Impact of early death recording on international comparison of acute myocardial infarction mortality - administrative hospital data study using the example of Germany and the United States.

BACKGROUND: In-hospital mortality from acute myocardial infarction (AMI) is widely used in international comparisons as an indicator of health system performance. Because of the high risk of early death after AMI, international comparisons may be biased by differences in the recording of early death cases in hospital inpatient data. This study examined whether differences in the recording of early deaths affect international comparisons of AMI in-hospital mortality by using the example of Germany and the United States, and explored approaches to address this issue. METHODS: The German Diagnosis-Related Groups Statistics (DRG Statistics), the U.S. National Inpatient Sample (NIS) and the U.S. Nationwide Emergency Department Sample (NEDS) were analysed from 2014 to 2019. Cases with treatment for AMI were identified in German and U.S. inpatient data. AMI deaths occurring in the emergency department (ED) without inpatient admission were extracted from NEDS data. 30-day in-hospital mortality figures were calculated according to the OECD indicator definition (unlinked data) and modified by including ED deaths, or excluding all same-day cases. RESULTS: German age-and-sex standardized 30-day in-hospital mortality was substantially higher compared to the U.S. (in 2019, 7.3% vs. 4.6%). The ratio of German vs. U.S. mortality was 1.6. After inclusion of ED deaths in U.S. data this ratio declined to 1.4. Exclusion of same-day cases in German and U.S. data led to a similar ratio. CONCLUSIONS: While short-duration treatments due to early death are generally recorded in German inpatient data, in U.S. inpatient data those cases are partially missing. Excluding cases with short-duration treatment from the calculation of mortality indicators could be a feasible approach to account for differences in the recording of early deaths, that might be existent in other countries as well.

Seasonal variation and prognosis in patients with acute myocardial infarction complicated by cardiogenic shock.

Background: Little is known about the association between seasonal variation and prognosis in patients with CS caused by AMI. Objectives: We investigated the 12-month clinical outcomes in patients treated with percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) according to season. Methods: A total of 695 patients undergoing PCI for AMI complicated by CS was enrolled from 12 centers in South Korea. The study patients were divided into four groups according to season in which the AMI with CS occurred (spring, n = 178 vs. summer, n = 155 vs. autumn, n = 182 vs. winter, n = 180). We compared major adverse cardiovascular events (MACEs; the composite of cardiac death, myocardial infarction, re-hospitalization due to heart failure, and any revascularization) between the four groups. Results: The risk of MACE during the 12 months after CS was similar in the four groups: spring, 68 patients, vs. summer, 69, vs. autumn, 73, vs. winter, 68 (p = 0.587). Multivariate Cox-regression analysis revealed no significant difference in 12-month MACE among groups compared to the spring group after inverse probability of treatment weighting adjustment (summer, HR 1.40, 95 % CI 0.98-1.99, p = 0.062; autumn, HR 1.26, 95 % CI 0.89-1.80, p = 0.193; winter, HR 1.18, 95 % CI 0.83-1.67, p = 0.356). The similarity of MACE between the four groups was consistent across a variety of subgroups. Conclusions: After adjusting for baseline differences, seasonal variation seems not to influence the mid-term risk of 12-month MACE in patients treated with PCI for AMI complicated by CS. Condensed abstract: Data are limited regarding the association between seasonal variation and prognosis in patients with cardiogenic shock (CS) caused by AMI. This study divided patients undergoing PCI for AMI complicated by CS into four groups based on the season of occurrence and found no significant differences in 12-month MACE between the groups after adjusting for bias and confounding factors. Multivariate analysis revealed consistent MACE similarity across subgroups. The study suggests that seasonal variation has no impact on the mid-term risk of 12-month MACE in patients with CS caused by AMI, after adjusting for baseline differences. Trial registration: ClinicalTrials.gov NCT02985008RESCUE (REtrospective and prospective observational Study to investigate Clinical oUtcomes and Efficacy of left ventricular assist device for Korean patients with cardiogenic shock), NCT02985008, Registered December 5, 2016 - retrospectively and prospectively. Irb information: This study was approved by the institutional review board of Samsung Medical Center (Reference number: 2016-03-130).

VA-ECMO weaning strategy using adjusted pulse pressure by vasoactive inotropic score in AMI complicated by cardiogenic shock.

AIMS: This study evaluated how well serial pulse pressure (PP) and PP adjusted by the vasoactive inotropic score (VIS) predicted venoarterial extracorporeal membrane oxygenation (VA-ECMO) weaning success and clinical outcomes in acute myocardial infarction complicated by cardiogenic shock (AMI-CS) patients. METHODS AND RESULTS: A total of 213 patients with AMI-CS who received VA-ECMO between January 2010 and August 2021 were enrolled in the institutional ECMO registry. Serial PP and VIS were measured immediately, 12, 24, and 48 h after VA-ECMO insertion. PP adjusted by VIS was defined as PP/√VIS. The primary outcome was successful VA-ECMO weaning. Successful weaning from VA-ECMO was observed in 151 patients (70.9%). Immediately after VA-ECMO insertion, PP [successful vs. failed weaning, 26.0 (15.5-46.0) vs. 21.0 (12.5-33.0), P = 0.386] and PP/√VIS [11.1 (5.1-25.0) vs. 6.0 (3.1-14.2), P = 0.118] did not differ between the successful and failed weaning groups. Serial PP and PP adjusted by VIS at 12, 24, and 48 h after VA-ECMO insertion were significantly higher in patients with successful weaning than those with failed weaning [successful vs. failed weaning, 24.0 (4.0-38.0) vs. 12.5 (6.0-25.5), P = 0.007 for 12 h PP, and 10.1 (5.7-22.0) vs. 2.9 (1.7-5.9), P < 0.001 for 12 h PP/√VIS]. The 12 h PP/√VIS showed better discriminative function for successful weaning than 12 h PP alone [area under the curve (AUC) 0.80, 95% confidence interval (CI) 0.72-0.88, P < 0.001 vs. AUC 0.67, 95% CI 0.57-0.77, P = 0.002]. Patients with a low 12 h PP/√VIS (≤7) had higher rates of in-hospital mortality (44.4% vs. 19.8%, P < 0.001) and 6 month follow-up mortality (hazard ratio 2.41, 95% CI 1.49-3.90, P < 0.001) than those with a high 12 h PP/√VIS (>7). CONCLUSIONS: PP adjusted by VIS taken 12 h following VA-ECMO initiation can predict weaning from VA-ECMO more successfully than PP alone, and its low value was associated with a higher risk of mortality in AMI-CS patients.

Cardiac arrest and post-discharge mortality in patients with myocardial infarction: A large-scale nationwide registry analysis.

Background: Cardiac arrest is a serious complication of acute myocardial infarction. The implementation of contemporary approaches to acute myocardial infarction management, including urgent revascularization procedures, has led to significant improvements in short-term outcomes. However, the extent of post-discharge mortality in patients experiencing cardiac arrest during acute myocardial infarction remains uncertain. This study aimed to determine the post-discharge outcomes of patients with cardiac arrest. Methods: We analysed data from the J-PCI OUTCOME registry, a Japanese prospectively planed, observational, multicentre, national registry of percutaneous coronary intervention involving consecutive patients from 172 institutions who underwent percutaneous coronary intervention and were discharged. Patients who underwent percutaneous coronary intervention for acute myocardial infarction between January 2017 and December 2018 and survived for 30 days were included. Mortality in patients with and without cardiac arrest from 30 days to 1 year after percutaneous coronary intervention for acute myocardial infarction was compared. Results: Of the 26,909 patients who survived for 30 days after percutaneous coronary intervention for acute myocardial infarction, 1,567 (5.8%) had cardiac arrest at the onset of acute myocardial infarction. Patients with cardiac arrest were younger and more likely to be males than patients without cardiac arrest. The 1-year all-cause mortality was significantly higher in patients with cardiac arrest than in those without (11.9% vs. 2.8%, p < 0.001) for all age groups. Multivariable analysis showed that cardiac arrest was an independent predictor of all-cause long-term mortality (hazard ratio: 2.94; 95% confidence interval: 2.29-3.76). Conclusions: Patients with acute myocardial infarction and concomitant cardiac arrest have a worse prognosis for up to 1 year after percutaneous coronary intervention than patients without cardiac arrest.

Factors Associated With Mortality During the First Year Post Infarction: Survival Analysis of Patients With Acute Myocardial Infarction in Colombia.

INTRODUCTION: Cardiovascular diseases account for over 80% of global deaths. Risk factors and social determinants influence mortality in patients post acute myocardial infarction (AMI). OBJECTIVE: To evaluate factors associated with post-AMI mortality during the one-year follow-up. MATERIALS AND METHODS: The study is a prospective cohort study of adults aged 18 years and older with type 1 AMI conducted between October 2021 and January 2024. Intrahospital and outpatient information was collected. Statistical analyses included the Kaplan-Meier survival curve and Cox regression analysis. Proportional hazards and model predictive capacity were evaluated. RESULTS: A total of 1873 patients were included, with a 9.4% mortality rate in the first year. At one year, the estimated survival probability was 88.61% (95% CI: 86.82-90.18). Cox analysis identified several factors associated with mortality, highlighting age (HR = 1.04, 95% CI: 1.02-1.06, p = 0.001), diabetes (HR = 1.77, 95% CI: 1.09-2.87, p = 0.020), renal insufficiency (HR = 2.25, 95% CI: 1.32-3.84, p = 0.003), and type of intervention. The model evaluation showed strong predictive capacity. CONCLUSIONS: It is essential to emphasize the importance of comprehensive management in AMI patients with risk factors such as diabetes and chronic kidney disease, as they are significant predictors of mortality during the first year post infarction.

Development and Validation of an Explainable Deep Learning Model to Predict In-Hospital Mortality for Patients With Acute Myocardial Infarction: Algorithm Development and Validation Study.

BACKGROUND: Acute myocardial infarction (AMI) is one of the most severe cardiovascular diseases and is associated with a high risk of in-hospital mortality. However, the current deep learning models for in-hospital mortality prediction lack interpretability. OBJECTIVE: This study aims to establish an explainable deep learning model to provide individualized in-hospital mortality prediction and risk factor assessment for patients with AMI. METHODS: In this retrospective multicenter study, we used data for consecutive patients hospitalized with AMI from the Chongqing University Central Hospital between July 2016 and December 2022 and the Electronic Intensive Care Unit Collaborative Research Database. These patients were randomly divided into training (7668/10,955, 70%) and internal test (3287/10,955, 30%) data sets. In addition, data of patients with AMI from the Medical Information Mart for Intensive Care database were used for external validation. Deep learning models were used to predict in-hospital mortality in patients with AMI, and they were compared with linear and tree-based models. The Shapley Additive Explanations method was used to explain the model with the highest area under the receiver operating characteristic curve in both the internal test and external validation data sets to quantify and visualize the features that drive predictions. RESULTS: A total of 10,955 patients with AMI who were admitted to Chongqing University Central Hospital or included in the Electronic Intensive Care Unit Collaborative Research Database were randomly divided into a training data set of 7668 (70%) patients and an internal test data set of 3287 (30%) patients. A total of 9355 patients from the Medical Information Mart for Intensive Care database were included for independent external validation. In-hospital mortality occurred in 8.74% (670/7668), 8.73% (287/3287), and 9.12% (853/9355) of the patients in the training, internal test, and external validation cohorts, respectively. The Self-Attention and Intersample Attention Transformer model performed best in both the internal test data set and the external validation data set among the 9 prediction models, with the highest area under the receiver operating characteristic curve of 0.86 (95% CI 0.84-0.88) and 0.85 (95% CI 0.84-0.87), respectively. Older age, high heart rate, and low body temperature were the 3 most important predictors of increased mortality, according to the explanations of the Self-Attention and Intersample Attention Transformer model. CONCLUSIONS: The explainable deep learning model that we developed could provide estimates of mortality and visual contribution of the features to the prediction for a patient with AMI. The explanations suggested that older age, unstable vital signs, and metabolic disorders may increase the risk of mortality in patients with AMI.

Intra-hospital variation of gut microbiota product, trimethylamine N-oxide (TMAO) predicts future major adverse cardiovascular events after myocardial infarction.

BACKGROUND AND AIMS: Trimethylamine N-oxide (TMAO) has been associated with atherosclerosis and poor outcome. We evaluated the prognostic impact of intra-hospital TMAO variation on patient outcome. METHODS AND RESULTS: Blood samples from 149 patients with acute myocardial infarction (AMI) were taken on admission and discharge. Plasma TMAO was determined by HPLC-MS. The endpoint was a composite three-point MACE (major adverse cardiovascular events) including all-cause mortality, re-infarction or the heart failure (HF) development. Median TMAO concentration on admission was significantly higher than on discharge, (respectively, 7.81 [3.47 - 19.98] vs 3.45 [2.3 - 4.78] µM,p<0.001). After estimating the 3.45 µM TMAO cut-off with the analysis of continuous hazard ratio, we divided our cohort into two groups. The first group included 75 (50.3%) patients whose TMAO levels remained below or decreased under cut-off (low-low/high-low; LL/HL), while the second group included 74 (49.7%) patients whose TMAO levels remained high or increased above the cut-off during hospitalisation (high-high/low-high; HH/LH). During the median 30-month follow-up, 21.5% patients experienced the composite endpoint. At Kaplan-Meier analysis, a trend of increasing MACE risk was observed in patients in the HH/LH group (p=0.05). At multivariable Cox analysis, patients from HH/LH group had more than two times higher risk of MACE during the follow-up than LL/HL group (HR=2.15 [95% CI, 1.03 - 4.5], p=0.04). Other independent predictors of MACE were older age and worse left ventricular systolic function. CONCLUSIONS: In patients with AMI, permanently high or increasing TMAO levels during hospitalisation are associated with a higher risk of MACE during long-term follow-up.

Clinical value of BRE-AS1 in myocardial infarction and its role in myocardial infarction-induced cardiac muscle cell apoptosis.

Objectives. The aim of this study was to investigate the expression of long non-coding RNA (lncRNA) brain and reproductive organ-expressed protein (BRE) antisense RNA 1 (BRE-AS1) in patients with acute myocardial infarction (AMI) and its effect on ischemia/reperfusion (I/R)-induced oxidative stress and apoptosis of cardiomyocytes. Methods. Serum BRE-AS1 levels in patients with AMI was detected using quantitative real-time polymerase chain reaction (qRT-PCR). The diagnostic and prognostic values of BRE-AS1 were evaluated. H9c2 cells were treated with hypoxia/reoxygenation to establish an in vitro myocardial infarction cell model. The levels of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6 were detected by enzyme-linked immunosorbent assay (ELISA). Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were determined by commercial kits. Cell counting kit-8 (CCK-8) and flow cytometry were used to evaluate the cell viability and cell apoptosis. Results. The expression of BRE-AS1 in serum of patients with AMI is upregulated, which shows the clinical diagnostic value for AMI. In the I/R injury cell model, the knockout of BRE-AS1 can significantly alleviate the increase in TNF-α, IL-1ß, and IL-6 levels, inhibit the production of LDH and MDA, increase the activities of SOD and GSH-Px, promote the cell viability and suppress cell apoptosis. Conclusions. Abnormally elevated BRE-AS1 has a high diagnostic value for AMI as well as a prognostic value for major adverse cardiovascular events (MACEs). The elevation of BRE-AS1 promoted oxidative stress injury and cell apoptosis in vitro.

Pyroptosis inhibitors MCC950 and VX-765 mitigate myocardial injury by alleviating oxidative stress, inflammation, and apoptosis in acute myocardial hypoxia.

Acute myocardial infarction (AMI) is a prevalent cardiovascular disease with high morbidity and mortality rates worldwide. Pyroptosis is an inflammatory form of programmed cell death that has been linked to various pathological conditions. However, its exact contribution to the onset and progression of heart injury in AMI has not yet fully elucidated. Herein, we established mouse AMI model by ligating the left anterior descending artery and performed transcriptome analysis during the early phase of AMI. Mouse HL-1 and human AC-16 cardiomyocytes were subjected to hypoxia to simulate ischemic injury in vitro. Our results revealed a significant activation of the inflammatory response at 3 h post-ligation, as confirmed by RNA sequencing. We identified the occurrence of NLRP3 inflammasome-mediated pyroptosis in the cardiac tissues of human cases with AMI, as well as in mouse models of AMI and hypoxia-induced cardiomyocytes, using immunohistochemistry staining and Western blotting assays. Concurrently, pharmacological inhibition of NLRP3 inflammasome-mediated pyroptosis with MCC950 and VX-765 effectively decreased hypoxia-induced cardiomyocytes injury, while mitigating myocardial oxidative stress, apoptosis and inflammation caused by hypoxia. Moreover, the circulating levels of gasdermin D (GSDMD), the pyroptosis executor, were remarkably elevated in the plasma of mice with early AMI and in the supernatant of hypoxia-exposed cardiomyocytes in a time-dependent manner using ELISA and Western blotting. Furthermore, the change in circulating GSDMD positively correlated with Creatine Kinase-MB (CK-MB) in the plasma of early-stage AMI mouse. In summary, these findings indicated a critical role for NLRP3 inflammasome-mediated pyroptosis in the progression of AMI, the administration of MCC950 and VX-765 may be attractive candidate therapeutic approaches for cardiac injury caused by acute hypoxia or even AMI. Additionally, the circulating GSDMD exhibits potential as a newly diagnostic biomarker for AMI.

Identification of co-expressed central genes and transcription factors in acute myocardial infarction and diabetic nephropathy.

BACKGROUND: Acute myocardial infarction (AMI) and diabetic nephropathy (DN) are common clinical co-morbidities, but they are challenging to manage and have poor prognoses. There is no research on the bioinformatics mechanisms of comorbidity, and this study aims to investigate such mechanisms. METHODS: We downloaded the AMI data (GSE66360) and DN datasets (GSE30528 and GSE30529) from the Gene Expression Omnibus (GEO) platform. The GSE66360 dataset was divided into two parts: the training set and the validation set, and GSE30529 was used as the training set and GSE30528 as the validation set. After identifying the common differentially expressed genes (DEGs) in AMI and DN in the training set, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses and protein-protein interaction (PPI) network construction were performed. A sub-network graph was constructed by MCODE, and 15 hub genes were screened by the Cytohubba plugin. The screened hub genes were validated, and the 15 screened hub genes were subjected to GO, KEGG, Gene MANIA analysis, and transcription factor (TF) prediction. Finally, we performed TF differential analysis, enrichment analysis, and TF and gene regulatory network construction. RESULTS: A total of 46 genes (43 up-regulated and 3 down-regulated) were identified for subsequent analysis. GO functional analysis emphasized the presence of genes mainly in the vesicle membrane and secretory granule membrane involved in antigen processing and presentation, lipopeptide binding, NAD + nucleosidase activity, and Toll-like receptor binding. The KEGG pathways analyzed were mainly in the phagosome, neutrophil extracellular trap formation, natural killer cell-mediated cytotoxicity, apoptosis, Fc gamma R-mediated phagocytosis, and Toll-like receptor signaling pathways. Eight co-expressed hub genes were identified and validated, namely TLR2, FCER1G, CD163, CTSS, CLEC4A, IGSF6, NCF2, and MS4A6A. Three transcription factors were identified and validated in AMI, namely NFKB1, HIF1A, and SPI1. CONCLUSIONS: Our study reveals the common pathogenesis of AMI and DN. These common pathways and hub genes may provide new ideas for further mechanistic studies.

JMJD6 Autoantibodies as a Potential Biomarker for Inflammation-Related Diseases.

Inflammation is closely associated with cerebrovascular diseases, cardiovascular diseases, diabetes, and cancers, and it is accompanied by the development of autoantibodies in the early stage of inflammation-related diseases. Hence, it is meaningful to discover novel antibody biomarkers targeting inflammation-related diseases. In this study, Jumonji C-domain-containing 6 (JMJD6) was identified by the serological identification of antigens through recombinant cDNA expression cloning. In particular, JMJD6 is an antigen recognized in serum IgG from patients with unstable angina pectoris (a cardiovascular disease). Then, the serum antibody levels were examined using an amplified luminescent proximity homogeneous assay-linked immunosorbent assay and a purified recombinant JMJD6 protein as an antigen. We observed elevated levels of serum anti-JMJD6 antibodies (s-JMJD6-Abs) in patients with inflammation-related diseases such as ischemic stroke, acute myocardial infarction (AMI), diabetes mellitus (DM), and cancers (including esophageal cancer, EC; gastric cancer; lung cancer; and mammary cancer), compared with the levels in healthy donors. The s-JMJD6-Ab levels were closely associated with some inflammation indicators, such as C-reactive protein and intima-media thickness (an atherosclerosis index). A better postoperative survival status of patients with EC was observed in the JMJD6-Ab-positive group than in the negative group. An immunohistochemical analysis showed that JMJD6 was highly expressed in the inflamed mucosa of esophageal tissues, esophageal carcinoma tissues, and atherosclerotic plaques. Hence, JMJD6 autoantibodies may reflect inflammation, thereby serving as a potential biomarker for diagnosing specific inflammation-related diseases, including stroke, AMI, DM, and cancers, and for prediction of the prognosis in patients with EC.

Determinants and effects of microvascular obstruction on serial change in left ventricular diastolic function after reperfused acute myocardial infarction.

Background: Although left ventricular (LV) diastolic dysfunction is more related to functional capacity after acute myocardial infarction (AMI), the determinants of LV diastolic functional change after reperfused AMI remain unknown. This study aimed to investigate the effects of microvascular obstruction (MVO) on mid-term changes in LV diastolic function after reperfused AMI. Methods: In a cohort of 72 AMI patients who underwent successful revascularization, echocardiography and cardiovascular magnetic resonance imaging were repeated at 9-month intervals. The late gadolinium enhancement (LGE) amount, segmental extracellular volume fraction, global LV, and left atrial (LA) phasic functions, along with mitral inflow and tissue Doppler measurements, were repeated. Results: Among the included patients, 31 (43%) patients had MVO. During the 9-month interval, LV ejection fraction (EF) and LV global longitudinal strain (GLS) were significantly improved in accordance with a decrease in LGE amount (from 18.2 to 10.3 g, p < 0.001) and LV mass. The deceleration time (DT) of early mitral inflow (188.6 ms-226.3 ms, p < 0.001) and LV elastance index (Ed; 0.133 1/ml-0.127 1/ml, p = 0.049) were significantly improved, but not in conventional diastolic functional indexes. Their improvements occurred in both groups; however, the degree was less prominent in patients with MVO. The degree of decrease in LGE amount and increase in LVEF was significantly correlated with improvement in LV-Ed or LA phasic function, but not with conventional diastolic functional indexes. Conclusions: In patients with reperfused AMI, DT of early mitral inflow, phasic LA function, and LV-Ed were more sensitive diastolic functional indexes. The degree of their improvement was less prominent in patients with MVO.

Patient knowledge about risk factors, achievement of target values and guideline adherent secondary prevention therapies 12 months after acute myocardial infarction.

AIMS: The prospective GULLIVE-R study aimed to evaluate adherence to guideline recommended secondary prevention, physicians' and patients' estimation of cardiac risk, and patients' knowledge about target values of risk factors after acute myocardial infarction (AMI). METHODS: We performed a prospective study enrolling patients 9-12 months after AMI. Guideline recommended secondary prevention therapies and physicians as well as patients' estimation about their risk, and patients' knowledge about target values were prospectively collected. RESULTS: Between 07/2019 and 06/2021 a total of 2509 outpatients were enrolled in 150 German centers 10 months after AMI. The mean age was 66 years, 26.4% were women, 45.3% had STEMI, 54.7% had NSTEMI, 93.6% had revascularization (84.0% PCI, 7.4% CABG, 1.8% both). Guideline recommended secondary drug therapies were prescribed in over 80% of patients, while only about 50% received all five recommended drugs (aspirin, P2Y12 inhibitors, statins, beta-blockers, RAAS inhibitors) and regular exercise was performed by only one third. About 90% of patients felt well informed about secondary prevention, but the correct target value for blood pressure was known in only 37.9% and for LDL-C in only 8.2%. Both, physicians and patients underestimated the objective risk for future AMIs as determined by the TIMI risk score for secondary prevention. CONCLUSIONS: There is still room for improvement in patient education and implementation of guideline recommended non-pharmacological and pharmacological secondary prevention therapies in patients in the chronic phase after AMI.

Bullet points: Between 07/2019 and 06/2021 a total of 2509 outpatients were enrolled in 150 German centers 10 months after AMI. Guideline recommended secondary drug therapies were applied in over 80% of patients, while only about 50% received all five recommended drugs (aspirin, P2Y12 inhibitors, statins, beta-blockers, RAAS inhibitors) and regular exercise was performed by only one third. About 90% of patients felt well informed about secondary prevention, but the correct target value for blood pressure was known in only 37.9% and for LDL-C in only 8.2%. ESC recommended target values for systolic blood pressure and LDL-cholesterol were achieved in 38.8% and 36.0%, respectively. There was an underestimation of risk for future AMIs as determined by the TIMI Risk Score for Secondary Prevention (TRS2P) both by physicians and patients.

Risk factors and prognosis of postoperative acute myocardial infarction in elderly hip fracture patients combined with coronary heart disease.

INTRODUCTION: This article mainly studies the risk factors for postoperative acute myocardial infarction (AMI) in elderly hip fracture patients combined with coronary heart disease (CHD), constructs a prediction model, and evaluates the prognosis of all the patients. METHODS: This article retrospectively collected elderly patients with hip fracture and CHD who underwent hip fracture surgery at the Third Hospital of Hebei Medical University from January 2019 to December 2021. Demographic data, laboratory indicators, and imaging examination results were collected from the medical case system. The risk factors of postoperative AMI were determined by univariate and multivariate logistic regression, and a nomogram prediction model was established. The ROC curve, calibration curve and DCA decision curve were plotted by R language software. The patients in the training set were followed up for 2 years to evaluate their survival situation. RESULTS: 1094 eligible patients were divided into a training set (n = 824 from January 1, 2019 to September 31, 2021) and a validation set (n = 270 from October 1, 2021 to December 31, 2022). In the training set, women accounted for 58.6%; The average age of the patients was 79.45 years old; The main type of fracture was intertrochanteric fracture. There were 64.7% patients taken B receptor blockers; A total of 166 (20.1%) patients underwent percutaneous coronary intervention (PCI); Hypertension accounted for 55.5%; 520 (63.1%) patients had a preoperative waiting time greater than 3 days; The average hemoglobin value upon admission was 101.36 g/L; The average intraoperative bleeding volume was 212.42 ml; The average surgical time was 2.5 ± 0.3 h; Reginal anesthesia accounted for 29.7%; 63 (68.5%) AMI patients had no obvious clinical symptoms; 68 (73.9%) AMI patients did not show ST-segment elevation in ECG; The risk factors of postoperative AMI were age, hemoglobin at admission, diabetes, chronic kidney disease, intraoperative bleeding, and reginal anesthesia. The AUC of the nomogram prediction model was 0.729. The AUC in the validation set was 0.783. Survival analysis showed a significant statistical difference in 2-year mortality between patients with AMI and without AMI, among all the patients with AMI, patients with ECG ST-segment elevation has higher mortality than patients without ECG ST-segment elevation. CONCLUSION: Our research results found that the incidence of postoperative AMI in elderly patients with hip fractures and CHD was 11.1%. Age, diabetes, hemoglobin at admission, regional anesthesia, chronic kidney disease, and intraoperative bleeding are risk factors. The AUC of the nomogram in training set is 0.729. The 2-year mortality rate of the patients with AMI is higher than that of patients without AMI.

Comprehensive bioinformatics analytics and in vivo validation reveal SLC31A1 as an emerging diagnostic biomarker for acute myocardial infarction.

BACKGROUND: Globally, Acute Myocardial Infarction (AMI) is a common cause of heart failure (HF), which has been a leading cause of mortality resulting from non-communicable diseases. On the other hand, increasing evidence suggests that the role of energy production within the mitochondria strongly links to the development and progression of heart diseases, while Cuproptosis, a newly identified cell death mechanism, has not yet been comprehensively analyzed from the aspect of cardiovascular medicine. MATERIALS AND METHODS: 8 transcriptome profiles curated from the GEO database were integrated, from which a diagnostic model based on the Stacking algorithm was established. The efficacy of the model was evaluated in a multifaced manner (i.e., by Precision-Recall curve, Receiver Operative Characteristic curve, etc.). We also sequenced our animal models at the bulk RNA level and conducted qPCR and immunohistochemical staining, with which we further validated the expression of the key contributor gene to the model. Finally, we explored the immune implications of the key contributor gene. RESULTS: A merged machine learning model containing 4 Cuproptosis-related genes (i.e., PDHB, CDKN2A, GLS, and SLC31A1) for robust AMI diagnosis was developed, in which SLC31A1 served as the key contributor. Through in vivo modeling, we validated the aberrant overexpression of SLC31A1 in AMI. Besides, further transcriptome analysis revealed that its high expression was correlated with significant potential immunological implications in the infiltration of many immune cell types, especially monocyte. CONCLUSIONS: We constructed an AMI diagnostic model based on Cuproptosis-related genes and validated the key contributor gene in animal modeling. We also analyzed the effects on the immune system for its overexpression in AMI.

Construction and validation of nomogram model for predicting the risk of ventricular arrhythmia after emergency PCI in patients with acute myocardial infarction.

OBJECTIVE: To make predictions about the risk of MVA (Malignant Ventricular Arrhythmia) after primary PCI (Percutaneous Coronary Intervention) in patients with AMI (Acute Myocardial Infarction) through constructing and validating the Nomogram model. METHODS: 311 AMI patients who suffered from emergency PCI in Hefei Second People's Hospital from January 2020 to May 2023 were selected as the training set; 253 patients suffering from the same symptom in Hefei First People's Hospital during the same period were selected as the validation set. Risk factors were further screened by means of multivariate logistic and stepwise regression. The nomogram model was constructed, and then validated by using C-index, ROC curve, decision curve and calibration curve. RESULTS: Multivariate logistic analysis revealed that urea, systolic pressure, hypertension, Killip class II-IV, as well as LVEF (Left Ventricular Ejection Fraction) were all unrelated hazards for MVA after emergency PCI for AMI (P<0.05); a risk prediction nomogram model was constructed. The C-index was calculated to evaluate the predictive ability of the model. Result showed that the index of the training and the validation set was 0.783 (95% CI: 0.726-0.84) and 0.717 (95% CI: 0.65-0.784) respectively, which suggested that the model discriminated well. Meanwhile, other tools including ROC curve, calibration curve and decision curve also proved that this nomogram plays an effective role in forecasting the risk for MVA after PCI in AMI patients. CONCLUSIONS: The study successfully built the nomogram model and made predictions for the development of MVA after PCI in AMI patients.

Association of Lipoprotein (a) and Standard Modifiable Cardiovascular Risk Factors With Incident Myocardial Infarction: The Mass General Brigham Lp(a) Registry.

BACKGROUND: Lipoprotein (a) [Lp(a)] is a robust predictor of coronary heart disease outcomes, with targeted therapies currently under investigation. We aimed to evaluate the association of high Lp(a) with standard modifiable risk factors (SMuRFs) for incident first acute myocardial infarction (AMI). METHODS AND RESULTS: This retrospective study used the Mass General Brigham Lp(a) Registry, which included patients aged ≥18 years with an Lp(a) measurement between 2000 and 2019. Exclusion criteria were severe kidney dysfunction, malignant neoplasm, and prior known atherosclerotic cardiovascular disease. Diabetes, dyslipidemia, hypertension, and smoking were considered SMuRFs. High Lp(a) was defined as >90th percentile, and low Lp(a) was defined as <50th percentile. The primary outcome was fatal or nonfatal AMI. A combination of natural language processing algorithms, International Classification of Diseases (ICD) codes, and laboratory data was used to identify the outcome and covariates. A total of 6238 patients met the eligibility criteria. The median age was 54 (interquartile range, 43-65) years, and 45% were women. Overall, 23.7% had no SMuRFs, and 17.8% had ≥3 SMuRFs. Over a median follow-up of 8.8 (interquartile range, 4.2-12.8) years, the incidence of AMI increased gradually, with higher number of SMuRFs among patients with high (log-rank P=0.031) and low Lp(a) (log-rank P<0.001). Across all SMuRF subgroups, the incidence of AMI was significantly higher for patients with high Lp(a) versus low Lp(a). The risk of high Lp(a) was similar to having 2 SMuRFs. Following adjustment for confounders and number of SMuRFs, high Lp(a) remained significantly associated with the primary outcome (hazard ratio, 2.9 [95% CI, 2.0-4.3]; P<0.001). CONCLUSIONS: Among patients with no prior atherosclerotic cardiovascular disease, high Lp(a) is associated with significantly higher risk for first AMI regardless of the number of SMuRFs.

Quantitative Analysis of Innate Lymphoid Cells in Patients with ST-Segment Elevation Myocardial Infarction.

BACKGROUND: Acute myocardial infarction (AMI) is one of the principal causes of death in Mexico and worldwide. AMI triggers an acute inflammatory process that induces the activation of different populations of the innate immune system. Innate lymphoid cells (ILCs) are an innate immunity, highly pleiotropic population, which have been observed to participate in tissue repair and polarization of the adaptive immune response. OBJECTIVE: We aimed to analyze the levels of subsets of ILCs in patients with ST-segment elevation myocardial infarction (STEMI), immediately 3 and 6 months post-AMI, and analyze their correlation with clinical parameters. RESULTS: We evaluated 29 STEMI patients and 15 healthy controls and analyzed the different subsets of circulating ILCs, immediately 3 and 6 months post-AMI. We observed higher levels of circulating ILCs in STEMI patients compared to control subjects and a significant correlation between ILC levels and cardiac function. We also found increased production of the cytokines interleukin 5 (IL-5) and interleukin 17A (IL-17A), produced by ILC2 cells and by ILC3 cells, respectively, in the STEMI patients. CONCLUSION: This study shows new evidence of the role of ILCs in the pathophysiology of AMI and their possible involvement in the maintenance of cardiac function.