challenges. Considering the patient’s clinical picture, there was a strong suspicion of viral-induced cardiomyopathy, and a COVID-19 infection was confirmed by PCR testing; his last COVID-19 booster dose was in 2021. The patient was promptly started on remdesivir and IV steroids. Unfortunately, the patient's condition continued to deteriorate, and he succumbed to his illness. Discussion: A myriad of cardiovascular manifestations have been implicated with COVID-19, including ACS, myocarditis, and heart failure. Although the exact underlying mechanisms for each of these conditions are unclear, a complex interplay between direct viral injury, systemic inflammation, and cytokine storm has been hypothesized. Our case illustrates the quick progression of heart failure into cardiogenic shock requiring pressor support, with subsequent rapid decompensation rendering CMR, cardiac catheterization, and biopsy timely impractical. It serves as a reminder to explore COVID-19 as a potential cause of biventricular failure in individuals with no evident reason and rapid clinical deterioration, particularly as early initiation of antiviral therapy could improve prognoses.
Abstract 4144952: A Meta-analysis of Folic Acid Supplementation Efficacy in Cardiovascular Diseases Prevention.
Authors: Ernesto Calderon Martinez, Joanne Arvelaez Pascucci, Jaqueline Livier Castillo, Angie Carolina Alonso Ramirez, Patricia Ghattas, Maria Marcela Giron de Marza, Briggitte Solange Sosaya Zuñiga, Jonathan David Martinez Lilan, Enrique Paredes Romero, Karen Fabiola Camacho Davila, Rafael Pinto, Victor Arruarana
Journal: Circulation (2024)

Introduction: Cardiovascular diseases are among the leading causes of morbidity and mortality worldwide. A key component is arteriopathy due to oxidative stress, involving homocysteine as a modifiable risk factor by supplementing folic acid. Hypothesis: This meta-analysis hypothesizes that folic acid supplementation reduces the risk of cardiovascular diseases by lowering homocysteine levels. Methods: Following PRISMA guidelines, a systematic search was conducted in PubMed, Cochrane, Scopus, Web of Science, CINAHL, and EMBASE databases up to March 18, 2024. Randomized controlled trials (RCTs) were included, comparing folic acid supplementation with placebo or alternative treatments in adult patients. The primary outcomes were impact on cardiovascular diseases, stroke, coronary heart disease, peripheral arterial disease, and mortality. Data were extracted and analyzed using random-effects models to calculate risk ratios (RR) and 95% confidence intervals (CI). Results: Our analysis included 16 studies with 39,034 participants meeting the inclusion criteria. The meta-analysis found a statistically significant reduction in stroke risk [RR: 0.87; 95%CI: 0.79, 0.96; P = 0.004] and mortality [RR: 0.92; 95%CI: 0.85, 0.99; P = 0.01]. It showed no statistically significant risk reduction in cardiovascular disease, coronary heart disease, or peripheral arterial disease. Additionally, when evaluating its effectiveness on HDL and LDL, folic acid supplementation showed no statistically significant difference in any of these values between the studies. Conclusions: Folic acid supplementation showed efficacy in reducing the risk of stroke and mortality. However, future research is necessary to investigate homocysteine's role in cardiovascular diseases and events. Systematic review registration number: PROSPERO registry— CRD42024525945.
Abstract 4144997: Pro-B-Type Natriuretic Peptide Kinetics across Pre-, Index, and Post-Acute COVID-19 in Hospitalized Acute on Chronic Heart Failure Patients: A Learning Health System Science Initiative
Authors: Caroline Wojtas, Ian Vargas, Robert Taylor, Manuel Rosario, Aman Khurana, Karen Hamad, richard heibel
Journal: Circulation (2024)

Introduction: Myocardial injury in patients hospitalized with acute on chronic heart failure concurrent with index SARS-CoV-2 (CoV-2) infection is well described, though studies incorporating pre- and post-acute COVID-19 (PAC) are lacking. We address this gap by estimating intensity of acutely decompensated heart failure (ADHF) using time-series pro-BNP levels across hospitalizations pre- vs. respectively index and initial readmission (PAC1). Hypothesis: Case time series analysis will reveal association (p&lt;0.05) between changes in baseline (&lt;24h of admission) pro-BNP levels at pre-index (&lt;180d) vs. respectively index and PAC1 (&lt;90d) with hospital length of stay (LOS) / Medicare Severity Diagnosis Related Groups Geometric Length of Stay (GMLOS) ratio (LOS/GMLOS) &gt;1.0. Methods: Electronic health records underwent IRB exempted extraction of administrative, demographic, and clinical-pathophysiologic data. Continuous data summarized with median [IQR] were compared using repeated-measures ANOVA and discrete data with chi-squared testing. Confounders were statistically balanced. Results: Among 1,413 patients hospitalized between March 10, 2020 and February 29, 2024 discharged alive, not to hospice, harboring ADHF and CoV-2 infection, 91 respectively had baseline pro-BNP at Index and a pre-index hospitalization. Twenty-two underwent PAC1. Statistically isomorphic age, sex and race included 76 (68, 84) years, 43% females distributed by White (83%), Black (11%) and other races (6%). Similarly,chronic comorbidities were pooled for summary including hypertension (87%), chronic lung disease (46%), diabetes (41%), renal disease (36%), obesity (35%), and deficiency anemia (35%). Median times pre-DC to index hospitalization (56 [23, 114]) vs. Pre-DC to PAC1 admission (37 [15, 45]) days (p&lt;0.001). Median pro-BNP (pg/mL) at Pre- (1948 [903, 4309]), Index (3081 [1458, 7230]), and PAC1 (2505 [ 1628, 8048]). Threshold increase in baseline pro-BNP associated with increased risk of LOS/GMLOS &gt;1.0 between pre-COVID-19 vs. index and PAC1 respectively was &gt;20% (p=0.013) and &gt;14% (p=0.039). Conclusions: Time series pro-BNP levels obtained at serial hospitalizations can identity ADHF patients likely to exceed MS DRG GMLOS. Moreover, self-matched designs may strengthen patient-oriented learning health system science aiming to understand causal relationships between exposures and identify treatable traits to blunt or obviate duration of ADHF requiring hospitalization.
Abstract 4144953: Prognostic Value Of sST2 Added To Mosaic Loss Of Y Chromosome As A Fibrosis-Related Disease-Specific Biological-Genomic Marker In Aortic Valve Stenosis
Authors: Silvia Mas-Peiro, Tina Rasper, Alexander Berkowitsch, Thimoteus Speer, Stefanie Dimmeler, Andreas Zeiher
Journal: Circulation (2024)

Background: Risk stratification in severe aortic valve stenosis (AVS), even after contemporary TAVR therapy, is a significant unmet need. General risk scores (STSscore) or heart status biomarkers (NTproBNP) are useful, but prognostic value of potential disease-specific and mechanistically-based indexes is still low. Myocardial replacement fibrosis, as assessed by cMRI, appears to be the most important prognostic factor after TAVR. Soluble ST2 (sST2), a general cardiac biomarker originally reported in inflammatory diseases, was shown to be an independent factor for myocardial fibrosis; and men have higher levels of sST2 in patients with AVS. Experimentally, mosaic loss of Y chromosome in monocytes (mLOY) was associated with increased diffuse myocardial fibrosis, and we recently reported that mLOY is associated with a worse prognosis in severe AVS. Aim: We aimed at assessing the prognostic value of sST2 added to mLOY as a disease-specific biological-genomic marker focused on fibrosis in male patients with severe AVS. Methods: A cohort of 243 consecutive elderly male patients undergoing TAVR was studied. mLOY (i.e., Y/X ratio) was assessed with a digital PCR method in peripheral blood cells DNA, by targeting a 6 bp sequence difference between genes AMELX and AMELY using TaqMan. The previously established mLOY cut-off value of 17% was used. sST2 serum levels were measured, and its optimal cut-off point was calculated based on ROC-curve and Youden index. 2-year survival in the following groups was compared using KM-curves: LOY-low/sST2-low, LOY-low/sST2-high, LOY-high/sST2-low, LOY-high/sST2-high. A multivariate Cox regression analysis was used to assess mortality risk independent from most important comorbidity, echocardiographic and laboratory risk factors. Results: Optimal cut-off value for sST2 was 32.665 ng/ml. Separately, both mLOY (HR: 2.9 [1,7-4.9] and sST2 (4.2 [2.5-7.0]) predicted mortality (both, p&lt;0.0001), but prognosis in LOY-high/sST2-high patients was significantly worse than in all other groups (p&lt;0.001) and showed a substantial risk difference over time (see K-M curves). Multivariate analysis confirmed the risk prediction to be independent from other risk factors (HR 4.620, 95% IC 2.35-9.07, p&lt;0.0001). Conclusion: In male patients with severe AVS undergoing TAVR, LOY-high/sST2-high, a combined biological-genomic marker for fibrosis, is a strong disease-specific and mechanistically-based mortality predictor, independent from general and cardiac risk markers.
Abstract 4144996: General Capillary Endothelial Cells Undergo Reprogramming into Arterial Endothelial Cells in Pulmonary Hypertension
Authors: Bin Liu, Dan Yi, Xiaomei Xia, Karina Ramirez, Hanqiu Zhao, Ankit Tripathi, Michael Fallon, Zhiyu Dai
Journal: Circulation (2024)

Introduction: Pulmonary arterial hypertension (PAH) is characterized by a progressive increase of pulmonary vascular resistance and obliterative pulmonary vascular remodeling that result in right heart hypertrophy, failure, and premature death. The underlying mechanisms of loss of distal capillary endothelial cells (ECs) and obliterative vascular lesion formation remain unclear. Method and Results: Our recent single-cell RNA sequencing, spatial transcriptomics analysis, RNASCOPE, and immunostaining analysis showed that arterial ECs accumulation and loss of capillary ECs were evident in human PAH patients and pulmonary hypertension (PH) rodents. Pseudotime trajectory analysis of the single-cell RNA sequencing data suggests that lung capillary ECs transit to arterial ECs during the development of PH. Our study also identified CXCL12 as the marker for distal arterial ECs in PH. General capillary EC lineage tracing approach using Plvap-DreERT2; Tdtomato mice demonstrated that general capillary ECs gave rise to arterial ECs during PH development. Genetic deletion of HIF-2a or Notch4 neutralized antibodies normalized the arterial programming in PH. Conclusion: In conclusion, our study demonstrates that general capillary endothelium transits to arterial endothelium through the HIF-2a-Notch4 pathway during the development of PAH. Thus, targeting arterial EC transition might be a novel approach for treating PAH patients. Acknowledgment: This work was supported in part by NIH grants R00HL138278, R01HL158596, R01HL62794, R01HL169509, R01HL170096, AHA Career Development Award 20CDA35310084, The Cardiovascular Research and Education Foundation, Arizona Biomedical Research Centre funding (RFGA2022-01-06), and University of Arizona institution funding to Z.D.
Abstract 4144801: Risk Assessment for Cardiac Adverse Events with Bruton’s Tyrosine Kinase Inhibitors in Patients with Mantle Cell Lymphoma
Authors: Abdelrahman Ali, Leslie Ynalvez, Juhee Song, Efstratios Koutroumpakis, Hyeon-Ju Ali, Shaden Khalaf, KEILA MENDOZA, Syed Yusuf, Nicolas Palaskas, Cezar Iliescu, Preetesh Jain, Anita Deswal
Journal: Circulation (2024)

Introduction: Bruton’s tyrosine kinase inhibitors (BTKi) have significantly advanced treatment of mantle cell lymphoma (MCL). This study evaluates the incidence and risk factors for cardiovascular adverse events (CVAEs) in MCL patients receiving BTKi, correlating CVAEs with risk stratification by the European Heart Failure Association (HFA) and International Cardio-Oncology Society (ICOS). Methods: In this retrospective study, demographic and clinical variables, and CVAEs were extracted from clinical records of MCL patients treated with BTKi. Patients were stratified into low, medium, high, and very high-risk groups using the HFA/ICOS tool. Exposure time, from BTKi initiation to 90 days post-treatment, was expressed per 100 person-years. The incidence rate (IR) of CVAEs included palpitations, arrhythmias, blood pressure medication initiation, heart failure, coronary artery disease, stroke, CVAE-related hospitalizations, bleeding, and death. Cox regression models analyzed the association of clinical and demographic characteristics with CVAEs. Results: We included 298 patients (85% untreated, 15% relapsed MCL), median age 65.6 years (IQR 57.6-71.5), predominantly White males (92%, 79%). Comorbidities at BTKi initiation included hypertension (44%), hyperlipidemia (37%), diabetes (11%), and history of atrial fibrillation (AF, 8%), with 2% having AF at therapy initiation. Median left ventricular ejection fraction was 60% (IQR 57-63) and the left atrial volume index 24.6 ml/m 2 (IQR 19.0-30.3). Ibrutinib was used in 60% and second-generation BTKis in 40%. Over a median BTKi exposure of 1 year (range 0.06-8.34), 99 subjects experienced AEs with an IR of 20.8 per 100 person-years. HFA/ICOS low-risk patients had the lowest IR (16.7/100 person-years, 95% CI 6.1-32.5), and the very high-risk group the highest IR (31.9/100 person-years, 95% CI 19.2-47.8). Seventeen patients (5.7%) developed new-onset AF, 7.2% on Ibrutinib and 4.3% on second-generation BTKi. Independent predictors of CVAEs included a history of AF (HR 1.80, 95% CI 1.01-3.22; p=0.047) and prior BTKi exposure within 90 days (HR 3.67, 95% CI 1.77-7.59; p&lt;0.001). Conclusions: Patients with a history of AF were at higher risk for CVAEs when treated with BTKi for MCL. The HFA/ICOS risk tool identified MCL patients at the highest risk for CVAEs with BTKi, highlighting the need for tailored monitoring strategies to optimize patient care and resource utilization.
Abstract 4145034: Drug-Coated Balloon Versus Drug-Eluting Stent in Small Vessel Coronary Artery Disease: A Meta-Analysis of Randomized Controlled Trials
Authors: Napat Suriyathumrongkul, Nisha Wanichwecharungruang, Natnicha leelaviwat, Phuuwadith Wattanachayakul, Narathorn Kulthamrongsri, Thitiphan Srikulmontri, Wasawat Vutthikraivit
Journal: Circulation (2024)

Background: Revascularization of small vessel coronary artery disease (SvCAD) is still challenging despite the extensive use of drug-eluting stents (DESs), mainly because of an increase in target vessel failure. Drug-coated balloon (DCB) has emerged as an alternative strategy in SvCAD. However, the safety and efficacy of DCB in SvCAD is still controversial. We conducted a meta-analysis comparing the clinical outcomes of DCB and DES in SvCAD patients. Methods: We comprehensively searched the databases of MEDLINE and EMBASE from inception to May 2024. Included studies were published randomized control trials (RCTs) that compared major adverse cardiac events (MACE), target-lesion revascularization (TLR), and target-vessel revascularization (TVR) between DCB and DES in SvCAD patients. Data from each study were combined using the random-effects model. Results: Six RCTs were included in this meta-analysis involving 1,534 SvCAD patients (775 underwent revascularization with DCB and 759 with DES). There was no difference in MACE, TLR, and TVR between DCB and DES groups ([OR] 1.14, 95% CI 0.64-2.00, I 2 =58.2%, p=0.657, [OR] 1.34, 95% CI 0.56-3.23, I 2 =48.5%, p=0.516, and [OR] 1.09, 95% CI 0.59-2.01, I 2 =49.6%, p=0.795, respectively) (Figure 1). There was no publication bias observed in Funnel plot as well as no small-study effect observed in Egger’s test. Conclusions: As compared to DES, our study showed that DCB was associated with similar clinical outcomes and could be a potential alternative strategy in SvCAD patients.
Abstract 4144918: Association of iron deficiency correction with the improvement of left ventricular systolic function in patients within 12 months after myocardial infarction
Authors: Dilyara Khastieva, Natalia Tarasova, Niiaz Khasanov
Journal: Circulation (2024)

Background: The adverse effects of iron deficiency (ID) on left ventricular function and outcomes in patients with acute coronary syndrome have been established. However, the effects of ID and its treatment in patients with myocardial infarction (MI) have not been adequately studied. Aim: To study left ventricular systolic function, assessed by evaluation of the wall motion score index (WMSI) and left ventricular ejection fraction (LVEF), in patients with corrected ID and persistent ID within 12 months after MI. Methods: This is open prospective study. 100 patients, 53 males (53%), and 47 females (47%) hospitalized with MI in "Kazan city clinical hospital 7" were enrolled in 2022 year. The mean age was 62±13 years. All patients had ID. ID is assumed to be present when serum ferritin &lt;100 ng/mL or 100 ng/mL ≤ serum ferritin ≤299 ng/mL with transferrin saturation&lt;20%. All patients were treated with iron supplements. After 3 months iron status was evaluated again, and the patients were divided into 2 groups: Group 1 - 70 (70%) patients with corrected ID and group 2 - 30 (30%) patients with persistent ID after the treatment. Echocardiography is performed within 24 hours and 3, 6, 12 months after MI. Results: The groups did not differ in major clinical parameters, comorbidities, medications, laboratory parameters, including hemoglobin level. The median (Me) of WMSI in the 24 hours after admission was 1.25 [1.19;1.62] in group 1 and 1.25 [1.12;1.56] in group 2 (p=0.55). In group 1, the Me WMSI at 3 months remained unchanged (1.25 [1.19;1.5], p =0,5), and was significantly lower than baseline at 6 months (1.19 [1.06-1.56], p &lt; 0.001) and at 12 months (1.12 [1.0;1.44], p &lt; 0.001). In patients in group 2, the Me WMSI remained unchanged at 3 months (1.25 [1.03;1.5], p=0.5), 6 months (1.25 [1.03;1.5], p=0.8) and 12 months (1.25 [1.0;1.5], p=0.6)(Pic. 1). The Me LVEF in the 24 hours after admission was 48% [45;54] in group 1 and 53% [48;54] in group 2 (p=0.06). In group 1, the Me LVEF remained unchanged at 3 months (48% [46;54], p=0.25) and was significantly increased than baseline after 6 months (53% [45;58], p&lt;0,001) and 12 months (55% [47;58], p&lt;0,001). In group 2, LVEF remained unchanged at 3 months (53% [46;57], p=0.75), at 6 months (53% [47;57], p=0.2) and 12 months (53% [46;58], p=0.7). Conclusion: Corrected ID is associated with a significant improvement of left ventricular systolic function in comparison with persistent ID in patients within 12 months after MI.