bluuebunny/crossref_metadata_2025 huggingface dataset:
The impact of smoking status on platelet reactivity and its association on clinical outcomes in east asian AMI patients with stent implantation
Authors: Song Z Y , Kim M H , Lee K M , Jin X , Yuan S L , Youk G S , Jung A H
Published: November 2023

Background

Smoking is one of the major risk factors as well as prognostic factors for cardiovascular disease including AMI.

Purpose

We sought to investigate the impact of smoking on major adverse cardiac and cerebrovascular events (MACCE) in AMI patient with stent implantation and also, we tried to confirm the issue’s of Smoker's paradox.

Methods

The multicenter PTRG-DES (Platelet function and geno Type-Related long-term proGnosis in DES-treated patients) consortium is a multicenter, real-world registry of patients who underwent PCI with DES and received DAPT of aspirin and clopidogrel in South Korea. We assessed PRUs as continuous and categorical measures. Additionally, the cutoff of HPR to ADP was defined as ≥ 252 PRU according to the time-dependent receiver-operating characteristic (ROC) curve analysis for East Asian patients. In this present analysis, smoking patients was defined according to data recorded at the time of admission. The primary outcome was the occurrence of major adverse cardiac and cerebrovascular events (MACCE) were evaluated at 5-year follow-up.

Results

The 3,285 patients (28.0%) were smoker, and 4,001 patients (34.2%) were HPR patients. Smoker significantly increased the risk of death (HR=1.302 [95% CI: 1.019-1.664]), but did not increase the risk of MACCE. In smoking patients, HPR phenotype was significant association with MACCE (HR=1.532 [95% CI: 1.139-2.061]), death (HR=1.995 [95% CI: 1.335-2.983]), stent thrombosis (HR=3.986 [95% CI: 1.559-10.193]), in non-smoker patients, HPR was significantly associated with stent thrombosis (HR=3.018 [95% CI:1.591-5.726]).

Conclusion

Smoking was significantly associated with 5-year risks of all-cause death and MACCE. Smoking exaggerate HPR effect on MACCE. However, the smoker’s paradox was not observed in our study.
Incidence and outcomes of type 2 myocardial infarction: a cohort study of a national population-based registry
Authors: Ho J S Y , Zheng H , Ho A F W , Foo D , Foo L L , Lim P Z Y , Liew B W , Chua T , Hausenloy D J , Yeo T C , Tan H C , Yip J W L , Chai P , Chan M Y Y , Sia C H
Published: November 2023

Background/introduction

Type 2 myocardial infarction (T2MI), caused by myocardial oxygen supply/demand mismatch without acute thrombotic plaque disruption, makes up 2-25% of reported MI. T2MI may be triggered by conditions such as arrhythmias, anaemia, sepsis, heart failure, but the incidence, outcomes and predictors of poor outcomes post-T2MI requires further study.

Aims

In this study, we characterised the incidence, outcomes and predictors of poor outcomes in T2MI in Singapore.

Methods

We performed an ambidirectional cohort study of 10720 consecutive T2MI patients from January 2012 to December 2018 from the national Singapore MI Registry (SMIR). The primary outcome was major adverse cardiovascular events (MACE; composite of MI, stroke and mortality) within 30 days and 1 year. The secondary outcomes were all-cause mortality, cardiovascular death and stroke.

Results

Of 10,724 patients with T2MI, 3852 (35.9%) had MACE within 30 days and 5947 (51.4%) had MACE within 1 year (Table 1). The incidence of T2MI increased from 20 per 100,000 residents in 2012 to 80 per 100,000 residents in 2017 (Figure 1A). Significant independent predictors of MACE at 30 days on multivariable analysis include age (hazard ratio [HR] 1.01, 95% confidence interval (CI) 1.00-1.01), history of hypertension (HR 1.23, 95% CI 1.06-1.42) or diabetes mellitus (HR 1.32, 95% CI 1.17-1.48), Killip classes 2-4 and left ventricular ejection fraction <50% during hospitalization. Low hemoglobin (Hb) 8-9 (HR 1.42, 95% CI 1.07-1.88) and 10-11 (HR 1.36, 95% CI 1.05-1.76) compared to Hb 14-15, were predictors of MACE at 30 days and Hb <13 showed significant associated with MACE at 1 year. Hb <12 was also significantly associated with all-cause mortality at 1 year, but not cardiovascular death or stroke. Significant predictors of stroke at 1 year included current smoking (HR 1.53, 95% CI 1.04-2.23) and atrial fibrillation (AF) (HR 1.54, 95% CI 1.21-1.97). Troponin levels were not significantly associated with MACE at 30 days or 1 year.

Conclusions

The incidence of T2MI has been increasing since 2012, with generally poor outcomes within 1 year. Predictors of poor outcomes include age, history of cardiovascular risk factors, AF, reduced LVEF during hospitalization, and low hemoglobin. A higher target Hb may be needed post-T2MI, and further research is needed to establish this.
Point-of-care biomarkers of thrombotic status predict spontaneous reperfusion in ST-segment elevation MI and clinical outcomes
Authors: Kanji R , Gue Y X , Memtsas V , Spencer N H , Gorog D A
Published: November 2023

Background

Spontaneous reperfusion, seen in ∼20% of patients with ST-segment elevation myocardial infarction (STEMI), manifests as normal epicardial flow in the infarct-related artery (IRA), with or without ST-segment resolution, before percutaneous coronary intervention (PCI). The drivers mediating this are unknown.

Purpose

We aimed to assess whether the thrombotic profile of patients with and without spontaneous reperfusion differed significantly, and whether such patients had better outcomes.

Methods

We performed a prospective, observational study in consecutive patients presenting with STEMI. Blood samples were taken from a 6 Fr arterial sheath immediately before emergency angiography, before PPCI, after dual antiplatelet therapy loading, but before the administration of heparin or other anticoagulant. Blood samples were tested using a point-of-care global test of thrombotic status, measuring occlusion (OT) and endogenous fibrinolysis (LT) times. Spontaneous reperfusion was defined as IRA TIMI III flow pre-PCI. Patients were followed for major cardiovascular events (MACE; death, myocardial infarction, stroke).

Results

Spontaneous reperfusion was associated with longer OT (435s vs. 366s, p<0.001) and shorter LT (1257s vs. 1616s, p<0.001), lower troponin and better LV function. LT was superior to OT for predicting spontaneous reperfusion (AUC for LT: 0.707, 95% CI 0.661-0.753; AUC for OT: 0.629, 95% CI 0.581-0.677). Amongst patients with spontaneous reperfusion, those with complete, versus partial ST-segment resolution, had longer OT (p=0.002) and shorter LT (p<0.001). Spontaneous reperfusion was unrelated to clinical characteristics or pain-to-angiography times.

Over 4-years, patients with spontaneous reperfusion experienced fewer MACE than those without (4.1% vs. 10.6%, p=0.013), especially in those with both spontaneous reperfusion and complete ST-segment resolution (1.5% vs. 10.1%, p=0.029).

Conclusions

We demonstrate a novel haematological signature in STEMI patients with spontaneous reperfusion, namely reduced platelet reactivity and faster endogenous fibrinolysis, relating to smaller infarcts and improved survival. This indicates a role for modulating thrombotic status early following STEMI-onset, to facilitate spontaneous reperfusion and improve outcomes.Visual abstractThrombotic profile predicts outcome
Association of inflammatory activation with acute stent thrombosis
Authors: Krychtiuk K A , Braeu K , Schauer S , Sator A , Galli L , Gangl C , Roth C , Hengstenberg C , Lang I M , Berger R , Speidl W S
Published: November 2023

Background

Acute stent thrombosis (ST) is a rare but deleterious event. Acute infection and inflammation may lead to activation of the coagulation system and of platelets. Coronary angiography with stent implantation is often deferred because of increased inflammatory markers.

Purpose

The aim of this study was to investigate whether an acute inflammatory state is associated with increased risk of early stent thrombosis.

Methods

Within a prospective single-center registry, the association between pre-procedural acute inflammatory activation, defined as C-reactive protein (CRP) plasma levels >5mg/dL or leukocytes >12 G/L, and occurrence of early stent thrombosis within 30 days after PCI was evaluated.

Results

We included 11327 patients that underwent coronary stenting. 3964 (35%) were treated for acute coronary syndrome (ACS) and 7363 (65%) had chronic coronary artery disease. The number of definite early ST within 30 days was 91 (0.8 %). Leukocyte count and plasma levels of C-reactive protein (CRP) were available in 6880 patients (87 patients with ST). 1715 patients showed signs of an acute inflammatory state as defined by a leukocyte count > 12 G/L or plasma levels of CRP > 5mg/dL. Stent implantation in patients with acute inflammation was associated with significant increased risk for ST (HR 3.01; p<0.0000001) independent of age, gender, kidney function, number and type of stents, presence of multivessel disease, choice of P2Y12 inhibitor and clinical presentation. This was the case in patients with (HR 2.48; p<0.001) and without acute coronary syndromes (HR 3.59; p<0.001). The incidence of ST in patients with ACS with and without signs of inflammation was 2.7% vs. 1.1% (p<0.001) and in patients with chronic coronary artery disease with and without inflammation was 2.3% vs 0.7% (p<0.001)

Conclusions

An acute inflammatory state as defined by a leukocyte count > 12 G/L or plasma levels of CRP > 5mg/dL at time of stent implantation was associated with a significant increased risk of acute ST. In particular in patients with chronic coronary artery disease acute inflammatory activation should lead to a deferral of elective interventions. In patients with ACS and increased inflammatory parameters, in which acute PCI is mandatory, future studies are needed, whether more intensive therapy could reduce risk of early ST in this particular high-risk cohort.
Analysis of immune infiltration and cuproptosis-related genes in acute myocardial infarction
Authors: Xiao Y , Pan R J , An Z H , Liu Q M , Zhou S H
Published: November 2023

Background

Acute myocardial infarction (AMI) is a major global health concern. The identification of key genes associated with AMI and cuproptosis is crucial for developing effective diagnostic and prognostic tools.

Purpose

To identify differentially expressed genes (DEGs) associated with AMI, and investigate their correlation with cuproptosis and immune infiltration to improve diagnosis and prognosis.

Methods

Six datasets (GSE48060, GSE83500, GSE97320, GSE974, GSE19339, and GSE66360) containing normal control and AMI samples were integrated from the Gene Expression Omnibus (GEO) database. DEGs between AMI and control samples were identified and cross-referenced with ferroptosis-associated genes. GO and KEGG analyses were performed to explore the functions and pathways associated with the identified genes. Immune infiltration analysis was also conducted to investigate the correlation between the genes and immune infiltration. An AMI prediction model was constructed using statistical analysis.

Results

Fifteen DEGs were identified, including nine upregulated and six downregulated genes. Among these genes, 11 were found to be associated with cuproptosis, including SLC31A1, PDHB, PDHA1, LIPT1, LIAS, FDX1, DLS1, DLD, DLAT, DBT, and ATP7B. These genes were mainly enriched in the TCA cycle, pyruvate metabolism, glycolysis/gluconeogenesis, and carbon metabolism pathways. Immune infiltration analysis revealed significant differences in macrophages, Th1 cells, Th2 cells, tumor-infiltrating lymphocytes, cytolytic activity, and MHC class 1 between normal and AMI samples. A correlation between these genes and immune infiltration was also observed. The AMI prognostic model constructed had an AUC of 0.61047.

Conclusion

Cuproptosis-related genes (SLC31A1, PDHB, PDHA1, LIPT1, LIAS, FDX1, DLS1, DLD, DLAT, DBT, and ATP7B) may play significant roles in AMI and its immune infiltration. The identified genes and pathways could potentially serve as biomarkers for improving the diagnosis and prognosis of AMI.Flow chart of research designCuproptosis-related AMI genes
In patients with acute myocardial infarction interleukin-8 levels are related to impaired renal function and predict recurrent infarction or death at 1-year follow-up - a case-control study
Authors: Wang Y , Matter M A , Rossi V A , Heg D , Costantino S , Staehli B E , Raeber L , Windecker S , Mach F , Gencer B , Rodondi N , Nanchen D , Levesque M , Ruschitzka F , Matter C M
Published: November 2023

Introduction

Acute myocardial infarction (AMI) induces a surge of inflammatory cytokines. IL-8, secreted by endothelial cells and monocyte-macrophages, rapidly recruits immune cells to the infarcted tissue. Previous studies in chronic kidney disease reported IL-8 to be associated with an increased inflammatory burden. Little is known about the diagnostic and prognostic value of IL-8 plasma levels in patients with AMI.

Purpose

We aimed to explore the diagnostic and prognostic value of IL-8 plasma levels in AMI patients.

Methods

Patients with AMI (STEMI and NSTEMI) were included from the SPUM-ACS cohort selecting a time window <24 h from symptom onset to blood sampling before PCI. Patients with malignancies or on immunosuppressive therapies were excluded. 160 patients with recurrent AMI or death within 1-year follow-up (cases) were compared to 160 counterparts with favorable outcome matched for age, sex, AMI subtype, and pain onset time (controls). 45 healthy blood donors (HD) without cardiovascular disease were added as an age- and sex-matched reference group. Heparin-plasma was used for Mesoscale U Plex cytokine analyses. The median and interquartile ranges (IQR) were compared using the non-parametric Kruskal-Wallis test. Relation of baseline characteristics to IL-8 levels within cases and controls was assessed with linear regression analyses. Kaplan-Meier curves were computed, selecting the cut-off value in consideration of the overall median IL-8 level.

Results

Cases (median=59.5, IQR=112.0 pg/mL) showed higher IL-8 plasma levels than HD (median=38.6, IQR=25.1 pg/mL, p=0.0006, Figure 1). Cases also had higher plasma IL-8 levels compared to controls (median=41.2, IQR=51.7 pg/mL, p=0.0006, Figure 1). Considering the median IL-8 level (50.1 pg/ml) as cut-off, cases with higher IL-8 had higher rates of recurrent MI or all-cause death than those with lower IL-8 levels within one year (log-rank p=0.002, Figure 2) with divergence between the subgroups seen early within the first two months. After correction for possible confounding factors (BMI, hypertension history, dyslipidaemia, diabetes, smoking, use of statins, LDL, Troponin, LVEF, and NT-proBNP), eGFR (estimated glomerular filtration rate) remained the only predictor for increased IL-8 (SRC: -0.178, p=0.016) in AMI patients.

Conclusions

In patients with AMI increased IL-8 levels predict subsequent MI or death at one-year follow-up. Lower eGFR is related to elevated IL-8 levels. Patients with AMI may thus profit from early IL-8 blocking therapies, particularly in the setting of impaired renal function.
Heterogeneity of plaque burden natural history within individual human coronary atherosclerotic plaques is based on local endothelial shear stress: insights for culprit areas and clinical events
Authors: Wentzel J J , Papafaklis M , Antoniadis A , Takahashi S , Cefalo N , Cormier M , Saito S , Coskun A , Stone P H
Published: November 2023

Background

Patterns of local endothelial shear stress (ESS) are heterogeneous along the course of individual coronary artery plaques. It is unknown how this heterogeneity affects the local natural history of plaque burden (PB) over time.

Objectives

To determine the effect of local ESS patterns along the course of coronary plaques at baseline on the heterogeneity of subsequent PB progression, regression, and quiescence in human coronary arteries and its link to clinical events.

Methods

302 patients from the PREDICTION study were included in the study. The PREDICTION study was an anatomic natural history followup study of patients treated for an acute coronary syndrome (ACS) performed in 15 Japanese clinical sites, as previously published [1]. Invasive imaging was performed at baseline and, per protocol, at 6-10 months follow-up. Arterial geometry and ESS were derived from angiography/intravascular ultrasound-based vascular profiling. Plaques were identified as regions with plaque thickness > 0.5 mm in at least 3 consecutive 3-mm segments. Plaque progression was defined as change in PB (plaque area/total vessel area*100%) PB >+5% increase, regression as <-5% decrease, and quiescence as no change. The location of each sequential 3-mm segment along the plaque was related to the minimum lumen area (MLA). Performance of PCI in followup was assessed relative to the magnitude of PB change over time.

Results

661 plaques (5,658 3-mm segments) from 591 coronary arteries were identified. 56% of 3-mm segments per plaque manifested PB progression, 60% PB regression, and 96% quiescence, and the presence and number of these PB changes were significantly related to plaque length (p<0.002). PB change >20% was associated with low ESS (0.75±0.31 Pa) and marked regression (PB change <-20%) with high ESS (3.94±0.04 Pa) (p<0.001, Figure 1 right panel). 3-mm segments exhibiting substantial PB progression were located along the full length of the plaque, and seldom at the MLA (p=0.874, (Figure 1 left panel), while substantial PB regression was significantly located at the MLA (p<0.001). With increasing ∆PB progression in individual 3-mm segments, a significant increase in performance of PCI was observed (p=0.012, Figure 2).

Conclusions

PB natural history of 3-mm segments within an individual plaque is heterogeneous, driven by local ESS, with substantial plaque progression/luminal encroachment developing along the entire course of the plaque, and typically not near the MLA. PCI was associated with the magnitude of PB progression/luminal encroachment, regardless of where the progression occurred.Figure 1Figure 2
Triglyceride levels predict high-risk coronary artery plaque progression in asymptomatic patients with type 2 diabetes and normal LDL cholesterol
Authors: Heinsen L J , Pararajasingam G , Andersen T , Auscher S , Sheta H , Lambrechtsen J , Egstrup K
Published: November 2023

Background

Type 2 diabetes mellitus (T2D) is associated with an increased risk of coronary artery disease (CAD) and a significant residual risk remains despite management of conventional risk factors.

Purpose

The purpose of the present study was to assess the association of triglycerides and high-risk plaque progression in patients with asymptomatic T2D without known CAD.

Methods

Asymptomatic patients with T2D and no history of CAD were studied with serial computed tomography angiography with an inter-scan interval of 13 ± 0.8 months. The total atheroma volume (TAV), and plaque composition (dense calcium, fibrous, fibrous-fatty, and necrotic core plaque) were assessed at baseline and at follow-up. Lipid status was assessed at baseline and after a one-year follow-up. Patients were divided into two groups depending on progression in triglyceride (TG) levels (TG+) and regression of TG levels (TG-).

Results

Of the 261 patients who were enrolled, 209 patients (157 men and 52 women) were included in the final analysis. Based on changes in TG levels, 107 patients were categorized as (TG+) and 102 patients were categorized as (TG-). The mean age was 62 ± 10 years, and the mean diabetes duration was 11 ± 8 years. At baseline, 76 % of the patients received lipid-lowering treatment, and low-density lipoprotein (LDL) cholesterol was 2.0 ± 0.8 mmol/L. A significantly higher progression of TAV was observed in patients with TG+ compared to TG- (50.2 ± 144.3 vs. -28.5 ± 176.9 mm3, P<0.001). This observation was primarily driven by an increase of fibrous fatty plaque (8.6 ± 41.2 vs. -12.8 ± 39.2 mm3, P<0.001) and necrotic core plaque (-3.9 ± 51.4 vs. -23.7 ± 71.8 mm3, P=0.002). Furthermore, an increase in TG levels predicted rapid plaque progression independent of LDL and other risk factors (OR 1.36, 95% CI; 1.02 – 1.81, P=0.04).

Conclusion

Changes in TG levels are associated with the progression of total and high-risk plaque volumes in asymptomatic patients with T2D and well-controlled LDL cholesterol.Low attenuation plaque vs. triglycerides
Influence of wall shear and structural stress on plaque progression of different phenotype in human coronary arteries
Authors: Wentzel J J , Tziotziou A , Hartman E , Korteland S , Van Der Steen A F W , Daemen J , Akyildiz A
Published: November 2023

Introduction

Atherosclerotic plaque progression is affected by local wall shear stress (WSS), .i.e. the frictional force of the blood at the vessel wall [1,2]. However, the blood pressure also induces stress inside the vessel wall (wall stress, WMS) and is mainly studied for plaque rupture [3]. Little is known on the impact of WMS on plaque progression.

Purpose

In order to have a comprehensive understanding of the involvement of the biomechanical factors (WSS and WMS) in atherosclerotic artery disease, we studied the individual and combined effects of WMS and WSS in plaque free as well as in atherosclerotic coronary segments.

Methods

Forty non-stented, non-culprit human coronary arteries (IMPACT study) were imaged with near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) at the baseline and after 12 months [3]. The 2D and 3D lumen, vessel wall and lipid-rich necrotic core (LRNC) geometries were reconstructed based on the co-registration of NIRS-IVUS and OCT. WSS was computed with Computational Fluid Dynamics [3]. The WMS on the peri-luminal region was calculated via ABAQUS with hyperelastic material models [4] using intraluminal pressure of 120mmHg. The vessels were divided into 1.5mm/45° sectors. In each sector wall growth was quantified as plaque burden (plaque area/total vessel area*100%) change over time. Plaque was defined as wall thickness > 0.5 mm. The sectors were categorized as "plaque with lipid rich necrotic core (LRNC)", "plaque w/o lipid rich necrotic core (LRNC)", or "plaque free wall". The individual and combined effect of WSS and WMS on plaque progression was evaluated using Linear Mixed Model in SPSS and all stress metrics were divided into artery-based tertiles.

Results

Vessel sectors exposed to low WSS at baseline demonstrated a higher plaque burden increase over the follow up period compared to the vessel sectors exposed to mid or high WSS (Fig.1), which was significantly different for all the 3 categories (Plaque free wall, Plaque without LRNC, Plaque with LRNC). Vessel sectors exposed to increasing WMS demonstrated increasing plaque progression (Fig.1) Sectors that were simultaneously exposed to low WSS and high WMS revealed the highest change in plaque size and in particular in plaque sectors that were lipid rich (Fig.2).

Conclusion

Our findings suggest that the local atherosclerotic disease progression in coronary arteries is not only associated with the well-known WSS, but also with WMS. Moreover, our results show that there is an complex interplay between WSS, WMS and plaque composition, such that lipid rich plaques exposed to low WSS and high WMS demonstrated the highest plaque progression.Figure 1Figure 2
A long-term prognostic factor for cardiovascular risk in patients with chest pain without diabetes mellitus and significant coronary stenosis
Authors: Rha S W , Choi B G , Choi S Y , Byun J K , Cha J , Hyun S , Park S , Kim J B , Choi C U
Published: November 2023

Background

Chest pain is the most common symptom of coronary artery disease (CAD); diabetes mellitus (DM) is a well-known single largest risk factor for cardiovascular diseases and survival worldwide. So, the impact of CAD and DM on long-term clinical effects is reported widely. This study aimed to evaluate the long-term prognostic factor for major adverse cardiac and clinical events (MACCE) in patients with chest pain without DM and CAD who underwent coronary angiography (CAG) and acetylcholine (ACH) provocation test.

Methods

A total of 1,046 patients with chest pain without DM and significant CAD who underwent CAG and ACH tests were finally enrolled. Propensity score matching and multivariate Cox-proportional hazard ratio analysis were performed to adjust for baseline potential confounders. All subjects were followed clinically for up to 5 years.

Results

Coronary spasm (CAS) seems the most common cause of chest pain. However, long-term MACCE of CAS is not worse than those of patients with chest pain without CAS when patients with CAS had subsequent optimal anti-anginal medication therapy. However, a repeated chest pain remains a problem even with continuous anti-anginal medication therapy. Up to 5-year follows, MACCE has occurred 7.3%, including recurrent angina of 6.9%. Dyslipidemia, mild to moderate CAD, and the use of aspirin/nitrates are associated with long-term MACCE.

Conclusions

Among the patients with chest pain without DM and significant CAD, the occurring major adverse cardiac events, including death, MI, and de novo CAD, are rare, but recurrent angina is still a challenging problem who had the treatment by anti-anginal medications.
Clinical presentation and cardiovascular risk factors in patients with STEMI due to spontaneous coronary artery dissection (SCAD)
Authors: Malleier S , Troebs M , Achenbach S
Published: November 2023

Background

Spontaneous coronary artery dissection (SCAD) may occur in the absence of atherosclerotic and traumatic etiology and can lead to severe clinical manifestations such as ST-segment elevation myocardial infarction (STEMI). Compared to atherosclerotic STEMI, younger patients and females are predominantly affected. Hence, underdiagnosis is an important concern. We therefore systematically analyzed the prevalence of SCAD among a large cohort of young patients presenting with STEMI, as well as risk factors and presenting symptoms.

Methods

We retrospectively identified a consecutive cohort of 631 patients younger than 55 years who underwent coronary angiography due to STEMI between 01/2005 and 10/2022. Systematic review of coronary angiograms allowed identification of all STEMI caused by SCAD (n=20, 3.2%), including patients previously misdiagnosed as atherosclerotic STEMI. By reviewing medical records, we identified symptoms at presentation and cardiovascular risk factors in patients with SCAD-STEMI.

Results

Out of the 20 patients <55 years presenting with SCAD-STEMI, 16 (80%) were female, and the mean age was 49.5 years. By far the most common presentation was typical angina (75%, n=15), being reported by all 4 male and 11/16 female patients (100% vs. 69%, respectively). Importantly, three patients presented with cardiac arrest due to malignant ventricular arrhythmia (15%). In 6 patients, symptoms were mild and atypical (nausea/vomiting, n = 3, 15%; atypical chest pain, n = 2, 10%; and diaphoresis, n = 1, 5%). There was no significant difference of symptoms between men and women.

11 patients (55%) were treated by primary PCI, none received emergency coronary artery bypass grafting (CABG). The mean maximum serum creatin kinase (CK) level was 1410 U/l (range 139-86144 U/l). Mean left ventricular ejection fraction (LVEF) was 50% (range 30-60%). Symptoms at presentation did not correlate with maximum CK levels, nor with LVEF.

In this caucasian cohort, the most common cardiovascular risk factor was arterial hypertension (n = 12, 60%), followed by smoking (n = 9, 45%). Six patients had hyperlipidemia (30%), and three (15%) were obese. Diabetes and a positive family history for cardiovascular events were rare (n = 2, 10% vs. n = 1, 5%, respectively).

Conclusion

In this large caucasian cohort of young patients with STEMI, SCAD accounted for 3.2 % of cases. Typical angina was the most common symptom at presentation, but cardiac arrest due to ventricular fibrillation was frequent. Symptoms in men and women were similar and did not correlate with LVEF, nor with maximum CK levels.
Machine learning for in-hospital cardiac events prediction in patients with acute coronary syndrome: results from ADDICT-ICCU study
Authors: Gall E , Dillinger J G , Hamzi K , Elbaz M , Gerbaud E , El Beze N , Lequipar A , Toupin S , Picard F , Trimaille A , Goralski M , Bedossa M , Boccara A , Pezel T , Henry P
Published: November 2023

Background

Acute coronary syndrome (ACS) remains a major cause of mortality worldwide. However, the accuracy of current prediction tools for in-hospital cardiac events after an ACS remains insufficient for individualized patient management strategies.

Purpose

To assess in patients with ACS the feasibility and accuracy of machine learning (ML)-based model using all data available at admission to predict in-hospital cardiac events.

Methods

We conducted a sub-study of ADDICT-ICCU registry, an observational prospective study including all consecutive patients admitted to intensive cardiac care unit (ICCU) in 39 centres throughout France between 7 and 22 April 2021. We evaluated 16 clinical, 4 biological and 6 transthoracic echocardiogram (TTE) features. ML involved automated feature selection with model building by random forest (RF), and then hyperparameter tuning was done by repeated cross-validation. The primary outcome was the occurrence of composite outcomes defined by death, resuscitated cardiac arrest or cardiogenic shock requiring medical and/or mechanical haemodynamic support.

Results

Of 1,499 consecutive patients, 765 (mean age 63±15 years, 70% male) were admitted for ACS. The overall in-hospital cardiac events rate for ACS patients was 4.0 %. Feature selection was performed using RF with the log-rank–based variable importance, and 6 of the available features at admission were selected for the RF model (1 clinical, 1 biological, and 4 from TTE) including mean blood pressure, renal function, cardiac output, filling pressures, tricuspid annular plane systolic excursion and pulmonary arterial systolic pressure. The ML model exhibited a higher area under the curve compared with TIMI score, GRACE score, and traditional stepwise model score for prediction of in-hospital cardiac events (ML score: 0.96 vs TIMI: 0.54, GRACE: 0.68, traditional stepwise score: 0.87; all P < 0.001).

Conclusions

The ML-model exhibited a higher prognostic value to predict in-hospital cardiac events compared with all traditional scores.

ML model for MACEs prediction ML model performance (AUC)
Family history of myocardial infarction with non-obstructive coronary arteries (MINOCA)
Authors: Hakansson H F K , Svensson P , Tornvall P
Published: November 2023

Introduction

Genetic factors play an important role in the development of myocardial infarction (MI), and a positive family history is a risk factor for MI. The significance of family history among patients with a working diagnosis of myocardial infarction with non-obstructive coronary arteries (MINOCA) is not known, and previous studies of family history in MI have not made a distinction between MINOCA and MI due to coronary artery disease (MI-CAD) based on angiographic findings.

Purpose

To investigate family history of MI with and without obstructive coronary arteries in patients with a working diagnosis of MINOCA.

Methods

A nationwide register-based case-control study of 15 462 MINOCA cases and 38 220 controls without MI with a non-obstructive coronary angiography due to chest pain, together with 204 424 MI-CAD cases, defined as MI with obstructive coronary arteries with a degree of stenosis >50%, between the years 1995-2020. Data from the Swedish coronary angiography and angioplasty register with information about angiographic findings was merged with information on first-degree relatives from the Swedish multi-generation register. Odds ratio (OR) was calculated with a 95% confidence interval (CI), to analyze the probability of MINOCA patients having first-degree relatives with 1) MINOCA, 2) MI-CAD, and 3) MI-CAD patients having first-degree relatives with MI-CAD. Logistic regression models adjusted for age, sex, hypertension, diabetes, hyperlipidemia and smoking status.

Results

A total of 161 MINOCA patients (1%) had ≥1 first-degree relative with MINOCA and the probability of having a positive family history of MINOCA did not differ compared to controls, with age and sex adjusted OR 1.08 (95% CI 0.89-1.31) and when adjusting for all covariates 1.08 (95% CI 0.87-1.34).

Conversely, 1436 MINOCA patients (9%) had ≥1 first-degree relative with MI-CAD and the probability of having a positive family history of MI-CAD was higher compared to controls with age and sex adjusted OR 1.12 (95% CI 1.05-1.20) and when adjusting for all covariates OR 1.16 (95% CI 1.04-1.20).

The sensitivity analysis showed that 24 972 MI-CAD (9%) patients had a positive family history of MI-CAD compared to controls, OR adjusted for age and sex 1.68 (95% CI 1.61-1.75), and OR adjusted for all covariates 1.68 (95% CI 1.60-1.75).

Conclusions

In this first study that examines family history of MINOCA, including data from over 250 000 coronary angiograms, a positive family history of MI-CAD was more common among patients with a working diagnosis of MINOCA compared to controls without MI and with non-obstructive coronary arteries. A family history of MINOCA was uncommon and was not associated with MINOCA. These results indicate that genetic factors and shared environmental factors within a family leading to CAD are important also for MINOCA, thus MI-CAD and MINOCA share underlying mechanisms.
Temporal trends in the prevalence of cardiovascular and non-cardiovascular comorbidities in patients presenting with acute myocardial infarction: Insights from the AMIS Plus registry
Authors: Loosli J , Stahli B E , Foster-Witassek F , Rickli H , Roffi M , Pedrazzini G , Radovanovic D
Published: November 2023

Background

Little is known about temporal trends in the prevalence of cardiovascular and non-cardiovascular comorbidities in patients presenting with acute myocardial infarction (AMI).

Methods

AMIS Plus registry patients enrolled between 2004 and 2021 were stratified based on comorbidities in 3 groups: (1) «cardiovascular comorbidity»: at least one among past history of myocardial infarction, coronary artery bypass grafting or percutaneous coronary intervention, heart failure, peripheral vascular disease, cerebrovascular disease, or atrial fibrillation; (2) «non-cardiovascular comorbidity»: at least one among dementia, chronic lung disease, connective tissue disease, peptic ulcer disease, moderate or severe renal disease, diabetes, liver disease, or cancer disease; and (3) «any comorbidity»: at least one of the mentioned comorbidities. Prevalence and mortality were analysed according to the type of comorbidity in 2-year periods and stratified by sex. Temporal trends were analysed using the Mantel-Haenszel linear-by-linear association Chi-squared test.

Results

Among the 48’848 patients enrolled, 24’215 (49.6%) had at least one comorbidity. Of these, 17’441 (72.0%) were male and 6’774 (28.0%) female. Over the years, there was a significant decrease in the prevalence of «any comorbidity» (p<0.001) as well as «cardiovascular comorbidity» (p<0.001). A significant decrease in the prevalence of «any comorbidity» as well as «cardiovascular comorbidity» was detected for both sexes. With respect to the prevalence of «non-cardiovascular comorbidity», a significant reduction over time was observed in men but not in women. The reduction of in-hospital mortality over time was significant across all groups, overall and for both sexes individually.

Conclusions

Over more than a decade, a significant reduction in the prevalence of comorbidities was observed in patients presenting with AMI, with the exception of non-cardiovascular comorbidities in women. This reduction may have contributed, in addition to the improvements in pharmacologic treatments as well as in revascularization, to the improved survival observed over time.Temporal trends of comorbidities
Association of baseline and changes in health related quality of life with mortality following myocardial infarction: multicentre longitudinal linked cohort study
Authors: Dondo T , Munyombwe T , Hurdus B , Aktaa S , Hall M , Nadarajah R , Farooq M , Haris M , West R M , Hall A S , Gale C P
Published: November 2023

Background/Introduction

Health related quality of life (HRQoL) for patients following myocardial infarction (MI) is frequently impaired and often deteriorates. However, the association between HRQoL and clinical endpoints in patients with MI is unknown.

Purpose

To investigate the association of baseline and temporal changes in HRQoL with long term all-cause mortality following MI.

Methods

This nationwide longitudinal linked health record study includes individuals with MI admitted to 77 hospitals in England between 1st November 2011 and 24th June 2015 in the EMMACE-3 and -4 studies. Self-reported HRQoL was collected using the EuroQol EQ-5D-3L (EuroQOL Visual Analogue Scale (EQ-VAS) and EuroQOL 5-Dimensional Classification (EQ-5D)) instrument during hospitalisation and at 1, 6 and 12-months following hospital discharge. Flexible parametric and multilevel survival models estimated associations of baseline and change in HRQoL with long term all-cause mortality.

Results

Of 9,474 individuals with MI, 25% (2,360) were women and 22.5% (2,135) participants died during the 9 years follow up period (median 6.9 years). There was an improvement in HRQoL over 12 months following MI (baseline mean, mean increase: EQ-5D 0.76, 0.003 per month; EQVAS 69.0, 0.5 per month). Better HRQoL at baseline was inversely associated with mortality (HR 0.55, 95% CI 0.47-0.63) (Figure 1A). At baseline, problems with self-care (HR 1.73, 95% CI 1.56-1.92), mobility (1.65, 1.50-1.81), usual activities (1.34, 1.23-1.47) and pain/discomfort (1.34, 1.22-1.46), were associated with increased mortality (Figure 1A). Improvements in EQ-5D (HR 0.69, 95% CI 0.60-0.80), but not EQ-VAS reduced the risk of death (Figure 1B). Deterioration in mobility, pain/discomfort, usual activities and self-care over 12 months increased the risk of death (HR 1.43, 95% CI 1.31-1.58; 1.21, 95% CI 1.11-1.32; 1.20, 95% CI 1.10-1.32; 1.44, 95% CI 1.30-1.59, respectively) (Figure 1B).

Conclusions

For patients with MI, poor HRQoL at baseline, its dimensions and deterioration over time are associated with mortality. Measuring HRQoL in routine clinical practice could delineate an at-risk group for targeted interventions to improve prognosis.Figure 1
Referral pathway in primary PCI - delays depend on the origin
Authors: Dias Claudio F , Neves D , Carias M , Almeida A , Figueiredo M , Viana R , Russo C , Rocha R , Bras D , Bento A , Fernandes R , Patricio L
Published: November 2023

Background

Ischaemic heart disease is the single most common cause of death and its frequency is increasing. The mortality in patients presenting with an acute coronary syndrome with ST-elevation (STEMI) is associated with many factors such as the time delay to treatment, which comprises primary angioplasty (pPCI) or fibrinolysis.

Therefore, treatment delays should be recorded systematically and audited, so as to improve standard of care.

Purpose

To analyse the response time and delays in the emergent coronary referral pathway for our centre, taking into consideration the place of first contact.

Methods

Primary data for this study was obtained by evaluating consecutive patients from the year 2015 to 2021, admitted for pPCI in our centre in the context STEMI. Time variables were collected for all patients – schematically represented in Figure 1. Statistical analyses were performed using IBM SPSS Statistics for Windows Version 27.0.

Results

We included a total of 1452 cases of pPCI with a median patient age of 64 years and 75,3% male. Over 7 years of pPCI were analysed and median times are displayed in table 1. We found that ECG median delays were significantly lower in the emergency first responders (EFR) group when comparing to PCI Centre group (11,0 vs 22,0; p<0,001), primary care physicians group(11,0 vs 23,0; p<0,001) and non-PCI Centre group (11,0 vs 28,0; p<0,001). Futhermore, median diagnostic delay was significantly lower in the EFR group compared to non-PCI centre group (28,0 vs 62,0; p<0,001) and primary care physician group (28,0 vs 59,0; p<0,001), as well as in the PCI Centre group compared to the non-PCI Centre group (30,0 vs 62,0; p<0,001) and to primary care physician group (30,0 vs 59,0; p<0,001).

Conclusions

Our data displays a clear heterogeneity in care which has an impact in the ischaemic time of STEMI patients. There seems to be a significant difference between the primary point of contact being the primary care physicians or a non-PCI centre when compared to our centre or the EFR, especially when it comes to the diagnostic timings. Hence, strategies must be developed to increase diagnostic sensibility and accuracy of STEMI patients throughout our geographical region.Time variable schemeTime according to groups
Performance of the High-STEACS Early Rule-Out Pathway for High Sensitivity Cardiac Troponin T at 30-days in a US population
Authors: Allen B , Millard M , Ashburn N , Snavely A , Nowak R , Mumma B , Madsen T , Wilkerson R G , Christenson R , Stopyra J , Mahler S
Published: November 2023

Background

The High-STEACS Early Rule-Out Pathway for High Sensitivity Cardiac Troponin T (hs-cTnT) is an algorithm designed to rule-out myocardial infarction (MI) in ED patients with symptoms concerning for acute coronary syndrome (ACS). High-STEACS was validated in the United Kingdom but has yet to be evaluated in the US.

Purpose

The objective of this secondary analysis of the STOP-CP (High Sensitivity Cardiac Troponin T to Optimize Chest Pain Risk Stratification) United States (US) multicenter study is to determine the performance of the High-STEACS hs-cTnT Pathway in a multisite US cohort.

Methods

Patients (≥ 21 years old) presenting to the (ED) with symptoms suggestive of ACS were enrolled (1/25/2017-9/6/2018) at 8 US medical centers. Participants with 0- and 1-hour hs-cTnT measures were stratified into outpatient and admission dispositions using the established High-STEACS hs-cTnT cut-points. Cardiac death or MI and major adverse cardiovascular events (MACE; a composite of cardiac death, MI, and coronary revascularization) at 30-days were adjudicated. Negative and positive predictive values (NPV and PPV) and negative and positive likelihood ratios (-LR and +LR) for the High-STEACS pathway were calculated for each outcome with 95% confidence intervals.

Results

Overall, 1430 patients were studied. 54.2% (775/1430) were male with a mean age of 57.6 ± 12.8 years. At 30-days, 12.8% (183/1430) of patients experienced cardiac death or MI and 14.2% (203/1430) had MACE. High-STEACS classified 59.9% (857/1430) to the outpatient disposition and 40.1% (573/1430) to admission. Among patients stratified to the outpatient group, 1.9% (16/857) experienced cardiac death or MI and 3.4% (29/857) had MACE at 30-days. The NPV and -LR for High-STEACS were 98.1% (95%CI 97.0-98.9) and 0.13 (95%CI 0.08-0.21) for 30-day cardiac death or MI and 96.6% (95%CI 95.2-97.7) and 0.21 (95%CI 0.15-0.30) for 30-day MACE. For patients stratified to admission, 29.1% (167/573) had 30-day cardiac death or MI and 30.4% (174/573) had MACE. This yielded a PPV and +LR for 30-day cardiac death or MI of 29.1% (95%CI 25.5-33.1) and 2.8 (95%CI 2.6-3.1) and 30.4% (95%CI 26.6-34.3) and 2.6 (95%CI 2.4-2.9) for 30-day MACE.

Conclusions

The High-STEACS hs-cTnT Pathway stratified nearly 60% of patients to an outpatient disposition, but these patients had high rates of 30-day cardiac events. These findings suggest that providers should be cautious before using this pathway among US patients with possible ACS.
Nourin miRNAs: novel biomarkers highly expressed in unstable angina patients with normal ECG and negative hs-troponin and dropped post percutaneous coronary intervention
Authors: Kandil H I , Yacoub B , Sadaka M , Yehia A , El-Khazragy N , Rashed L , El-Hadidi A S , Kreutzer D L , Christenson R H , Elgebaly S A
Published: November 2023

Background

We recently reported that Nourin-dependent miR-137 and miR-106b can identify reversible myocardial ischemia in chest pain patients with a confirmed diagnosis of chronic stable chronic artery disease (CAD) and unstable angina (UA). These patients showed normal resting ECG and hs-cTnI below the clinical decision (<99th of URL). Normal, low-grade, baseline expression levels of Nourin miRNAs were detected in healthy subjects and in non-cardiac chest pain patients with hs-cTnI <99th URL.

Purpose

1) To confirm the upregulation of Nourin miRNAs in chest pain patients with normal resting ECG and hs-cTnI < 99th URL, who are suspected of having UA; 2) whether Nourin miRNA expression levels change after relieving myocardial ischemia by PCI; and 3) whether there is an association between severity of chest of pain and Nourin miRNA expression levels prior to PCI.

Methods

This study enrolled 36 consecutive chest pain patients with normal resting ECGs and hs-cTnI <99th URL, from two large referral centers in Egypt. All enrolled patients had a single vessel disease with significant coronary stenosis (>70%) during diagnostic coronary angiography that was treated by PCI using standard techniques. The gene expression levels of miR-137 and miR-106b were measured in serum samples collected prior to PCI, as well as 12 hours and 24 hours post PCI. The angina class was evaluated at presentation, discharge, and after 4 weeks to verify angina relief.

Results

All patients (n=36) underwent successful PCI. Gene expression levels of miR-137 and miR-106b were significantly upregulated prior to PCI (mean ± SD: miR-137 = 355±150 and miR-106b =317±122) compared to healthy subjects (n=16) who showed minimal expression levels ranged from 0.615 to 1.05 (P <0.0001). Levels of both biomarkers dropped by 50% (12 hours) and 65% (24 hours) post PCI (P <0.05) (Figure 1). The expression levels of Nourin miRNAs did not associate with the Canadian class levels of angina severity. All patients were asymptomatic at discharge, while 84% remained asymptomatic after 4 weeks.

Conclusions

This study: 1) confirms that Nourin miR-137 and miR-106b can identify myocardial ischemia in patients presenting with unstable angina; 2) confirms that these two novel molecular biomarkers are elevated during myocardial ischemia, in the absence of myocardial injury; and 3) for the first time, we report a significant drop of Nourin miRNA expression levels post PCI, with myocardial ischemia relief.