tbuckley/cabot-search huggingface dataset:
Abstract 4139839: Sex, Race and Rural-Urban Disparities in Acute Myocardial Infarction-Related Mortality Rates Among Younger and Older Diabetic Adults; Data from CDC Wonder 1999-2020
Authors: Eman Ali, Fakhar Latif, Muhammad Ammar Samad, Urwah Afzal, Huzaifa Ahmad Cheema, Adeel Ahmad, Wajeeh Rehman, Hafsah Alim Ur Rahman, Sourbha Dani
Journal: Circulation (2024)

Introduction: Diabetes mellitus type 2 (T2DM) is an established risk factor for acute myocardial infarction (AMI). Current data suggests that mortality risk of AMI in diabetics remains significantly higher than non-diabetics. Therefore, we aim to examine the trends in AMI-related deaths among younger and older diabetic adults in the United States from 1999 to 2020. Methods: We used CDC Wide-ranging Online Data for Epidemiologic Research (CDC WONDER) to access mortality data from 1999 to 2020. AMI and T2DM-related deaths, age ≥ 35 years, were identified from multiple causes of death and were represented as age-adjusted mortality rates (AAMR) per 1,000,000 population using ICD codes for AMI including (I21.0-I21.9, I22.0-I22.1, I22.8-I22.9) and T2DM (E11.0-E11.9). Joinpoint regression was used to examine trends and annual percentage change (APC) overall and stratified by sex, race, and rural-urban distribution. Results: Between 1999-2020, 164,260 individuals died from AMI and T2DM with an overall AAMR of 43.2 (95% CI: 43, 43.4). AAMRs related to AMI and T2DM modestly increased from 42 in 1999 to 46.8 in 2005 (APC 2.84, 95% CI: 0.1, 8.43), followed by a significant decline to 38.8 in 2014 (APC -1.95, 95% CI: -4.17, -1.29), with subsequent significant increment to 52.2 in 2020 (APC 4.26, 95% CI: 2.73, 6.90). Men had higher AAMRs when compared to women (AAMRs men: 57.2; women: 32.5). After an initial rise from 1999-2003 in men and 1999-2005 in women, AAMRs declined in both men and women till 2014 (AAMRs men: 52; women: 28.3), followed by a significant rise till 2020 (AAMRs men: 71.5; women: 36.3). Among the race groups, AAMR was highest in American Indian or Alaska Natives (75.8), followed by Hispanics (56.4), Non-Hispanic (NH) Blacks (54.5), NH Whites (NHWs) (40.8), and lastly Asian or Pacific Islanders (38.2). According to the rural-urban classification, non-metropolitan areas demonstrated higher AAMRs than metropolitan areas (AAMRs: non metropolitan: 57.2; metropolitan: 40.3). Conclusion: Lesser urbanization, men, and American Indian or Alaska Natives are associated with higher mortality rates. Further in-depth research is needed to comprehend the underlying mechanisms interlinking AMI and T2DM and provide tailored interventions for mortality reduction among patients with concomitant AMI and T2DM.
Abstract 4139740: Left Atrial Strain and Genotype Associated with Clinical Outcomes in Genetic Hypertrophic Cardiomyopathy
Authors: Jin-Sun Park, Kimberly Hong, Cody Kelso, Pooja Nair, Apurv Prabhakar, Eric Adler
Journal: Circulation (2024)

Background: Genetic cardiomyopathies (CMP) are a group of inherited diseases that can lead to heart failure and sudden cardiac death. Hypertrophic CMP (HCMP) is a common genetic disorder. Despite the knowledge about the different causal genes, the relationship between individual genotypes and phenotypes is incomplete. Using the myocardial strain measurement, the relationship between individual genotypes and phenotypes could be evaluated. Methods: We consecutively enrolled 183 patients (123 males, 63 ± 19 year-old) with HCMP who underwent genetic testing. All patients were divided into three groups: gene (-) group, sarcomeric gene (+) group and non-sarcomeric gene (+) group. Echocardiographic images were reviewed and used to calculate myocardial strain. The data of clinical outcomes were obtained and analyzed according to the genotypes and myocardial strain. The primary composite end point of major cardiac adverse events (MACEs), consisting of left ventricular dysfunction (LVD) development, heart failure development, lethal arrhythmias and all-cause death, was analyzed. Results: Myocardial stains, including global LV longitudinal strain, LA strain and RV strain, were not statistically different among the groups. MACE-free survival rate in the gene (-) group was significantly lower than in other groups (log-rank p &lt;0.001). LA conduit strain was significantly related with lethal arrhythmia. Univariable regression for LA conduit strain and lethal arrhythmias showed an odds ratio of 1.137 (95% CI, 1.008–1.283) with p =0.037. For receiver operating characteristic analysis, the areas under the curve for LA conduit strain was 0.716 ( p =0.009). An absolute LA conduit strain cutoff of 10.0% yielded a sensitivity rate of 67% and specificity rate of 66%. The lethal arrhythmias-free survival rate in the group with LA conduit strain lower than 10.0% was significantly lower than in the other group (log-rank p =0.024). Conclusion: The genotype-positive patients with HCMP have worse clinical outcomes. The LA conduit strain was related to lethal arrhythmias in HCMP.
Abstract 4140281: Redefining atrial fibrillation treatment success: Institutional results of atrial fibrillation care using patient-defined pragmatic goals
Authors: Alexander Kolomaya, Brian Zenger, Michael Torre, Ann Lyons, Thomas Bunch, Rachel Hess, Jonathan Piccini, Trudie Lobban, Morgan Miller, Andrew Redd, John Spertus, yue Zhang, Benjamin Steinberg
Journal: Circulation (2024)

Background: While atrial fibrillation (AF) clinical trials define treatment success by time to first AF episode &gt; 30 seconds, our previous survey identified patient-defined success as a Toronto AF Severity Score (AFSS) of ≤ 5 (no-mild symptoms, 80% of participants) and an AF episode lasting ≤ 1 hour (60% of respondents). Our objective is to better understand patterns of AF treatment success and failure when defined by patient priorities. Methods: Using an institutional retrospective cohort of AF patients with either AFSS scores (53.8%) and/or ambulatory ECG (AECG) data (59.4%), we describe the proportion of patients failing to achieve an AFSS ≤ 5 or AF episodes ≤ 1 hour ( Figure 1 ). Results: Between 2019 and May 2024, 2087 patients with an AFSS symptom score, and 2305 with AECG monitoring were included, of whom 862 (41%) had AFSS scores ≤5 and 1130 (49%) had AF episodes ≤1 hour. Compared to patients with AFSS ≤ 5, 1225 patients (59%) with AFSS &gt; 5 were younger, more likely to be female, and have more comorbid conditions (hypertension, diabetes mellitus, obstructive sleep apnea, and heart failure) without significant differences in treatment, including rhythm control strategies (Table 1) . Compared to patients with AF episodes ≤ 1 hour, 1175 patients (51%) with AF episodes &gt; 1 hour were more likely to have received prior ablation, prior cardioversion, and anti-arrhythmic medications. Conclusion: Less than half of AF patients in clinical practice have AF symptom scores or arrhythmia burdens meeting patient-defined goals, with significant differences in both success measures by patient characteristics. Pursuing goal-oriented treatment in AF research and care may help clinicians identify uncontrolled patients, align treatment to patient priorities, and direct future medical intervention at an individual level.
Abstract 4139825: Impact of Non-Culprit Chronic Total Occlusion in Patients with Infarct-Related Cardiogenic Shock: Results from the RESCUE Registry
Authors: Min Chul Kim, Youngkeun Ahn, Ki Hong Choi, Jeong Hoon Yang, Hyeon-Cheol Gwon, Chul-Min Ahn, Cheolwoong Yu, Woojung Chun, Jang-whan Bae, Sung Uk Kwon, Wang Soo Lee, Jin-Ok Jeong, Sang-Don Park, Seong-Hoon Lim
Journal: Circulation (2024)

Background: About 25% of patients with acute myocardial infarction complicated by cardiogenic shock (AMI-CS) have chronic total occlusion (CTO) at non-culprit artery. However, the prognostic impact of CTO in these patients is still unclear. Aims: We aimed to investigate the impact of CTO at non-culprit artery on 1-year mortality in patients with AMI-CS using the multicenter registry of cardiogenic shock. Methods: A total of 1,247 patients presented with cardiogenic shock (CS) were enrolled in the SMART-RESCUE registry between January 2014 and December 2018. After exclusion of non-ischemic cause shock, ischemic cardiomyopathy, failed or no revascularization, vasospasm, and patients undergoing coronary artery bypass surgery, 695 patients underwent percutaneous coronary intervention (PCI). Among these, we analyzed 536 patients with multivessel disease (MVD) according to the presence of CTO at non-culprit artery. The study endpoint was a 1-year all-cause mortality. We also examined the incidence of 1-year cardiac death, and in-hospital death or renal replacement therapy (RRT). Results: A 141 patients (26.3%) of study population had CTO lesion at non-culprit artery. The CTO group had more patients with diabetes mellitus, and lesser patients with ST-elevation myocardial infarction. Although initial left ventricular ejection fraction was lower in CTO group (28.5 vs. 34.1%, P=0.005), initial systolic blood pressure (73.8 vs. 73.2 mmHg, P=0.822) and the level of lactate (6.6 vs. 6.4 mmol/L, P=0.804) were similar in both groups. Venoarterial extracorporeal membrane oxygenation was applied in 206 patients (38.4%), and its use rate was comparable in 2 groups (40.4 vs. 37.7%, P=0.571). Pre- (32.9 vs. 22.9, P &lt;0.001) and post-PCI SYNTAX score (16.7 vs. 5.3, P &lt;0.001) was significantly higher in CTO group. In CTO group, 53 patients (37.6%) had CTO at left main or left anterior descending artery, and only 19 patients (13.5%) in CTO group received PCI for CTO. In multivariate analysis, all-cause mortality at 1-year was significantly higher in CTO group (51.8 vs. 40.5%, hazard ratio [HR] 1.44, 95% confidence interval [CI] 1.09-1.90, P=0.011). The incidences of 1-year cardiac death (45.4 vs. 32.4%, HR 1.55, 95% CI 1.15-2.10, P=0.004) and in-hospital death or RRT (46.8 vs. 36.5%, P=0.031) were also higher in CTO group. Conclusions: Non-culprit CTO lesion was associated with higher 1-year mortality in patients with AMI-CS and multivessel disease.
Abstract 4140089: Lower low-lipoprotein cholesterol level at the time of acute myocardial infarction is associated with increased cardiovascular events
Authors: Takuya Onozato, Hideki Wada, Manabu Ogita, Keiki Abe, Yu Suresvar Singh, Jun Shitara, Satoru Suwa, Katsumi Miyauchi, Tohru Minamino
Journal: Circulation (2024)

Background: Lipid-lowering therapy for patients with acute myocardial infarction (AMI) is highly recommended, however, a paradox may exist where lower low-density lipoprotein cholesterol (LDL-C) levels at myocardial infarction (MI) are associated with poorer prognoses. Aim: To evaluate the association between baseline LDL-C levels and cardiovascular events after MI. Methods: We studied 1,987 consecutive AMI patients who underwent primary percutaneous coronary intervention and who had available data on preprocedural LDL-C between 1999-2015 at Juntendo University Shizuoka Hospital. Patients were divided into quartiles based on their LDL-C levels. The incidence of major adverse cardiac events (MACE), including all-cause death and recurrent MI up to 5-year, were evaluated. Results: Patients in the lowest LDL-C group were older and had higher prevalence of hypertension, diabetes mellitus and chronic kidney disease. During follow-up, 455 (20.9%) MACE were identified. Cumulative incidence of MACE was significantly higher in the lowest LDL-C group than in other groups (p&lt;0.0001, Figure). After adjustment for other risk factors, the lowest LDL-C group had a significantly higher risk of MACE compared with the highest group (hazard ratio, 1.52; 95% confidence interval, 1.11-2.08; p=0.009). On the other hand, no significant difference in cardiovascular risk was found for patients in the highest LDL-C group compared to patients in the second or third groups. Conclusions: Lower LDL-C level was associated with worse clinical outcomes among patients with MI. Patients with lower LDL-C level have a poor prognosis and require more attention.
Abstract 4139711: Does Left Ventricular Dysfunction Assessed by Global Longitudinal Strain Affect Outcomes After Transcatheter Aortic Valve Implantation?
Authors: yuki matsubara, Michiyo Yamano, Tetsuhiro Yamano, Tomotaka Fujimoto, Masaki Yashige, Kan Zen, Takeshi Nakamura, Satoaki Matoba
Journal: Circulation (2024)

Background: Left ventricular (LV) global longitudinal strain (GLS) has been reported to decline before LV ejection fraction (EF) in patients with aortic stenosis (AS). The decrease in LVEF has been reported to result in poor prognosis after transcatheter aortic valve implantation (TAVI). However, the relationship between the degree of LV dysfunction caused by AS and the post-procedural outcomes has not been fully elucidated. Research questions: Is there a difference in the clinical outcome after TAVI according to the degree of LV dysfunction? Aim: The purpose of this study is to determine the relationship between the degree of LV dysfunction and outcomes after TAVI. Methods: This was a single-center, retrospective cohort study, in which 150 of 347 consecutive patients undergoing TAVI were included, excluding atrial fibrillation, inadequate echo image for analysis, and loss to follow-up echocardiography. The degree of LV dysfunction was classified into Grade I (EF ≥50%, GLS ≤-15%), Grade II (EF ≥ 50%, GLS &gt; -15%), and Grade III (EF &lt; 50%), and baseline echocardiographic parameters and changes from baseline to intermediate follow-up (6 months to 1 year) were compared between groups. Results: Baseline characteristics showed significant differences in the incidence of symptomatic heart failure. Baseline echocardiographic parameters were significantly impaired according to grade progression (Table). Although patients with Grade III showed improvement in cardiac function, significant differences remained in LV diastolic diameter, LV mass index, LVEF, and LV-GLS compared with those with Grade I. On the other hand, patients with Grade II showed improvement in LV diastolic diameter, LV mass index, and LVEF, resulting in values comparable to Grade I. However, regarding LV-GLS, although patients with Grade II showed improvement as well as Grade III, it did not improve to the same level as Grade I (Figure). Conclusions: The present study suggests that patients with impaired LV-GLS without reduced LVEF have a better improvement in cardiac function after TAVI compared to patients with reduced LVEF. The optimal timing of TAVI may be in the earlier stages of the deterioration of LV-GLS.
Abstract 4140082: Mediation of Higher Coronary Heart Disease Risk in Non-White Populations by Lifestyle-Psychosocial and Genetic Factors: A Comparative Analysis
Authors: Mohammadreza Naderian, Kristjan Norland, Iftikhar Kullo
Journal: Circulation (2024)

Background: Coronary heart disease (CHD) results from environmental and genetic factors. Lifestyle-psychosocial factors that capture environmental risk and polygenic risk scores (PRS) that capture genetic risk have been associated with CHD in prior studies. Aim: To assess whether higher CHD risk traditionally attributed to non-White race/ethnicty is mediated by PSS CHD or PRS CHD . Methods: In UK Biobank, we ascertained incident CHD (MI/coronary revascularization) and calculated an ancestry-specific PRS for CHD (PGS000018). Based on self-reported race/ethnicity, participants were classified as White and non-White. An age, sex, and ethnicity-adjusted polysocial score for CHD (PSS CHD ) was derived from 100 self-reported lifestyle-psychosocial factors across nine domains: Adulthood Relationship, Education, Entertainment, Housing, Income, Occupation, Physical Activity, Psychological Health, and Sleep. Those with CHD or statin use at recruitment or missing age, sex, race/ethnicity or genotype were excluded. Machine learning (elastic net model) was used to develop PSS CHD . Cox and mediation analyses were performed. Results: In 398,403 participants (56±8 y, 43% male, 96.3% White, 1.8% Asian, 1.6% Black, and 0.3% Chinese), 10,033 had an incident CHD event during a 10-year follow-up. The HRs (95% CIs) for a 1 SD increase in PSS CHD and PRS CHD for CHD risk were 1.5 (1.4–1.5, P &lt;10 -16 ), and 1.6 (1.5 - 1.6, P &lt;10 -16 ), respectively (Figure 1A-B). Asians and Blacks had the highest PSS CHD (mean±SD: 0.5±1, and 0.5±1, respectively), followed by Chinese (0.1±0.9), and Whites (0.0±1) (Figure 1C). After adjustment for age, sex, diabetes, hypertension, LDL-C, and smoking, non-Whites had higher CHD risk: HR (95% CI): 1.2 (1.0–1.4, P &lt;10 -16 ), and the higher risk was mediated more substantially by PSS CHD than PRS CHD (63% (38%-100%) vs. 16% (8%-41%), both P &lt;10 -16 ). Conclusions: The higher CHD risk observed in non-Whites in UK Biobank was mainly due to unfavorable lifestyle-psychosocial factors, rather than PRS, consistent with the paradigm that race/ethnicity is not a biological but rather a social construct. Our findings support substituting race/ethnicity with lifestyle-psychosocial factors and social determinants of health in CHD risk equations.
Abstract 4140310: B cell-mediated antigen presentation promotes adverse cardiac remodeling in chronic heart failure
Authors: Jana Lovell, Carolina Duque, Sylvie Rousseau, Aashik Bhalodia, Kevin Bermea, Charles Cohen, Luigi Adamo
Journal: Circulation (2024)

Introduction: Acute myocardial infarction (MI) induces splenic remodeling and rapid mobilization of immune cells from the spleen to the injured myocardium. Activation of this “cardio-splenic” axis contributes to adverse cardiac remodeling and the development of chronic heart failure. B cells account for the majority of splenic immune cells, but their potential role within the cardio-splenic axis of heart failure remains incompletely explored. In this study, we provide evidence indicating that B cells play an essential role within the cardio-splenic axis via MHC II-mediated antigen presentation. Methods and Results: MI was induced in mice via permanent ligation of the left anterior descending coronary artery. Four weeks following MI or sham surgery, splenic B cells were isolated and transferred into healthy wild-type mice. Eight weeks after adoptive transfer, we assessed cardiac remodeling of recipient mice using echocardiography, gravimetric analysis, and histology. We found that the adoptive transfer of splenic B cells from post-MI mice was sufficient to induce adverse cardiac remodeling in recipient mice (Figure 1). Adoptively transferred splenic B cells were identified in the blood, spleen, and heart of recipient mice 8 weeks post-adoptive transfer. Single cell RNA sequencing (scRNAseq) of splenic B cells was then performed in mice following MI. Biological pathway analyses revealed dysregulation of signaling pathways related to antigen processing and presentation in post-MI mice, suggesting splenic B cells were modulating adverse cardiac remodeling via major histocompatibility complex class II (MHC II)-mediated antigen presentation (Figure 2). Therefore, we developed transgenic mice with B cell-specific MHC II deletion and repeated our adoptive transfer studies. The adoptive transfer of splenic B cells deficient in MHC II from post-MI mice did not induce adverse cardiac remodeling in naïve recipients (Figure 3). Transcriptomic analyses of peripheral blood B cells were also performed in post-MI human patients and healthy control patients, and showed similar dysregulation of antigen processing and presentation in B cells in both acute and chronic phases of MI. Conclusions: Following MI, splenic B cells recirculate along the cardio-splenic axis and contribute to adverse cardiac remodeling via MHC II-mediated antigen presentation. Our results thus point towards MHC II-mediated signaling in B cells as a novel and specific therapeutic target in heart failure.
Abstract 4140295: An Implementation Strategy Package to Improve Familial Hypercholesterolemia Recognition in Primary Care: The CAREFH Study
Authors: Samuel Gidding, Laney Jones, Dylan Cawley, Lauren Carr, Ryan Colonie, Katrina Romagnoli, H Lester Kirchner, Yirui Hu, Marc Williams
Journal: Circulation (2024)

Background: Familial hypercholesterolemia (FH) is under-diagnosed and under-treated. Goals/Aims/Hypothesis: We developed an implementation strategy package to increase primary care awareness regarding familial hypercholesterolemia. We hypothesized that providers would be more likely to order a screening lipid profile in those without one in the prior 5 years and would be more likely to diagnose FH and/or order genetic testing in eligible patients after intervention compared to the prior 6 months. Methods: The intervention included face to face education regarding FH at 20 primary care locations in the Geisinger Health System, development of electronic health record tools (Smart Set, Dutch Lipid Clinic Score calculator, Clinic Note Template), simplification of genetic test ordering procedures, and notification of primary care providers on the day that patients without a lipid profile in the last 5 years or eligible for an FH workup (presence of premature myocardial infarction or LDL-C &gt; 190 mg/dl) were on their schedule. Data was collected for 6 months prior to intervention and 6-12 months post intervention. Results: In patients without a recent test, lipid profiles were more likely to be ordered in patients post intervention (10,251/40,463 (25.3%) pre vs. 14,574/45,089 (32.3%) post; p &lt; 0.0001). An FH diagnosis was added to the chart more commonly post intervention in patients with phenotypic criteria (6/8129 (0.1%) pre vs 32/7879 (0.4%) post; p &lt; 00001). No patients had genetic testing ordered prior to intervention whereas 37 did afterwards. Electronic health record tools were used at &lt; 1% of encounters. Conclusions: An intervention that includes face to face education regarding FH, simplification of genetic test ordering, and reminders to primary care providers regarding patients eligible for an FH evaluation improves rates of lipid testing, FH diagnosis and genetic test ordering. FH specific electronic health record tools were not frequently used.