Targeted metabolomic profiling of acute ST-segment elevation myocardial infarction.

Myocardial infarction is a major cause of morbidity and mortality worldwide. Metabolomic investigations may be useful for understanding the pathogenesis of ST-segment elevation myocardial infarction (STEMI). STEMI patients were comprehensively examined via targeted metabolomic profiling, machine learning and weighted correlation network analysis. A total of 195 subjects, including 68 STEMI patients, 84 patients with stable angina pectoris (SAP) and 43 non-CVD patients, were enrolled in the study. Metabolomic profiling involving the quantitative analysis of 87 endogenous metabolites in plasma was conducted. This study is the first to perform targeted metabolomic profiling in patients with STEMI. We identified 36 significantly altered metabolites in STEMI patients. Increased levels of four amino acids, eight acylcarnitines, six metabolites of the NO-urea cycle and neurotransmitters, and three intermediates of tryptophan metabolism were detected. The following metabolites exhibited decreased levels: six amino acids, three acylcarnitines, three components of the NO-urea cycle and neurotransmitters, and three intermediates of tryptophan metabolism. We found that the significant changes in tryptophan metabolism observed in STEMI patients-the increase in anthranilic acid and tryptophol and decrease in xanthurenic acid and 3-OH-kynurenine-may play important roles in STEMI pathogenesis. On the basis of the differences in the constructed weighted correlation networks, new significant metabolite ratios were identified. Among the 22 significantly altered metabolite ratios identified, 13 were between STEMI patients and non-CVD patients, and 17 were between STEMI patients and SAP patients. Seven of these ratios were common to both comparisons (STEMI patients vs. non-CVD patients and STEMI patients vs. SAP patients). Additionally, two ratios were consistently observed among the STEMI, SAP and non-CVD groups (anthranilic acid: aspartic acid and GSG (glutamine: serine + glycine)). These findings provide new insight into the diagnosis and pathogenesis of STEMI.

The Role of Inflammation in Early Left Ventricular Thrombus Formation Following ST-Elevation Myocardial Infarction-A Matched Case-Control Study.

BACKGROUND: There is limited data on the association between inflammation and the formation of early left ventricular thrombus (LVT) following ST-elevation myocardial infarction (STEMI). This study aimed to explore the predictive value of several inflammatory biomarkers for LVT formation following STEMI. METHODS AND RESULTS: Our cohort included 2534 consecutive patients admitted to the cardiac intensive care unit (CICU) with STEMI. The final analysis included 51 patients with LVT and 102 patients without LVT, matched for age, sex, anterior infarct and ejection fraction. Upon admission, patients with LVT had higher white blood cell counts (WBC) (12.8 ± 7 vs. 12.4 ± 4 ×103/µL, p = 0.01), higher absolute neutrophil counts (10.5 ± 4 vs. 8.6 ± 4 ×103/µL, p = 0.003), neutrophil-to-lymphocyte ratio (8.2 ± 6 vs. 4.8 ± 4, p = 0.04), and C-reactive protein (CRP) levels (35.9 ± 62 vs. 18.6 ± 40 mg/L, p = 0.04). Peak values for WBC and CRP were also higher in the LVT group (17.8 ± 8 vs. 14.6 ± 5 ×103/µL, p = 0.003 and 95.8 ± 82 vs. 64.2 ± 76 mg/L, p = 0.02, respectively). In univariate regression analysis, WBC upon admission (OR: 1.12, 95% CI: 1.02-1.21, p = 0.02), peak WBC (OR: 1.09, 95% CI: 1.02-1.17, p = 0.009), neutrophil count upon admission (OR: 1.15, 95% CI: 1.04-1.26, p = 0.004), and peak CRP (OR: 1.01, 95% CI: 1-1.01, p = 0.03) predicted LVT formation, which was also evident in multivariate regression models. CONCLUSION: WBC and neutrophil counts upon admission, as well as peak WBC and CRP, have additional predictive value for LVT formation following STEMI, beyond classical risk factors.

Uric Acid to Albumin Ratio as a Predictive Marker for Intracoronary Thrombus Severity in ST-Segment Elevation Myocardial Infarction (STEMI) Patients Undergoing Primary Percutaneous Coronary Intervention (PCI).

BACKGROUND This study assessed the association between a novel inflammatory marker, uric acid (UA)-to-albumin ratio (UAR), and preprocedural intracoronary artery thrombus (ICAT) in ST elevation myocardial infarction (STEMI). MATERIAL AND METHODS A total of 171 STEMI patients treated by primary percutaneous coronary intervention between February and December 2023 were evaluated prospectively in this cross-sectional study. The patients were stratified into 2 groups as low (grades 1 to 3) and high-(ICAT) groups (grades 4 and 5). To determine the independent predictors of lower and higher ICAT, multivariate regression analysis was performed. RESULTS C-reactive protein (CRP), UA, and UAR were significantly higher in the high ICAT group (1.11 (0.3-2.8) vs 0.80 (0.10-2.8), P=0.037; 5.4 (3.5-7.2) vs 4.9 (3.4-5.6), P<0.001; 1.78 (0.82-3) vs 1.48 (0.77-2.57), P<0.001, respectively). However, albumin levels were similar between groups (3.1 (2.1-4.4) vs 3.3 (2.1-4.4), P=0.243). Higher UAR (OR: 3.95% CI: 1.23-12.7, P=0.021), lower left ventricular ejection fraction (LVEF) (OR=0.802; 95% CI 0.7537-0.872; P<0.001), longer pain-wire crossing time (OR=1; 95% CI: 1-1.02; P<0.001), and diabetes mellitus (OR=0.181; 95% CI 0.46-0.7; P<0.001) were independent predictors of ICAT. CONCLUSIONS UAR, a marker of inflammation, is an independent predictor of ICAT in patients with STEMI.

Association between haemoglobin decline and long-term outcomes in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention.

OBJECTIVE: To explore the association between in-hospital haemoglobin decline and long-term mortality and major adverse cardiovascular and cerebrovascular events (MACCE) among ST-segment elevation myocardial infarction (STEMI) patients treated with primary percutaneous coronary intervention (PCI). METHODS: This retrospective analysis included adult patients who underwent primary PCI for STEMI. Haemoglobin levels were recorded at admission and 48-72 h later. Patients were divided into two groups based on the extent of haemoglobin decline: low (<3 g/dl or no decline) and high (≥3 g/dl). The primary endpoint was all-cause mortality at long-term follow-up. The secondary endpoint was MACCE. RESULTS: Patients were divided into two groups: low group (n = 665) and high group (n = 111). The mortality rate was significantly higher in the high group (72 of 111 patients; 65%) than in the low group (185 of 655 patients; 28%). Propensity score matching confirmed this association, with higher mortality (41 of 79 patients [52%] versus 25 of 79 patients [32%]) and MACCE rates (56 of 79 patients [71%] versus 41 of 79 patients [52%]) in the high group compared with the low group, respectively. CONCLUSION: There was a significant association between in-hospital haemoglobin decline, even without visible bleeding, and increased long-term mortality and MACCE in STEMI patients undergoing primary PCI.

Design of a Robust Flow Cytometric Approach for Phenotypical and Functional Analysis of Human Monocyte Subsets in Health and Disease.

Human monocytes can be subdivided into phenotypically and functionally different classical, intermediate and non-classical monocytes according to the cell surface expression of CD14 and CD16. A precise identification and characterisation of monocyte subsets is necessary to unravel their role in inflammatory diseases. Here, we compared three different flow cytometric strategies (A-C) and found that strategy C, which included staining against CD11b, HLA-DR, CD14 and CD16, followed by several gating steps, most reliably identified monocyte subtypes in blood samples from healthy volunteers and from patients with stable coronary heart disease (CHD) or ST-elevation myocardial infarction (STEMI). Additionally, we established a fixation and permeabilisation protocol to enable the analysis of intracellular markers. We investigated the phagocytosis of lipid nanoparticles, the uptake of 2-NBD-glucose and the intracellular levels of CD74 and HLA-DM. This revealed that classical and intermediate monocytes from patients with STEMI showed the highest uptake of 2-NBD-glucose, whereas classical and intermediate monocytes from patients with CHD took up the largest amounts of lipid nanoparticles. Interestingly, intermediate monocytes had the highest expression level of HLA-DM. Taken together, we present a robust flow cytometric approach for the identification and functional characterisation of monocyte subtypes in healthy humans and patients with diseases.

Elevated Circulatory Levels of UL16 Binding Protein 1 Positive Microparticles Are Associated With Acute Myocardial Infarction and its Severity.

BACKGROUND/AIM: Atherosclerosis is a vascular inflammatory disease characterized by the activation and stress of various inflammatory cells, leading to the development of coronary artery disease and subsequently acute myocardial infarction (AMI). Among AMI cases, ST-segment elevation myocardial infarction (STEMI) is typically more severe than non-STEMI (NSTEMI). UL16-binding proteins (ULBPs), which are NKG2D ligands, can be expressed on the surface of stressed and activated cells, prompting these cells to generate microparticles (MPs). Consequently, MPs carrying ULBPs, particularly ULBP1 (ULBP1+ MPs), may be released into the bloodstream. This study aimed to investigate the association between ULBP1+ MPs and the presence of AMI and its severity. MATERIALS AND METHODS: We recruited 58 AMI patients and 45 age-matched control subjects. Levels of ULBP1+ MPs and ULBP1+ MPs originating from T lymphocytes (ULBP1+ TMPs) were measured using flow cytometry. RESULTS: Both ULBP1+ MP and ULBP1+ TMP levels were significantly elevated in AMI patients compared to controls. Elevated levels of these MPs were independent risk factors for AMI with odds ratios (OR) of 4.3 (95%CI=1.5-12.3) for ULBP1+ MPs and 5.8 (95%CI=2.0-17.0) for ULBP1+ TMPs. Additionally, ULBP1+ TMP levels were significantly higher in STEMI patients compared to NSTEMI patients, with an independent association observed between ULBP1+ TMPs and STEMI (OR=3.9; 95%CI=1.2-12.8). CONCLUSION: Elevated levels of ULBP1+ MPs and ULBP1+ TMPs are associated with AMI and its severity. These biomarkers could serve as indicators of vulnerable plaques that lead to AMI.

Temporal trends in concordance between ICD-coded and cardiac biomarker-classified hospitalisation rates for acute coronary syndromes: a linked hospital and biomarker data study.

BACKGROUND: Since 2000, the definition of myocardial infarction (MI) has evolved with reliance on cardiac troponin (cTn) tests. The implications of this change on trends of acute coronary syndrome (ACS) subtypes obtained from routinely collected hospital morbidity data are unclear. Using person-linked hospitalisation data, we compared International Classification of Diseases (ICD)-coded data with biomarker-classified admission rates for ST-segment elevation MI (STEMI), non-STEMI (NSTEMI) and unstable angina (UA) in Western Australia (WA). METHODS: We used linked hospitalisation data from all WA tertiary hospitals to identify patients with a principal diagnosis of STEMI, NSTEMI or UA between 2002 and 2016. Linked biomarker results were classified as 'diagnostic' for MI according to established criteria. We calculated age-standardised and sex-standardised rates (ASSRs) for ICD-coded versus biomarker-classified admissions by ACS subtypes and estimated annual change in admissions using Poisson regression adjusting for age and sex. RESULTS: There were 37 272 ACS admissions in 30 683 patients (64.2% male), and 96% of cases had linked biomarker data, predominantly conventional cTn at the start and high-sensitive cTn from late 2013. Despite lower ASSRs, trends in MI classified with a diagnostic biomarker were concordant with ICD-coded admissions rates for both STEMI and NSTEMI. Between 2002 and 2010, STEMI rates declined by 4.1% (95% CI 5.0%, 3.1%) and 3.4% (95% CI 4.6%, 2.3%) in ICD-coded and biomarker-classified admissions, respectively, and both plateaued thereafter. For NSTEMI between 2002 and 2010, the ICD-coded and biomarker-classified rates increased 8.0% per year (95% CI 7.2%, 8.9%) and 8.0% (95% CI 7.0%, 9.0%), respectively, and both subsequently declined. For UA, both ICD-coded and biomarker-classified UA admission rates declined in a steady and concordant manner between 2002 and 2016. CONCLUSIONS: The present study supports the validity of using administrative data to monitor population trends in ACS subtypes as they appear to generally reflect the redefinition of MI in the troponin era.

Effects of different doses of tirofiban combined with dual antiplatelet drugs on platelet indices, vascular endothelial function, and major adverse cardiovascular events in patients with acute ST-segment elevated myocardial infarction undergoing percutaneous coronary intervention.

This trial targeted to analyze the effects of different doses of tirofiban combined with dual antiplatelet drugs on platelet indices, vascular endothelial function, and major adverse cardiovascular events (MACE) in patients with acute ST-segment elevated myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). A total of 180 patients with STEMI who underwent PCI were divided into Group A, Group B, and Group C (60 cases per group). Group A was given conventional medication, and Groups B and C were given a standard dose (10 µg/kg) and a high dose (20 µg/kg) of tirofiban on the basis of Group A, respectively. Thrombolysis in myocardial infarction (TIMI) myocardial perfusion grade and TIMI blood flow grade were compared. Myocardial enzymes, platelet indices, vascular endothelial function, inflammatory factors, and cardiac function indices were detected. In-hospital bleeding events and follow-up MACE were recorded. After PCI, Group C had a higher number of TIMI myocardial perfusion grade III and TIMI blood flow grade III versus Group A. Group C achieved the greatest changes in myocardial enzymes, platelet indices, vascular endothelial function-related factors, inflammatory factors, and cardiac function indices, followed by Group B and Group A. The incidence of bleeding events was higher in Group C than in Group A, and that of MACE in Group C was lower than in Group A. The addition of high-dose tirofiban to PCI and dual antiplatelet drugs for STEMI patients can improve myocardial blood perfusion, cardiac function, and vascular endothelial function, inhibit platelet activation and aggregation, and reduce the occurrence of MACE.

What is the context?Acute myocardial infarction is a branch of acute coronary syndromes, which can be categorized into ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction. Percutaneous coronary intervention is a non-surgical, invasive treatment used to improve blood flow to ischemic tissues and relieve coronary artery stenosis or occlusion. Despite the fact that percutaneous coronary intervention allows for timely mechanical reperfusion, patients with myocardial infarction have to face an increased risk of adverse cardiovascular events.What is the new?The addition of high-dose tirofiban to percutaneous coronary intervention and dual antiplatelet drugs for ST-segment elevation myocardial infarction patients can improve myocardial blood perfusion, cardiac function, and vascular endothelial function, inhibit platelet activation and aggregation, and reduce the occurrence of major adverse cardiovascular events.What is the impact?These findings favor the future application of tirofiban combination therapies and can improve patients' conditions alone.

Thromboinflammation is associated with clinical outcome after ST-elevation myocardial infarction.

ABSTRACT: Platelets are crucial in thrombus formation during ST-elevation myocardial infarction (STEMI). In addition, they also play an important role in postischemic thromboinflammation, which is determined by the interplay between activated platelets and neutrophils. The latter form neutrophil extracellular traps, which are detectable in plasma as citrullinated histone H3-deoxyribonucleic acid-DNA complexes. Prediction of the risk of recurrent events is important in precision medicine. Therefore, we investigated whether circulating thromboinflammatory markers predict clinical outcome after STEMI. We performed a prospective, multicentric, observational, all-comer study of patients with STEMI (n = 361). Thromboinflammation, measured as H3Cit-DNA complexes, was assessed on day 1 after presentation with STEMI as well as 5 days and 6 months after STEMI by enzyme-linked immunosorbent assay. Twelve months of clinical follow-up was conducted. Multivariate analysis was performed investigating which variables were independently associated with major adverse cardiac events (MACEs). Patients were aged 64 ± 12 years; 80% were male; and 40% had diabetes mellitus. Thromboinflammation was enhanced during index hospitalization compared with 6-months follow-up (137.4 ± 100.0 µg/L vs 53.7 ± 54.7 µg/L; P < .001). Additionally, patients within the highest tertile of thromboinflammation at day 1 after STEMI showed worse outcome during follow-up (hazard ratio, 2.57; 95% confidence interval, 1.72-3.85; P < .001). Receiver operating characteristic analysis revealed a cutoff value of 219.3 µg/L. In multivariate logistic regression analysis, thromboinflammation was independently associated with outcome after STEMI. To sum it up, thromboinflammation is enhanced in STEMI. It identifies patients at high risk of MACE. Therefore, thromboinflammation might be a promising target and marker in precision medicine. The trial was registered at www.clinicaltrials.gov as #NCT03539133.

Association between peak troponin level and prognosis among patients admitted to intensive cardiovascular care unit.

INTRODUCTION: High-sensitivity cardiac troponin (hs-cTn) is a key biomarker for myocardial injury, yet its prognostic value in intensive cardiovascular care units (ICCU) remains poorly understood. We aimed to assess the association between peak hs-cTn levels and prognosis in ICCU patients. METHODS: All patients admitted to a tertiary care center ICCU between July 2019 - July 2023 were prospectively enrolled. Patients were divided into five groups according to their peak hs-cTnI levels: A) hs-cTnI <100 ng/L; B) hs-cTnI of 100-1000 ng/L; C) hs-cTnI of 1000-10,000 ng/L; D) hs-cTnI of 10,000-100,000 ng/L and E) hs-cTnI ≥100,000 ng/L. The primary outcome was all-cause mortality at one year. RESULTS: A total of 4149 patients (1273 females [30.7 %]) with a median age of 69 (IQR 58-79) were included. Group E was highly specific for myocardial infarction (97.4 %) and especially for ST segment elevation myocardial infarction (STEMI) (87.5 %). Patients in group E were 56 % more likely to die at 1-year in an adjusted Cox model (95 % CI 1.09-2.23, p = 0.014) as compared with group A. Subgroup analyses revealed that among STEMI patients, higher peak hs-cTnI levels were not associated with higher mortality rate (HR 1.04, 95 % CI 0.4-2.72, p = 0.9), in contrast to patients with NSTEMI (HR 7.62, 95 % CI 1.97-29.6, p = 0.003). CONCLUSIONS: Peak hs-cTnI levels ≥100,000 ng/L were linked to higher one-year mortality, largely indicative of large myocardial infarctions. Notably, the association between elevated hs-cTnI levels and mortality differed between STEMI and NSTEMI patients, warranting further investigation.

Kinetics and Prognosis Value of CCL5/RANTES at the Acute Phase of ST-Segment-Elevation Myocardial Infarction.

BACKGROUND: RANTES (regulated upon activation, normal T cell expressed, and secreted) or CCL5 (CC chemokine ligand 5) is a chemokine that mediates chemotaxis and activation of T cells, monocytes, mast cells, and dendritic cells. It is involved in the pathogenesis of several diseases, including atherosclerosis, but its role at the acute phase of myocardial infarction (MI) is unclear. Our objective is to determine whether the serum level of RANTES is a marker of the severity of acute MI. METHODS AND RESULTS: The study included 250 consecutive patients with ST-segment-elevation MI who underwent percutaneous coronary intervention in a prospective cohort. Peripheral venous blood samples were taken at 5 time points and ELISA was performed. Major adverse cardiovascular events were prospectively recorded over the 12-month follow-up. Serum RANTES level raised from 12.9 (8.0-20.7) ng/mL at H0 to 13.9 (7.4-22.4) ng/mL at H4 and decreased gradually until 1 month at 9.7 (5.4-13.6) ng/mL (P<0.0001). RANTES area under the curve (AUC) level was not correlated with infarct size (r=-0.03, P=0.70) or left ventricular ejection fraction assessed by magnetic resonance imaging (r=0.02, P=0.80). Patients with a RANTES AUC serum level below the first tertile value of the population (411.0 ng.h.mL-1) were more likely to have a major adverse cardiovascular event during the first 12 months after ST-segment-elevation MI (hazard ratio [HR], 2.9 [1.3-6.6], P=0.01). In a multivariable Cox regression analysis, serum level below the first tertile remained associated with an increased risk of experiencing major adverse cardiovascular event during the follow-up (adjusted HR, 2.6 [1.2-5.8], P=0.02). CONCLUSIONS: A low level of circulating RANTES post ST-segment-elevation MI was associated with an increased risk of experiencing major adverse cardiovascular event and might be a valuable prognostic marker in patients with ST-segment-elevation MI.

Establishment and validation of a nomogram model containing a triglyceride-glucose index and neutrophil-to-high-density lipoprotein ratio for predicting major adverse cardiac events in patients with ST-segment elevation myocardial infarction.

OBJECTIVE: To analyze the predictive value of the triglyceride-glucose (TyG) index and neutrophil-to-high-density lipoprotein ratio (NHR) for in-hospital major adverse cardiac events (MACE) after percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI), and to establish an associated nomogram model. METHODS: In this retrospective study, we collected data from consecutive STEMI patients who underwent PCI from October 2019 to June 2023 at the Second People's Hospital of Hefei and the Second Affiliated Hospital of Anhui Medical University, as training and validation sets. Stepwise regression and multivariate logistic regression analysis were performed to screen independent risk factors, and a nomogram model was constructed and evaluated for its predictive efficacy. RESULTS: The TyG index, NHR, urea, diastolic blood pressure, hypertension, and left ventricular ejection fraction were independent risk factors for in-hospital MACE after PCI, and were used to construct the nomogram model. The C-index of the training and validation sets were 0.799 and 0.753, respectively, suggesting that the model discriminated well. Calibration and clinical decision curves also demonstrated that the nomogram model had good predictive power. CONCLUSION: In STEMI patients, increased TyG index and NHR were closely related to the occurrence of in-hospital MACE after PCI. Our constructed nomogram model has some value for predicting the occurrence of in-hospital MACE in STEMI patients.

Intestinal fatty acid binding protein is associated with infarct size and cardiac function in acute heart failure following myocardial infarction.

BACKGROUND: In acute heart failure (HF), reduced cardiac output, vasoconstriction and congestion may damage the intestinal mucosa and disrupt its barrier function. This could facilitate the leakage of bacterial products into circulation and contribute to inflammation and adverse cardiac remodelling. We aimed to investigate gut leakage markers and their associations with inflammation, infarct size and cardiac function. METHODS: We examined 61 ST-elevation myocardial infarction (STEMI) patients who developed acute HF within 48 hours of successful percutaneous coronary intervention (PCI). Serial blood samples were taken to measure lipopolysaccharide (LPS), LPS-binding protein (LBP), soluble cluster of differentiation 14 (sCD14) and intestinal fatty acid binding protein (I-FABP). Cumulative areas under the curve (AUCs) from baseline to day 5 were calculated. Serial echocardiography was performed to assess left ventricular ejection fraction (LVEF), global longitudinal strain (GLS) and wall motion score index (WMSI). Single-photon emission CT (SPECT) was performed at 6 weeks to determine infarct size and LVEF. RESULTS: I-FABPAUC correlated positively with infarct size (rs=0.45, p=0.002), GLS (rs=0.32, p=0.035) and WMSI (rs=0.45, p=0.002) and negatively with LVEF measured by SPECT (rs=-0.40, p=0.007) and echocardiography (rs=-0.33, p=0.021) at 6 weeks. LPSAUC, LBPAUC and sCD14AUC did not correlate to any cardiac function marker or infarct size. Patients, who at 6 weeks had above median GLS and WMSI, and below-median LVEF measured by SPECT, were more likely to have above median I-FABPAUC during admission (adjusted OR (aOR) 5.22, 95% CI 1.21 to 22.44; aOR 5.05, 95% CI 1.25 to 20.43; aOR 5.67, 95% CI 1.42 to 22.59, respectively). The same was observed for patients in the lowest quartile of LVEF measured by echocardiography (aOR 9.99, 95% CI 1.79 to 55.83) and three upper quartiles of infarct size (aOR 20.34, 95% CI 1.56 to 264.65). CONCLUSIONS: In primary PCI-treated STEMI patients with acute HF, I-FABP, a marker of intestinal epithelial damage, was associated with larger infarct size and worse cardiac function after 6 weeks.

Predictive value of platelet-to-albumin ratio combined with the C2HEST score for New-Onset atrial fibrillation in elderly patients with acute ST-segment elevation myocardial infarction.

BACKGROUND: New-onset atrial fibrillation (NOAF) is a common adverse outcome in acute ST-segment elevation myocardial infarction (STEMI) patients following percutaneous coronary intervention (PCI) and is associated with a worse prognosis. The platelet-to-albumin ratio (PAR) has been utilized to predict the severity and prognosis of cardiovascular diseases. This study aims to investigate the predictive value of PAR combined with the C2HEST score for NOAF in the elderly population with STEMI undergoing PCI. METHODS: 445 elderly STEMI patients without a history of atrial fibrillation (AF) who underwent PCI were consecutively enrolled in this study. Multivariate logistic regression analysis was used to identify independent risk factors for NOAF after PCI. RESULTS: 50 patients (11.2%) developed NOAF after PCI. Multivariate logistic regression analysis revealed that heart rate (HR), systemic immune-inflammation index (SII), uric acid (UA), PAR, and C2HEST score were independent risk factors for NOAF. The area under the curve (AUC) of the combined PAR and C2HEST score was 0.839, and Delong's test indicated that the combined model had superior predictive value compared to individual markers (AUC of PAR: 0.738; AUC of C2HEST score: 0.752) (P < 0.05). The addition of PAR and C2HEST score to this model (HR, SII, and UA) significantly improved the reclassification and discrimination ability (IDI 0.175; NRI 0.734, both P < 0.001). During regular follow-up, the incidence of MACE was higher in the NOAF group compared to the non-NOAF group. CONCLUSION: The combination of PAR and the C2HEST score has a high predictive value for NOAF in elderly STEMI patients following PCI.

Senescent CD4+ T-Cell Phenotypes and Inflammatory Milieu in the Coronary and Systemic Circulation in ST-Elevation Myocardial Infarction: An Exploratory Study.

INTRODUCTION: In ST-elevation myocardial infarction (STEMI), inflammation is pivotal, with early senescent CD4+CD28null cells implicated in its pathogenesis. However, the functional phenotype of these cells within the coronary circulation remains unclear. METHODS: We examined CD4+ cell subpopulations in blood samples from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of seven healthy controls. RESULTS: Our findings revealed reduced CD4+ cell counts in STEMI patients compared to controls (1,998, 1,275-3,268 vs. 4,278, 3,595-4,449), alongside an increased proportion of CD4+ cells lacking CD28 expression (20.1 vs. 6.1%). These CD4+CD28null cells in STEMI predominantly exhibited a Th1 phenotype (47.8% vs. 6.6%). Intriguingly, no significant differences were detected in CD4+CD28null cells between coronary sinus and vena cava, and cytokine levels in these compartments remained similar. CONCLUSION: CD4+CD28null cells are increased in STEMI, mainly polarized toward a Th1 phenotype, and distributed equally between the different vascular beds.

The association between HbA1c/C-peptide levels and short-term mortality in patients diagnosed with myocardial infarction.

Introduction: In this study, we aimed to investigate the effect of HbA1C/C-peptide ratio on short-term mortality (this period is defined as 30 days after diagnosis) in the patients with myocardial infarction.Materials & Methods: Around 3245 patients who were admitted due to ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction underwent primary percutaneous coronary intervention between October 2020 and 2024 were included in this study.Results: In the receiver operating characteristic analysis, the predictive power of the HCR score for mortality in ST-elevation myocardial infarction patients was determined to be 83% sensitivity and 81% specificity. In non-ST-elevation myocardial infarction, this was determined to be 78% sensitivity and 75% specificity.Conclusion: The HbA1C/C-peptide ratio score can predict poor clinical outcomes early, reducing mortality and morbidity in patients with myocardial infarction.

[Box: see text].

Association of fibrotic markers with diastolic function after STEMI.

Galectin-3 and Suppression of tumorigenicity-2 (ST2) are known markers of cardiac fibrosis. We investigated the prognostic value of fibrotic markers for the development of diastolic dysfunction and long-term outcome in patients suffering an ST-elevated myocardial infarction (STEMI). We analyzed 236 patients from the GIPS-III cohort with available echocardiographic studies and plasma measurements at hospitalization and after 4 months follow-up. Adjusted logistic mixed effects modelling revealed no association between the occurrence of diastolic dysfunction over time with abnormal plasma levels of galectin-3 and ST2. We observed no differences regarding survival outcome at follow-up of 5 years between patients with normal versus abnormal values in both galectin-3 (P = 0.75), and ST2 (P = 0.85). In conclusion, galectin-3 and sST2 were not associated with the development of diastolic dysfunction in non-diabetic patients that presented with a STEMI.

Circular RNA Profile in Atherosclerotic Disease: Regulation during ST-Elevated Myocardial Infarction.

Circular (circ) RNAs are non-coding RNAs with important functions in the nervous system, cardiovascular system, and cancer. Their role in atherosclerosis and myocardial infarction (MI) remains poorly described. We aim to investigate the potential circRNAs in immune cells during atherogenesis and examine the most regulated during MI and the modulation by interleukin (IL)-6 receptor inhibition by tocilizumab. Wild-type (WT) and ApoE-/- mice were fed an atherogenic diet for 10 weeks, and the circRNA profile was analyzed by circRNA microarray. Whole blood from patients with ST-elevated MI (STEMI) and randomized to tocilizumab (n = 21) or placebo (n = 19) was collected at admission, 3-7 days, and at 6 months, in addition to samples from healthy controls (n = 13). Primers for human circRNA were designed, and circRNA levels were measured using RT-qPCR. mRNA regulation of predicted circRNA targets was investigated by RNA sequencing. The expression of 867 circRNAs differed between atherogenic and WT mice. In STEMI patients, circUBAC2 was significantly lower than in healthy controls. CircANKRD42 and circUBAC2 levels were inversely correlated with troponin T, and for circUBAC2, an inverse correlation was also seen with final infarct size at 6 months. The predicted mRNA targets for circUBAC2 and circANKRD42 were investigated and altered levels of transcripts involved in the regulation of inflammatory/immune cells, apoptosis, and mitochondrial function were found. Finally, tocilizumab induced an up-regulation of circANKRD42 and circUBAC2 3-7 days after percutaneous coronary intervention. CircRNA levels were dysregulated in STEMI, potentially influencing the immune system, apoptosis, and mitochondrial function.

Evaluation of a nomogram model for predicting in-hospital mortality risk in patients with acute ST-elevation myocardial infarction and acute heart failure post-PCI.

OBJECTIVES: This study aims to identify the risk factors contributing to in-hospital mortality in patients with acute ST-elevation myocardial infarction (STEMI) who develop acute heart failure (AHF) post-percutaneous coronary intervention (PCI). Based on these factors, we constructed a nomogram to effectively identify high-risk patients. METHODS: In the study, a collective of 280 individuals experiencing an acute STEMI who then developed AHF following PCI were evaluated. These subjects were split into groups for training and validation purposes. Utilizing lasso regression in conjunction with logistic regression analysis, researchers sought to pinpoint factors predictive of mortality and to create a corresponding nomogram for forecasting purposes. To evaluate the model's accuracy and usefulness in clinical settings, metrics such as the concordance index (C-index), calibration curves, and decision curve analysis (DCA) were employed. RESULTS: Key risk factors identified included blood lactate, D-dimer levels, gender, left ventricular ejection fraction (LVEF), and Killip class IV. The nomogram demonstrated high accuracy (C-index: training set 0.838, validation set 0.853) and good fit (Hosmer-Lemeshow test: χ2 = 0.545, p = 0.762), confirming its clinical utility. CONCLUSION: The developed clinical prediction model is effective in accurately forecasting mortality among patients with acute STEMI who develop AHF after PCI.