Risk Of Myocardial Infarction Research Articles

Invasive Treatment of Left Main Coronary Artery Disease: From Anatomical Features to Mechanistic Differences.

There is debate on the best treatment for significant stenoses of the left main (LM) coronary artery. The available evidence is based on four randomized trials, which were either performed specifically to assess patients with LM disease (EXCEL, NOBLE, PRECOMBAT) or had a significant fraction of patients with this disease pattern (SYNTAX). A meta-analysis revealed no difference in periprocedural and 5-year mortality but demonstrated a significant reduction of spontaneous myocardial infarction (MI) with CABG. Furthermore, the recently published SWEDEHEART registry data have shown survival advantage and fewer MACCE with CABG for LM disease after adjustment. In general, patients with more severe coronary artery disease (CAD) appear to have a survival advantage with CABG both over PCI and medical therapy (independent of the presence or absence of LM stenosis), which is always associated with a reduction of spontaneous MI in the CABG arm. Since the nomenclature of LM disease does not automatically reflect the complexity of CAD, we review the nature of LM disease in this article. We mechanistically assess the treatment effects of PCI and CABG for patients with LM disease, which is rarely isolated, often distal, and mostly associated with varying degrees of single and multi-vessel disease. We conclude that in patients with isolated LM shaft lesions and associated diseases of low complexity, the risk of spontaneous MI is lower, and PCI may achieve similar long-term outcomes compared to CABG. Thus, heart teams are essential for selecting the best treatment option and should focus on assessing infarction risk in chronic CAD.

Atrial fibrillation fact sheet in Korea 2024 (part 1): epidemiology of atrial fibrillation in Korea

Background and objectivesThis study aimed to analyze and present updated trends in atrial fibrillation (AF) epidemiology within the Korean population, providing a foundation for planning and implementing appropriate management and treatment strategies for patients with AF.Patients and methodsWe used the Korean National Health Insurance Service database to evaluate the prevalence, incidence, comorbidities, and clinical adverse outcomes of patients with AF in Korea between 2013 and 2022.ResultsAF prevalence in Korean adults aged ≥ 20 years doubled (1.1 to 2.2%) between 2013 and 2022, with significant increases observed across various sex and age groups. Similarly, the number of newly diagnosed patients with AF per year increased steadily, with the incidence rising from 184 to 275 per 100,000 person-years, particularly among older populations. Over this period, the mean age of patients with AF increased from 67.7 to 70.3 years, and comorbidities prevalence and CHA2DS2-VASc score rose significantly, indicating a higher stroke risk. Compared with patients without AF, AF was associated with an increased risk of mortality (hazard ratio [HR]: 1.78), ischemic stroke (HR: 2.39), major bleeding (HR: 2.10), myocardial infarction (HR: 1.44), and heart failure admission (HR: 2.42).ConclusionAF prevalence and incidence have steadily increased between 2013 and 2022, with a more pronounced increase in older patients. Patients with AF are increasingly becoming a high-risk population and are at increased risk of clinical adverse outcomes compared to non-AF patients. Therefore, a sustained national effort to improve AF awareness and comprehensive care quality for patients with AF is required.

Effect of empagliflozin on total myocardial infarction events by type and additional coronary outcomes: insights from the randomized EMPA-REG OUTCOME trial

BackgroundThe effect of empagliflozin, a sodium-glucose-co-transporter-2 inhibitor, on risk for myocardial infarction has not been fully characterized.MethodsThis study comprised prespecified and post-hoc analyses of the EMPA-REG OUTCOME trial in which 7020 people with type 2 diabetes (T2D) and cardiovascular disease [mostly atherosclerotic (ASCVD)] were randomized to empagliflozin or placebo and followed for a median 3.1 years. We assessed the effect of empagliflozin on total (first plus recurrent) events of centrally adjudicated fatal and non-fatal myocardial infarction (MI) using a negative binomial model with robust confidence intervals (CI) that preserves randomization and accounts for the within-patient correlation of multiple events. Post hoc, we analyzed types of MI: type 1 (related to plaque-rupture/thrombus), type 2 (myocardial supply–demand imbalance), type 3 (sudden-death related, i.e. fatal MI), type 4 (percutaneous coronary intervention-related), and type 5 (coronary artery bypass graft-related). MIs could be assigned to > 1 type.ResultsThere were 421 total MIs (including recurrent); 299, 86, 26, 19, and 1 were classified as type 1, 2, 3, 4, and 5 events, respectively. Overall, empagliflozin reduced the risk of total MI events by 21% [rate ratio for empagliflozin vs. placebo, 0.79 (95% CI, 0.620–0.998), P = 0.0486], largely driven by its effect on type 1 [rate ratio, 0.79 (95% CI, 0.61–1.04)] and type 2 MIs [rate ratio, 0.67 (95% CI, 0.41–1.10)].ConclusionsIn T2D patients with ASCVD, empagliflozin reduced the risk of MIs, with consistent effects across the two most common etiologies, i.e. type 1 and 2.Trail Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01131676.

Laboratory-confirmed respiratory viral infection triggers for acute myocardial infarction and stroke: Systematic review protocol.

Cardiovascular disease contributes substantially to global mortality and morbidity. Respiratory tract infections, particularly influenza, may trigger an increase in the short-term risk of acute myocardial infarction (AMI) and stroke. Recent studies have also linked this risk to other respiratory viruses, including respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the pathogen-specific relative contributions, the strength of their associations, and overall public health significance are poorly understood. Assuming causal links, understanding, quantifying, and comparing the effects of different pathogens as triggering factors for acute cardiovascular events is critical to guide future research and prevention. Our aim is to conduct a systematic review to examine the relative effects of laboratory-confirmed respiratory virus infections as triggers for acute myocardial infarction and stroke. We will conduct a comprehensive search of Ovid MEDLINE, PubMed, Ovid Embase, Cochrane Library Central Register of Controlled Trials, and Web of Science, from inception to the end of March 2024. Studies capturing respiratory viral infection(s) using laboratory-confirmatory methods, incidence of AMI or stroke (ischaemic or haemorrhagic), and those involving human participants in any country, will be assessed for eligibility. We will include the following analytical epidemiological study types: randomised controlled trials, cohort and case-control studies, self-controlled case series, and case-crossover designs. We will not impose restrictions on the date, language, study population, geographical region, or sample size, to minimise the risk of introducing biases. Search results will be screened for eligibility by two independent reviewers, and discrepancies resolved by consensus and/or arbitration by a third reviewer. We will assess the risk of bias among the included studies by adopting the Cochrane Collaboration tools for randomised and non-randomised studies. The overall quality of studies will be assessed using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. We will examine sources of heterogeneity, and if studies are sufficiently homogeneous, a meta-analysis will be conducted to calculate the pooled effect sizes. Reporting will adhere to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. International Prospective Register of Systematic Reviews (PROSPERO) registration number: CRD42024494997.

In-Hospital Outcomes of Revascularization in Patients with Left Ventricular Systolic Dysfunction and Coronary Chronic Total Occlusion

Background: The in-hospital outcomes of percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) in patients with left ventricular systolic dysfunction (LVSD) and chronic total occlusion (CTO) remain unclear. Methods: From 2014 to 2020, patients with LVSD and CTO who underwent PCI or CABG were collected. The primary endpoint was in-hospital major adverse cardiac or cerebrovascular events (MACCE), defined as the composite of all-cause mortality, cardiovascular mortality, stroke, myocardial infarction (MI), and target vessel revascularization. Inverse probability of treatment weighting (IPTW) was performed to evaluate the association between revascularization strategies and in-hospital outcomes. The hazard ratio (HR) and 95% confidence interval (CI) were calculated using the Cox proportional hazards model. Results: Of the 773 patients who met the inclusion criteria, 543 (70.2%) underwent PCI, and 230 (29.8%) underwent CABG. The primary endpoint was observed in 25 (3.2%) patients. The incidence of in-hospital MACCE (6.5% vs. 1.8%, p < 0.001) was significantly higher in the CABG group than in the PCI group. After IPTW, the risk of in-hospital MACCE was not found to be significantly different between CABG and PCI groups (HR = 1.81; 95% CI: 0.37–8.82; p = 0.460). Compared with patients who underwent PCI, those who underwent CABG exhibited a significantly higher risk of MI (HR = 6.92; 95% CI: 1.24–38.60; p = 0.027). Conclusions: Patients with LVSD and CTO could experience better outcomes with PCI, which offers a safer alternative coronary revascularization strategy and a reduced risk of MI.

In-Hospital Outcomes of Revascularization in Patients with Left Ventricular Systolic Dysfunction and Coronary Chronic Total Occlusion

Background: The in-hospital outcomes of percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) in patients with left ventricular systolic dysfunction (LVSD) and chronic total occlusion (CTO) remain unclear. Methods: From 2014 to 2020, patients with LVSD and CTO who underwent PCI or CABG were collected. The primary endpoint was in-hospital major adverse cardiac or cerebrovascular events (MACCE), defined as the composite of all-cause mortality, cardiovascular mortality, stroke, myocardial infarction (MI), and target vessel revascularization. Inverse probability of treatment weighting (IPTW) was performed to evaluate the association between revascularization strategies and in-hospital outcomes. The hazard ratio (HR) and 95% confidence interval (CI) were calculated using the Cox proportional hazards model. Results: Of the 773 patients who met the inclusion criteria, 543 (70.2%) underwent PCI, and 230 (29.8%) underwent CABG. The primary endpoint was observed in 25 (3.2%) patients. The incidence of in-hospital MACCE (6.5% vs. 1.8%, p < 0.001) was significantly higher in the CABG group than in the PCI group. After IPTW, the risk of in-hospital MACCE was not found to be significantly different between CABG and PCI groups (HR = 1.81; 95% CI: 0.37–8.82; p = 0.460). Compared with patients who underwent PCI, those who underwent CABG exhibited a significantly higher risk of MI (HR = 6.92; 95% CI: 1.24–38.60; p = 0.027). Conclusions: Patients with LVSD and CTO could experience better outcomes with PCI, which offers a safer alternative coronary revascularization strategy and a reduced risk of MI.

B-cell hub genes play a cardiovascular pathogenic role of in childhood obesity and Kawasaki disease as revealed by transcriptomics-based analyses.

The study aims to explore the central genes that Kawasaki disease (KD) and Obesity (OB) may jointly contribute to coronary artery disease. Investigating single-cell datasets (GSE168732 and GSE163830) from a comprehensive gene expression database, we identified characteristic immune cell subpopulations in KD and OB. B cells emerged as the common immune cell characteristic subgroup in both conditions. Subsequently, we analyzed RNA sequencing datasets (GSE18606 and GSE87493) to identify genes associated with B-cell subpopulations in KD and OB. Lastly, a genome-wide association study and Mendelian randomization were conducted to substantiate the causal impact of these core genes on myocardial infarction. Quantitative real-time PCR (qRT-PCR) to validate the expression levels of hub genes in KD and OB. The overlapping characteristic genes of B cell clusters in both KD and OB yielded 70 shared characteristic genes. PPI analysis led to the discovery of eleven key genes that significantly contribute to the crosstalk. Employing receiver operating characteristic analysis, we evaluated the specificity and sensitivity of these core genes and scored them using Cytoscape software. The inverse variance weighting analysis suggested an association between TNFRSF17 and myocardial infarction risk, with an odds ratio of 0.9995 (95% CI = 0.9990-1.0000, p = 0.049). By employing a single-cell combined transcriptome data analysis, we successfully pinpointed central genes associated with both KD and OB. The implications of these findings extend to shedding light on the increased risk of coronary artery disease resulting from the co-occurrence of OB and KD.

Long-term exposure to air pollution, road traffic noise and greenness, and incidence of myocardial infarction in women

BackgroundEmerging evidence shows that long-term exposure to air pollution, road traffic noise, and greenness can each be associated with cardiovascular disease, but only few studies combined these exposures. In this study, we assessed associations of multiple environmental exposures and incidence of myocardial infarction using annual time-varying predictors. Materials and MethodsIn a population-based cohort of 20,407 women in Sweden, we estimated a five-year moving average of residential exposure to air pollution (PM2.5, PM10 and NO2), road traffic noise (Lden), and greenness (normalized difference vegetation index, NDVI in 500 m buffers), from 1998 to 2017 based on annually varying exposures and address history. We used adjusted time-varying Cox proportional hazards regressions to estimate hazard ratios (HR) and 95 % confidence intervals (95 % CI) of myocardial infarction per interquartile range (IQR). Furthermore, we investigated interactions between the exposures and explored potential vulnerable subgroups. ResultsIn multi-exposure models, long-term exposure to greenness was inversely associated with incidence of myocardial infarction (HR 0.89; 95 % CI 0.80, 0.99 per IQR NDVI increase). Stronger associations were observed in some subgroups, e.g. among women with low attained education and in overweight (BMI ≥ 25 kg/m2) compared to their counterparts. For air pollution, we observed a tendency of an increased risk of myocardial infarction in relation to PM2.5 (HR 1.07; 95 % CI 0.93, 1.23) and the association appeared stronger in women with low attained education (HR 1.30; 95 % CI 1.06, 1.58). No associations were observed for PM10, NO2 or road traffic noise. Furthermore, there were no clear interaction patterns between the exposures. ConclusionOver a 20-year follow-up period, in multi-exposure models, we found an inverse association between residential greenness and risk of myocardial infarction among women. Furthermore, we observed an increased risk of myocardial infarction in relation to PM2.5 among women with low attained education. Road traffic noise was not associated with myocardial infarction.

Risk of venous thromboembolism and arterial events in patients with hypoalbuminemia: a comprehensive meta-analysis of more than 2 million patients

BackgroundAlbumin has antiplatelet and anticoagulant functions. Hypoalbuminemia, as defined by serum values of <3.5 g/dL, is associated with arterial thrombosis; its impact on venous thromboembolism (VTE) is unclear. ObjectivesThe objective of this meta-analysis is to assess the VTE risk in patients with hypoalbuminemia. MethodsMEDLINE and EMBASE were searched up to January 2024 for observational studies and randomized trials reporting data of interest. Primary outcome was the risk of VTE, while secondary outcomes were myocardial infarction and stroke risk in patients with hypoalbuminemia vs those without hypoalbuminemia. The risk of bias was evaluated using Newcastle–Ottawa scale and Cochrane tool. Risk ratios (RRs) with 95% CIs were calculated in a random-effects model. ResultsForty-three studies for a total of 2 531 091 patients (39 738 medical and 2 491 353 surgical) were included in primary analysis; 79.1% of the studies used 3.5 g/dL cut-off value for hypoalbuminemia definition. Follow-up duration was 30 days in 60.5% of studies. Patients with hypoalbuminemia had a higher risk of VTE (RR, 1.88; 95% CI, 1.66-2.13). RRs were similar in both medical (RR, 1.87; 95% CI, 1.53-2.27) and surgical patients (RR, 1.87; 95% CI, 1.61-2.16) and in patients with (RR, 1.86; 95% CI, 1.66-2.10) and without cancer (RR, 1.89; 95% CI, 1.47-2.44). Risk of myocardial infarction (RR, 1.88; 95% CI, 1.54-2.31) and stroke (RR, 1.77; 95% CI, 1.26-2.48) was higher in patients with hypoalbuminemia. ConclusionHypoalbuminemia is a risk factor for VTE in both medical and surgical patients irrespective of cancer coexistence. Serum albumin analysis may represent a simple and cheap tool to identify patients at VTE risk.

3D Printed Interdigitated Electrodes for Cardiac Biomarker Detection.

The identification of biomarkers has significant benefits for early disease diagnosis and treatment. Hence, there is an increasing demand for low-cost, disposable point-of-care diagnostic devices for rapid and specific biomarker detection, with good sensitivity and range. Interdigitated electrodes (IDEs) are among the most widely used transducers, especially in chemical and biological sensors, because of their high sensitivity, low cost, and straightforward manufacturing procedure. In this work, a simple 3D printed IDE structure has been developed for cardiac troponin I detection to indicate the risk of acute myocardial infarction (AMI). IDEs have been fabricated using 3D printing technique and the electrically conductive composite polylactic acid (PLA) filament being utilized for the fabrication of electrodes. The demonstrated cardiac troponin I sensor has a calculated quantification limit and detection limit of 0.233 ng ml-1 and 76.97 pg ml-1, respectively which are clinically significant ranges for AMI identification. Electrochemical analytical techniques, such as electrochemical impedance spectroscopy (EIS) and cyclic voltammetry (CV), were carried out for the detection of analyte concentration. Furthermore, using this fabrication methodology IDEs can be fabricated for under US$ 0.4 which can be utilized to detect several other biomarkers.

Myocardial infarction & C-reactive protein levels among Mexican adults with arthritis: Findings from the Mexican Health and Aging Study

BackgroundStudies of adult populations in high-income countries have found an association between arthritis and myocardial infarction (MI) due to high levels of systemic inflammation. Our objectives were to examine the association between arthritis and MI among Mexican adults and to assess the mediating effect of C-reactive protein (CRP) on this association. MethodsData came from the 2012, 2015, and 2018 observation waves of the Mexican Health and Aging Study. Our sample included 11,707 participants aged 50 and older with no prior MI before 2012. We used self-reported information for arthritis, joint pain, medication use, and limitations to daily activities in 2012. Logistic regression was used to model the association between arthritis and self-reported MI in 2015 or 2018. We used a sub-sample of 1602 participants to assess the mediating effect of CRP. ResultsIn the full sample, participants with arthritis that limited their daily activities had higher odds of MI than participants with no arthritis (OR = 1.40; 95 % CI = 1.04–1.88). In the sub-sample, arthritis that limited daily activities was associated with higher mean CRP (5.2 mg/dL; 95 % CI = 4.10–6.21) than arthritis with no limitations (3.5 mg/dL; 95 % CI = 2.93–4.01). However, CRP levels had a small mediating effect, and the relationship between arthritis with physical limitations and MI remained statistically significant. ConclusionMexican adults with arthritis that limits their daily activities are at an increased risk for MI. Continued research is needed to identify factors that contribute to this increased risk.

Long-term risk factors of recurrent stroke, myocardial infarction and death in patients leaving hospital with a diagnosis of ischemic stroke or TIA

Objectives. The prevalence of patients with prior stroke is increasing globally. Accordingly, there is a need for up-to-date evidence of patient-related prognostic factors for stroke recurrence, post stroke myocardial infarction (MI) and death based on long-term follow-up of stroke survivors. For this purpose, the RIALTO study was established in 2004. Design. A prospective cohort study in which patients diagnosed with ischemic stroke (IS) or transient ischemic attack (TIA) in three Copenhagen hospitals were included. Data were collected from medical records and by structured interview. Data on first stroke recurrence, first MI and all-cause death were extracted from the Danish National Patient Registry and the Danish Civil Registration System. Results. We included 1215 patients discharged after IS or TIA who were followed up by register data from April 2004 to end of 2018 giving a median follow-up of 3.5–6.9 years depending on the outcome. At the end of follow-up 406 (33%) patients had been admitted with a recurrent stroke, 100 (8%) had a MI and 822 (68%) had died. Long-term prognostic predictors included body mass index, diabetes, antihypertensive and lipid lowering treatment, smoking, a sedentary lifestyle as well as poor self-rated health and psychosocial problems. Conclusions. Long-term risk of recurrent stroke and MI remain high in patients discharged with IS or TIA despite substantial improvements in tertiary preventive care in recent decades. Continued attention to the patient risk profile among patients surviving the early phase of stroke, including comorbidities, lifestyle, and psychosocial challenges, is warranted.

Role of GLP-1 Receptor Agonist in Diabetic Cardio-renal Disorder: Recent Updates of Clinical and Pre-clinical Evidence.

Cardiovascular complications and renal disease is the growing cause of mortality in patients with diabetes. The subversive complications of diabetes such as hyperglycemia, hyperlipidemia and insulin resistance lead to an increase in the risk of myocardial infarction (MI), stroke, heart failure (HF) as well as chronic kidney disease (CKD). Among the commercially available anti-hyperglycemic agents, incretin-based medications appear to be safe and effective in the treatment of type 2 diabetes mellitus (T2DM) and associated cardiovascular and renal disease. Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have been shown to be fruitful in reducing HbA1c, blood glucose, lipid profile, and body weight in diabetic patients. Several preclinical and clinical studies revealed the safety, efficacy, and preventive advantages of GLP-1RAs against diabetes- induced cardiovascular and kidney disease. Data from cardio-renal outcome trials had highlighted that GLP-1RAs protected people with established CKD from significant cardiovascular disease, lowered the likelihood of hospitalization for heart failure (HHF), and lowered all-cause mortality. They also had a positive effect on people with end-stage renal disease (ESRD) and CKD. Beside clinical outcomes, GLP-1RAs reduced oxidative stress, inflammation, fibrosis, and improved lipid profile pre-clinically in diabetic models of cardiomyopathy and nephropathy that demonstrated the cardio-protective and reno-protective effect of GLP-1RAs. In this review, we have focused on the recent clinical and preclinical outcomes of GLP-1RAs as cardio-protective and reno-protective agents as GLP-1RAs medications have been demonstrated to be more effective in treating T2DM and diabetes-induced cardiovascular and renal disease than currently available treatments in clinics, without inducing hypoglycemia or weight gain.

Rationale and Design of SCOT-HEART 2Trial: CT Angiography for the Prevention of Myocardial Infarction.

Coronary artery disease continues to be the leading cause of death globally. Identifying patients who are at risk of coronary artery disease remains a public health priority. At present, the focus of cardiovascular disease prevention relies heavily on probabilistic risk scoring despite no randomized controlled trials demonstrating their efficacy. The concept of using imaging to guide preventative therapy is not new, but has previously focused on indirect measures such as carotid intima-media thickening or coronary artery calcification. In recent trials, patients found to have coronary artery disease on computed tomography (CT) coronary angiography were more likely to be started on preventative therapy and had lower rates of cardiac events. This led to the design of the SCOT-HEART 2 (Scottish Computed Tomography of the Heart 2) trial, which aims to determine whether screening with the use of CT coronary angiography is more clinically effective than cardiovascular risk scoring to guide the use of primary preventative therapies and reduce the risk of myocardial infarction.

Advancing non-ST-elevation myocardial infarction risk assessment with artificial intelligence-based algorithms

Advancing non-ST-elevation myocardial infarction risk assessment with artificial intelligence-based algorithms

Overview of Cochrane Systematic Reviews on Interventions for Rehabilitation in People with Ischemic Heart Disease: A Mapping Synthesis.

Objectives: This overview of Cochrane Systematic Reviews (CSRs) reports on current evidence and its certainty of the effectiveness of interventions for the rehabilitation of people with ischemic heart disease (IHD), included in the World Health Organization Rehabilitation Programme Package of Interventions for Rehabilitation. Methods: We included all the CSRs relevant to people with IHD. We used a mapping synthesis to group outcomes and comparisons of included CSRs, indicating the effectiveness of interventions for rehabilitation and the certainty of evidence. Results: The evidence map included a total of 13 CSRs. The effect of the interventions varied across comparisons, and the certainty of evidence was inconsistent, ranging from high to very low. We found the best evidence for exercise-based cardiac rehabilitation in the reduction of fatal and non-fatal myocardial infarction and all-cause hospital admission up to 12 months follow-up. Also, combined interventions (work-directed interventions, physical conditioning interventions, and psychological interventions) reduce the days needed for returning to work. Conclusions: The current effect and certainty of evidence for several comparisons investigated support the role of exercise-based cardiac rehabilitation in the management of people with IHD, specifically reducing the risk of fatal and non-fatal myocardial infarction and hospitalisation. However, our findings highlight the lack of high-certainty evidence about hard endpoints, particularly total mortality. Future research should prioritise these primary endpoints to enhance the credibility of cardiac rehabilitation.

The effect of incremental increases in the number of packed red blood cell units transfused on perioperative outcomes in open abdominal aortic aneurysm repair.

Despite abundant evidence in the surgical and critical care literature demonstrating inferior outcomes in transfused patients, liberal use of blood transfusion, particularly after the initial unit, remains common in vascular surgery. We therefore sought to investigate the incremental risk of each additional unit of blood transfused intraoperatively for patients undergoing elective open repair of abdominal aortic aneurysm (AAA) with regards to postoperative mortality and complications. Patients in the Vascular Quality Initiative registry undergoing elective open infrarenal AAA repair from 2003 to 2020 were included. Exclusion criteria were age greater than 90, prior aortic surgery, concomitant iliac aneurysm, and concomitant additional major procedure. Multivariable logistic regression was used to calculate adjusted odds ratios for in-hospital mortality with incremental increases in packed red blood cells (pRBCs) given intraoperatively. Univariate analysis was performed for secondary outcomes including postoperative cardiac, respiratory, renal, and wound complications. Of 4608 patients who underwent elective open AAA repair, 796 patients (16.9%) underwent perioperative transfusion. The overall in-hospital mortality rate was 2.5%. Adjusting for relevant factors, there was an increase in the odds of in-hospital mortality of 24% for each additional unit transfused. Incremental increases in the number of units transfused were associated with significantly higher risk of postoperative myocardial infarction, congestive heart failure, pulmonary complications, renal failure, and wound complications. There appears to be an important increase in the odds of mortality for each additional unit transfused during infrarenal open AAA repair even when controlling for confounders.

Air Quality Perceptions, Awareness, and Associated Behaviors Among U.S. Adults With and Without Heart Disease

IntroductionExposure to ambient air pollution can worsen cardiovascular disease and increase the risk of stroke, myocardial infarction, and cardiovascular disease mortality. Strategies to reduce air pollution exposure can therefore help prevent cardiovascular morbidity and mortality. This study was conducted to assess awareness among U.S. adults of the effect of air pollution on cardiovascular health and actions individuals can take to reduce their air pollution exposure. MethodsIn May–July 2022, 4,156 adults responded to the summer wave of the 2022 ConsumerStyles survey and self-reported their heart disease status and perceptions, awareness, and behaviors about ambient air pollution and health. In 2023, the data were analyzed to generate weighted population estimates representative of noninstitutionalized U.S. adults. Associations between heart disease and responses about perceptions, awareness, and behaviors were estimated using binomial and multinomial regression methods for weighted data. ResultsOverall, 90% of the weighted population estimate of U.S. adults reported that air pollution can impact a person's health and 44% reported that air pollution can cause or worsen heart disease. Percentages of adults reporting that air pollution can impact a person's health (prevalence ratio=1.09, 95% CI=1.06, 1.12) and that air pollution can cause or worsen heart disease (prevalence ratio=1.28, 95% CI=1.08, 1.51) were higher among adults with than without heart disease. ConclusionsLess than half of U.S. adults are aware that air pollution affects heart disease. Improvements in awareness of the effect of air pollution on cardiovascular health and strategies to reduce exposure could help protect individuals with heart disease.

Clinical impact of Academic Research Consortium for High Bleeding-Risk scores on clinical outcomes in patients with stable coronary artery disease undergoing percutaneous coronary intervention.

High bleeding risk (HBR), as defined by the Academic Research Consortium for High Bleeding Risk (ARC-HBR) criteria, has been recently reported to be associated with an increased risk of major bleeding events and cardiovascular events. We investigated the association between the ARC-HBR score and clinical outcomes in patients with stable coronary artery disease (CAD) who underwent percutaneous coronary intervention (PCI). We assessed 328 consecutive patients with stable CAD who underwent PCI between January 2017 and December 2020. We scored the ARC-HBR criteria by assigning 1 point to each major criterion and 0.5 points to each minor criterion. Patients were stratified into low (ARC-HBR score < 1), intermediate (1 ≤ ARC-HBR score < 2), and high (ARC-HBR score ≥ 2) bleeding-risk groups. The primary outcome measure was major adverse cardiovascular events (MACE), defined as a composite of all-cause death, nonfatal myocardial infarction, and nonfatal stroke. We compared the discriminative abilities of the ARC-HBR score with the Thrombolysis in Myocardial Infarction Risk Score for Secondary Prevention (TRS2°P) and ARC-HBR score with Coronary Revascularization Demonstrating Outcome Study in Kyoto (CREDO-Kyoto) thrombotic risk score. The mean patient age was 70.1 ± 10.2years (males, 76.8%). During the median follow-up period of 983 (618-1338) days, 44 patients developed MACE. Kaplan-Meier curves showed that a stepwise significant increase in the cumulative incidence of MACE as the ARC-HBR score increased (log-rank p < 0.001). In the time-dependent receiver-operating characteristic curve analysis for predicting MACE within 2years, the area under the curve (AUC) of the ARC-HBR score was significantly higher than that of the TRS2°P (AUC: 0.825 vs. 0.725, p value for the difference = 0.023) and similar to that of CREDO-Kyoto thrombotic risk score (AUC: 0.825 vs. 0.813, p value for the difference = 0.627). Conclusions: The ARC-HBR score adequately stratified future risk of MACE in patients with stable CAD who underwent PCI. The ARC-HBR score showed a higher discriminative ability for predicting mid-term MACE than the TRS2°P.

LncRNA CDKN2B-AS1 regulates collagen expression.

The long noncoding RNA CDKN2B-AS1 harbors a major coronary artery disease risk haplotype, which is also associated with progressive forms of the oral inflammatory disease periodontitis as well as myocardial infarction (MI). Despite extensive research, there is currently no broad consensus on the function of CDKN2B-AS1 that would explain a common molecular role of this lncRNA in these diseases. Our aim was to investigate the role of CDKN2B-AS1 in gingival cells to better understand the molecular mechanisms underlying the increased risk of progressive periodontitis. We downregulated CDKN2B-AS1 transcript levels in primary gingival fibroblasts with LNA GapmeRs. Following RNA-sequencing, we performed differential expression, gene set enrichment analyses and Western Blotting. Putative causal alleles were searched by analyzing associated DNA sequence variants for changes of predicted transcription factor binding sites. We functionally characterized putative functional alleles using luciferase-reporter and antibody electrophoretic mobility shift assays in gingival fibroblasts and HeLa cells. Of all gene sets analysed, collagen biosynthesis was most significantly upregulated (Padj=9.7 × 10- 5 (AUC > 0.65) with the CAD and MI risk gene COL4A1 showing strongest upregulation of the enriched gene sets (Fold change = 12.13, Padj = 4.9 × 10- 25). The inflammatory "TNFA signaling via NFKB" gene set was downregulated the most (Padj=1 × 10- 5 (AUC = 0.60). On the single gene level, CAPNS2, involved in extracellular matrix organization, was the top upregulated protein coding gene (Fold change = 48.5, P < 9 × 10- 24). The risk variant rs10757278 altered a binding site of the pathogen responsive transcription factor STAT1 (P = 5.8 × 10- 6). rs10757278-G allele reduced STAT1 binding 14.4% and rs10757278-A decreased luciferase activity in gingival fibroblasts 41.2% (P = 0.0056), corresponding with GTEx data. CDKN2B-AS1 represses collagen gene expression in gingival fibroblasts. Dysregulated collagen biosynthesis through allele-specific CDKN2B-AS1 expression in response to inflammatory factors may affect collagen synthesis, and in consequence tissue barrier and atherosclerotic plaque stability.