The Association between Major Adverse Cardiovascular Events and Peripheral Artery Disease Burden.

OBJECTIVE: The aim of the present study was to investigate the possible relationship between the segmental burden of lower limb atherosclerosis and Major Adverse Cardiovascular Events (MACEs). METHODS: All the consecutive symptomatic peripheral artery disease (PAD) patients admitted for digital subtraction angiography (DSA) at Turku University Hospital department of Vascular Surgery between 1 January 2009 and 30 July 2011 were retrospectively analyzed. Angiography due to symptomatic PAD was used as the index date for the inclusion in the study. The segmental burden of atherosclerosis based on DSA was divided into three categories according to the highest disease burden of the defined artery segment: aorto-iliac, femoropopliteal, or tibial segments. The major association for the study was MACEs (defined as a cerebrovascular event, heart failure (HF) and myocardial infarction requiring hospital admission). Demographic data and MACEs were obtained from the hospital electronic medical records system. RESULTS: The lower limb atherosclerosis burden of tibial vessels was related to an increased probability for HF (OR 3.9; 95%CI 2.4-6.5) and for MACEs overall (OR 2.3; 95%CI 1.4-3.6). The probability of both HF and MACEs overall rose with the increasing severity of the atherosclerosis burden. Moreover, the more severe the tibial vessel atherosclerosis, the higher the risk of HF and MACEs. The most extensive tibial atherosclerosis patients had an OR 4.5; 95%CI 2.6-8.0 for HF and an OR 3.1; and 95%CI 1.7-5.6 for MACEs overall. The femoropopliteal disease burden was also associated with an increased risk of HF (OR 2.3; 95%CI 1.6-3.2) and MACE (OR 1.9; 95%CI 1.3-2.7). However, the increasing extent of atherosclerosis of the femoropopliteal segment solely increased the risk of MACEs. CONCLUSIONS: PAD patients with severe tibial atherosclerosis are likely to present with MACEs. The risk is further enhanced as the extent of tibial vessel atherosclerosis is increased. An association between MACE and severe atherosclerosis on the aortoiliac segment was not detected. However, when the femoropopliteal segment was the most affected artery segment, the risk of MACEs was increased.

Effect of Cangrelor on Infarct Size in ST-Segment-Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention: A Randomized Controlled Trial (The PITRI Trial).

BACKGROUND: The administration of intravenous cangrelor at reperfusion achieves faster onset of platelet P2Y12 inhibition than oral ticagrelor and has been shown to reduce myocardial infarction (MI) size in the preclinical setting. We hypothesized that the administration of cangrelor at reperfusion will reduce MI size and prevent microvascular obstruction in patients with ST-segment-elevation MI undergoing primary percutaneous coronary intervention. METHODS: This was a phase 2, multicenter, randomized, double-blind, placebo-controlled clinical trial conducted between November 2017 to November 2021 in 6 cardiac centers in Singapore. Patients were randomized to receive either cangrelor or placebo initiated before the primary percutaneous coronary intervention procedure on top of oral ticagrelor. The key exclusion criteria included presenting <6 hours of symptom onset; previous MI and stroke or transient ischemic attack; on concomitant oral anticoagulants; and a contraindication for cardiovascular magnetic resonance. The primary efficacy end point was acute MI size by cardiovascular magnetic resonance within the first week expressed as percentage of the left ventricle mass (%LVmass). Microvascular obstruction was identified as areas of dark core of hypoenhancement within areas of late gadolinium enhancement. The primary safety end point was Bleeding Academic Research Consortium-defined major bleeding in the first 48 hours. Continuous variables were compared by Mann-Whitney U test (reported as median [first quartile-third quartile]), and categorical variables were compared by Fisher exact test. A 2-sided P<0.05 was considered statistically significant. RESULTS: Of 209 recruited patients, 164 patients (78%) completed the acute cardiovascular magnetic resonance scan. There were no significant differences in acute MI size (placebo, 14.9% [7.3-22.6] %LVmass versus cangrelor, 16.3 [9.9-24.4] %LVmass; P=0.40) or the incidence (placebo, 48% versus cangrelor, 47%; P=0.99) and extent of microvascular obstruction (placebo, 1.63 [0.60-4.65] %LVmass versus cangrelor, 1.18 [0.53-3.37] %LVmass; P=0.46) between placebo and cangrelor despite a 2-fold decrease in platelet reactivity with cangrelor. There were no Bleeding Academic Research Consortium-defined major bleeding events in either group in the first 48 hours. CONCLUSIONS: Cangrelor administered at the time of primary percutaneous coronary intervention did not reduce acute MI size or prevent microvascular obstruction in patients with ST-segment-elevation MI given oral ticagrelor despite a significant reduction of platelet reactivity during the percutaneous coronary intervention procedure. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03102723.

Radiomics-based detection of acute myocardial infarction on noncontrast enhanced midventricular short-axis cine CMR images.

Cardiac magnetic resonance cine images are primarily used to evaluate functional consequences, whereas limited information is extracted from the noncontrast pixel-wise myocardial signal intensity pattern. In this study we want to assess whether characterizing this inherent contrast pattern of noncontrast-enhanced short axis (SAX) cine images via radiomics is sufficient to distinguish subjects with acute myocardial infarction (AMI) from controls. Cine balanced steady-state free-precession images acquired at 1.5 T from 99 AMI and 49 control patients were included. First, radiomic feature extraction of the left ventricular myocardium of end-diastolic (ED) and end-systolic (ES) frames was performed based on automated (AUTO) or manually corrected (MAN) segmentations. Next, top features were selected based on optimal classification results using a support vector machine (SVM) approach. The classification performances of the four radiomics models (using AUTO or MAN segmented ED or ES images), were measured by AUC, classification accuracy (CA), F1-score, sensitivity and specificity. The most accurate model was found when combining the features RunLengthNonUniformity, ClusterShade and Median obtained from the manually segmented ES images (CA = 0.846, F1 score = 0.847). ED analysis performed worse than ES, with lower CA and F1 scores (0.769 and 0.770, respectively). Manual correction of automated contours resulted in similar model features as the automated segmentations and did not improve classification results. A radiomics analysis can capture the inherent contrast in noncontrast mid-ventricular SAX cine images to distinguishing AMI from healthy subjects. The ES radiomics model was more accurate than the ED model. Manual correction of the autosegmentation did not provide significant classification improvements.

Hyperbaric Oxygen Upregulates Mst1 to Activate Keap1/Nrf2/HO-1 Pathway Resisting Oxidative Stress in a Rat Model of Acute Myocardial Infarction.

This study aimed to investigate the protective effects and mechanisms of hyperbaric oxygen (HBO) preconditioning in a rat model of acute myocardial infarction (MI) established by ligation of the left anterior descending (LAD) coronary artery. Microarray, real-time PCR, and western blotting (WB) results demonstrated that the Mst1 gene was downregulated in the heart tissue of the MI rat model. HBO preconditioning significantly increased Mst1 expression in cardiac tissues of rats after MI modeling. Lentiviral infection was used to silence the Mst1 gene in rats treated with HBO to probe the effect of Mst1 on HBO cardioprotection. HBO preconditioning decreased heart infarct size and ameliorated cardiac function in MI rats, whereas Mst1 silencing reversed the effect of HBO administration, as indicated after heat infarct size determination via TTC staining, histological examination via HE staining, and measurements of cardiac function. HBO preconditioning reduced oxidative stress and inflammation in cardiac tissue of MI rat model, evidenced by alteration of malondialdehyde (MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG), and protein carbonyl contents, as well as production of inflammation-associated myeloperoxidase (MPO), IL-1ß, and TNF-α. These findings provide a new signaling mechanism through which HBO preconditioning can protect against acute MI injury through the Mst1-mediating Keap1/Nrf2/HO-1-dependent antioxidant defense system.

Prospects of Intravenous Coenzyme Q10 Administration in Emergency Ischemic Conditions.

Coenzyme CoQ10 (CoQ10) is an endogenous lipid-soluble antioxidant that effectively protects lipids, proteins, and DNA from oxidation due to its ability to undergo redox transitions between oxidized and reduced forms. Various oxidative stress-associated infectious and somatic diseases have been observed to disrupt the balance of CoQ10 concentration in tissues. As a high molecular weight polar lipophilic compound, CoQ10 exhibits very limited oral bioavailability, which restrains its therapeutic potential. Nevertheless, numerous studies have confirmed the clinical efficacy of CoQ10 therapy through oral administration of high doses over extended time periods. Experimental studies have demonstrated that in emergency situations, intravenous administration of both oxidized and reduced-form CoQ10 leads to a rapid increase in its concentration in organ tissues, offering protection for organ tissues in ischemic conditions. This suggests that the cardio- and neuroprotective efficacy of intravenously administered CoQ10 forms could present new opportunities in treating acute ischemic conditions. Based on these findings, the review provides reasoning supporting further research and implementation of CoQ10 dosage forms for intravenous administration in emergency situations into clinical practice.

Clinical efficacy of buprenorphine after oral dosing in rats undergoing major surgery.

Serum corticosterone, serum buprenorphine, body weight change, consumption of food and water and behaviour-based pain assessment were measured in catheterised and non-catheterised male Wistar rats undergoing myocardial infarct (MI) surgery under general anaesthesia following buprenorphine dosing by subcutaneous (Bup-SC, 0.05 mg/kg) and oral (Bup-O, 0.4 mg/kg) routes. Buprenorphine was dosed subcutaneously at half an hour before and 8, 16 and 24 hours after surgery (Bup-SC), orally at one hour before surgery (Bup-O1) or at one hour before and 12 hours after surgery (Bup-O2) in catheterised rats and at one hour before and 24 hours after surgery (Bup-O24) in non-catheterised rats. Serum corticosterone, body weight changes and food and water consumption were not significantly different between treatments in catheterised rats. Bup-SC resulted in rapidly decreasing serum concentrations below the clinically effective concentrations (1 ng/mL) already at two hours after the first dose. Bup-O provided significantly higher and slowly decreasing serum concentrations, at or above clinically effective concentrations, for 24 hours (Bup-O1) and 42 hours (Bup-O2) after surgery. In non-catheterised rats, body weight development and food consumption were significantly higher in Bup-O24 rats compared to Bup-SC rats. The results indicate that a SC buprenorphine dose of 0.05 mg/kg every eight hours provides long periods of serum concentrations below clinically effective levels, and that a higher dose and/or more frequent dosage are required to provide stable serum concentrations at or above clinically effective levels. A single oral buprenorphine dose of 0.4 mg/kg provides clinically effective and stable serum concentrations for 24 hours in rats after MI surgery.

Automated spatially targeted optical micro proteomics identifies fibroblast- and macrophage-specific regulation of myocardial infarction scar maturation in rats.

Myocardial infarction (MI) results from occlusion of blood supply to the heart muscle causing death of cardiac muscle cells. Following myocardial infarction (MI), extracellular matrix deposition and scar formation mechanically stabilize the injured heart as damaged myocytes undergo necrosis and removal. Fibroblasts and macrophages are key drivers of post-MI scar formation, maturation, and ongoing long-term remodelling; however, their individual contributions are difficult to assess from bulk analyses of infarct scar. Here, we employ state-of-the-art automated spatially targeted optical micro proteomics (autoSTOMP) to photochemically tag and isolate proteomes associated with subpopulations of fibroblasts (SMA+) and macrophages (CD68+) in the context of the native, MI tissue environment. Over a time course of 6-weeks post-MI, we captured dynamic changes in the whole-infarct proteome and determined that some of these protein composition signatures were differentially localized near SMA+ fibroblasts or CD68+ macrophages within the scar region. These results link specific cell populations to within-infarct protein remodelling and illustrate the distinct metabolic and structural processes underlying the observed physiology of each cell type.

Common and specific proteins and pathways in heart and cerebral ischemia.

OBJECTIVE: To understand the similarities and differences between acute ischemic stroke and acute myocardial infarction (AMI) to help in the development of specific or common treatment strategies. METHODS: Using an aptamer-based proteomic array, we measured and compared 1310 circulating proteins in the blood of 40 patients with AIS, 9 patients with AMI, and 31 healthy controls. Pathway enrichment analysis was performed using GSEA and g:profiler. RESULTS: Ninety-four proteins were differentially expressed in AIS, and 284 were differentially expressed in AMI. Of these, 8 were specific to cerebral ischemia, and 197 were specific to myocardial infarction. Forty-two proteins were altered in both ischemia processes. Most altered pathways in AIS could be classified as immune response, cell cycle processing, molecular transport, or signaling. Pathways altered in AMI were mostly related to lipid metabolism and transport, highlighting cholesterol metabolic processes and estrogen signaling. In both types of ischemia, we found pathways related to metabolism, specifically purine metabolism, and signaling processes, such as TNF signaling or MAPK1/3. CONCLUSIONS: The present study revealed proteins and pathways that were specifically altered in cerebral ischemia, in cardiac ischemia, or in both diseases, providing information on the similarities and differences of ischemic conditions. The role of common and specific proteins and pathways should be explored in detail to find possible therapeutic targets.

Myocardial infarct size for predicting improvements in cardiac function in patients with ischemic cardiomyopathy following coronary artery bypass grafting.

Background: This study used late gadolinium enhancement-cardiac magnetic resonance (LGE-CMR) to assess myocardial infarct size, with the data being employed to predict whether patients with ischemic cardiomyopathy (ICM) would experience improvements in left ventricular function at 6 months following coronary artery bypass grafting (CABG). Methods: The data of patients with ICM with left ventricular ejection fraction (LVEF) ≤40% who underwent CABG were retrospectively analyzed. All patients underwent preoperative LGE-CMR imaging. Echocardiography results from 6 months post-CABG were used to assess improvements in LVEF, with improvement being defined as ΔLVEF ≥5%. The value of myocardial infarction segments and infarct size as predictors of improved cardiac function following CABG was analyzed. Results: Of the included patients, 66.7% (52/78) exhibited improved cardiac function at 6 months post-CABG. LGE-CMR imaging data revealed that compared to improved group, the improved group had significantly more myocardial infarct segments [improved group: median 1.0, interquartile range (IQR) 0-3; nonimproved group: median 4.0, IQR 3.0-6.0; P<0.001] and significantly greater myocardial infarct size (improved group: 22.4%±8.2%; nonimproved group: 34.7%±5.9%; P<0.001). The area under the receive operating characteristic curve values for myocardial infarct size in predicting cardiac function improvement were significantly higher than those of myocardial infarct segments (0.88 vs. 0.81; P=0.041). The respective sensitivity and specificity values for using a myocardial infarct size cutoff of 26.4% in differentiating between these 2 patient groups were 92.3% and 71.2%, respectively. According to logistic regression analysis, myocardial infarct size was an independent predictor of nonimprovement in cardiac function [odds ratio (OR) =1.244; 95% confidence interval (CI): 1.114-1.389; P<0.001]. A median 1.6-year follow-up interval (range, 0.5-4.1 years) revealed that the incidences of major adverse cerebrovascular events and cardiovascular events were significantly higher in the nonimproved group (5.8% vs. 26.9%; P<0.001), with these individuals having a higher New York Heart Association grading than patients with improved cardiac function (P=0.019). Conclusions: Myocardial infarct size can be measured to reliably predict improvements in cardiac function in patients with ICM following CABG. These results can guide clinicians in their efforts to identify those patients most likely to achieve positive outcomes following CABG.

Clinical outcomes of hundred large Impella implantations in cardiogenic shock patients based on individual clinical scenarios.

BACKGROUND: Large Impella systems (5.0 or 5.5; i.e., Impella 5+) (Abiomed Inc., Danvers, MA, USA) help achieve better clinical outcomes through relevant left ventricular unloading in acute cardiogenic shock (CS). Here, we report our experience with Impella 5+, while focusing on the clinical outcomes depending on individual case scenarios in patients with acute CS. METHODS: This single-center retrospective observational study included 100 Impella 5+ implantations conducted on patients with acute CS from November 2018 to October 2021. After excluding 10 reimplantation cases, 90 cases were enrolled for further analysis. RESULTS: In-hospital and 30-day mortality rates were 56.7% (n = 51) and 48.9% (n = 44), respectively. In-hospital mortality was lower in patients with acute myocardial infarction (AMI) than in non-AMI patients (p = 0.07). Young age and low lactate levels were the independent predictors of successful transition and survival after permanent mechanical circulatory support/heart transplantation (pMCS/HTX) (age, p = 0.03; lactate level, p = 0.04; survived after pMCS/HTX, n = 11; died on Impella, n = 41). During simultaneous utilization of venoarterial extracorporeal membrane oxygenation therapy and Impella 5+, termed ECMELLA therapy, high dose of noradrenaline was a predictive factor for in-hospital mortality by multivariate analysis (n = 0.02). CONCLUSIONS: Our results suggest that enhanced Impella support might have better clinical outcomes among acute CS patients supported with large Impella, those with AMI than those with no AMI. Young age and low lactate levels were predictors of successful bridging to pMCS/HTX and favorable clinical outcomes thereafter. The clinical outcomes of ECMELLA therapy might depend on noradrenaline dose at the time of Impella 5+ implantation.

Impact of myocardial deformation on risk prediction in patients following acute myocardial infarction.

Background: Strain analyses derived from cardiovascular magnetic resonance-feature tracking (CMR-FT) provide incremental prognostic benefit in patients sufferring from acute myocardial infarction (AMI). This study aims to evaluate and revalidate previously reported prognostic implications of comprehensive strain analyses in a large independent cohort of patients with ST-elevation myocardial infarction (STEMI). Methods: Overall, 566 STEMI patients enrolled in the CONDITIONING-LIPSIA trial including pre- and/or postconditioning treatment in addition to conventional percutaneous coronary intervention underwent CMR imaging in median 3 days after primary percutaneous coronary intervention. CMR-based left atrial (LA) reservoir (Es), conduit (Ee), and boosterpump (Ea) strain analyses, as well as left ventricular (LV) global longitudinal strain (GLS), circumferential strain (GCS), and radial strain (GRS) analyses were carried out. Previously identified cutoff values were revalidated for risk stratification. Major adverse cardiac events (MACE) comprising death, reinfarction, and new congestive heart failure were assessed within 12 months after the occurrence of the index event. Results: Both atrial and ventricular strain values were significantly reduced in patients with MACE (p < 0.01 for all). Predetermined LA and LV strain cutoffs enabled accurate risk assessment. All LA and LV strain values were associated with MACE on univariable regression modeling (p < 0.001 for all), with LA Es emerging as an independent predictor of MACE on multivariable regression modeling (HR 0.92, p = 0.033). Furthermore, LA Es provided an incremental prognostic value above LVEF (a c-index increase from 0.7 to 0.74, p = 0.03). Conclusion: External validation of CMR-FT-derived LA and LV strain evaluations confirmed the prognostic value of cardiac deformation assessment in STEMI patients. In the present study, LA strain parameters especially enabled further risk stratification and prognostic assessment over and above clinically established risk parameters. Clinical Trial Registration: ClinicalTrials.gov, identifier NCT02158468.

Performance of a prehospital HEART score in patients with possible myocardial infarction: a prospective evaluation.

INTRODUCTION: The History, Electrocardiogram (ECG), Age, Risk Factors and Troponin (HEART) score is commonly used to risk stratify patients with possible myocardial infarction as low risk or high risk in the Emergency Department (ED). Whether the HEART score can be used by paramedics to guide care were high-sensitivity cardiac troponin testing available in a prehospital setting is uncertain. METHODS: In a prespecified secondary analysis of a prospective cohort study where paramedics enrolled patients with suspected myocardial infarction, a paramedic Heart, ECG, Age, Risk Factors (HEAR) score was recorded contemporaneously, and a prehospital blood sample was obtained for subsequent cardiac troponin testing. HEART and modified HEART scores were derived using laboratory contemporary and high-sensitivity cardiac troponin I assays. HEART and modified HEART scores of ≤3 and ≥7 were applied to define low-risk and high-risk patients, and performance was evaluated for an outcome of major adverse cardiac events (MACEs) at 30 days. RESULTS: Between November 2014 and April 2018, 1054 patients were recruited, of whom 960 (mean 64 (SD 15) years, 42% women) were eligible for analysis and 255 (26%) experienced a MACE at 30 days. A HEART score of ≤3 identified 279 (29%) as low risk with a negative predictive value of 93.5% (95% CI 90.0% to 95.9%) for the contemporary assay and 91.4% (95% CI 87.5% to 94.2%) for the high-sensitivity assay. A modified HEART score of ≤3 using the limit of detection of the high-sensitivity assay identified 194 (20%) patients as low risk with a negative predictive value of 95.9% (95% CI 92.1% to 97.9%). A HEART score of ≥7 using either assay gave a lower positive predictive value than using the upper reference limit of either cardiac troponin assay alone. CONCLUSIONS: A HEART score derived by paramedics in the prehospital setting, even when modified to harness the precision of a high-sensitivity assay, does not allow safe rule-out of myocardial infarction or enhanced rule-in compared with cardiac troponin testing alone.

Acute Cardiovascular Complications of COVID-19: A Systematic Review.

Since the pandemic in 2019, coronavirus 2019 (COVID-19) has continued to be linked with a variety of organ systems and complications. While it is generally considered a respiratory disease, its link with the heart is widely discussed in the literature. This article focuses on the acute cardiovascular complications of COVID-19 and the possible predictors of these complications. Our study included 97 articles (58 case reports, eight case series, 23 retrospective cohort studies, five prospective cohort studies, and three cross-sectional studies). Several mechanisms have been proposed to explain COVID-19-induced cardiovascular complications, with cytokine-induced inflammation and direct cardiac damage noted as the significant focus. Patients with underlying cardiovascular complications such as hypertension and diabetes were noted to be at increased risk of acute cardiovascular complications, as well as an increased risk of severe disease and death. Also, acute myocardial infarction and arrhythmias were two of the most common acute cardiovascular complications noted in our review. Other acute cardiovascular complications are myocarditis, takotsubo syndrome, acute thromboembolic events, and pericardial complications. This article provides an updated review of acute cardiovascular complications of COVID-19, its pathogenesis, and risk stratification and emphasizes the need for high suspicion in patients with underlying cardiovascular risk factors.

Interaction of exercise training with taurine attenuates infarct size and cardiac dysfunction via Akt-Foxo3a-Caspase-8 signaling pathway.

This research aimed to investigate the synergistic protective effect of exercise training and taurine on Akt-Foxo3a-Caspase-8 signaling related to infarct size and cardiac dysfunction. Therefore, 25 male Wistar rats with MI were divided into five groups: sham (Sh), control-MI(C-MI), exercise training-MI(Exe-MI), taurine supplementation-MI(Supp-MI), and exercise training + taurine-MI(Exe + Supp-MI). The taurine groups were given a 200 mg/kg/day dose of taurine by drinking water. Exercise training was conducted for 8 weeks (5 days/week), each session alternated 2 min with 25-30% VO2peak and 4 min with 55-60% VO2peak for 10 alternations. Then, the left ventricle tissue samples were taken from all groups. Exercise training and taurine activated Akt and decreased Foxo3a. Expression of the caspase-8 gene was increased in cardiac necrosis after MI, While, after 12 weeks of intervention decreased. Results exhibited that exercise training combined with taurine has a greater effect than either alone on activating the Akt-Foxo3a-caspase signaling pathway (P < 0.001). MI-induced myocardial injury leads to increase collagen deposition (P < 0.001) and infarct size and results in cardiac dysfunction via reduced stroke volume, ejection fraction, and fractional shortening (P < 0.001). Exercise training and taurine improved cardiac functional parameters (SV, EF, FS) and infarct size (P < 0.001) after 8 weeks of intervention in rats with MI. Also, the interaction of exercise training and taurine has a greater effect than alone on these variables. Interaction of exercise training with taurine supplementation induces a general amelioration of the cardiac histopathological profiles and improves cardiac remodeling via activating Akt-Foxo3a-Caspase-8 signaling with protective effects against MI.

External validation of the Manchester Acute Coronary Syndromes ECG risk model within a pre-hospital setting.

OBJECTIVES: The Manchester Acute Coronary Syndromes ECG (MACS-ECG) prediction model calculates a score based on objective ECG measurements to give the probability of a non-ST elevation myocardial infarction (NSTEMI). The model showed good performance in the emergency department (ED), but its accuracy in the pre-hospital setting is unknown. We aimed to externally validate MACS-ECG in the pre-hospital environment. METHODS: We undertook a secondary analysis from the Pre-hospital Evaluation of Sensitive Troponin (PRESTO) study, a multi-centre prospective study to validate decision aids in the pre-hospital setting (26 February 2019 to 23 March 2020). Patients with chest pain where the treating paramedic suspected acute coronary syndrome were included. Paramedics collected demographic and historical data and interpreted ECGs contemporaneously (as 'normal' or 'abnormal'). After completing recruitment, we analysed ECGs to calculate the MACS-ECG score, using both a pre-defined threshold and a novel threshold that optimises sensitivity to differentiate AMI from non-AMI. This was compared with subjective ECG interpretation by paramedics. The diagnosis of AMI was adjudicated by two investigators based on serial troponin testing in hospital. RESULTS: Of 691 participants, 87 had type 1 AMI and 687 had complete data for paramedic ECG interpretation. The MACS-ECG model had a C-index of 0.68 (95% CI: 0.61 to 0.75). At the pre-determined cut-off, MACS-ECG had 2.3% (95% CI: 0.3% to 8.1%) sensitivity, 99.5% (95% CI: 98.6% to 99.9%) specificity, 40.0% (95% CI: 10.2% to 79.3%) positive predictive value (PPV) and 87.6% (87.3% to 88.0%) negative predictive value (NPV). At the optimal threshold for sensitivity, MACS-ECG had 50.6% sensitivity (39.6% to 61.5%), 83.1% specificity (79.9% to 86.0%), 30.1% PPV (24.7% to 36.2%) and 92.1% NPV (90.4% to 93.5%). In comparison, paramedics had a sensitivity of 71.3% (95% CI: 60.8% to 80.5%) with 53.8% (95% CI: 53.8% to 61.8%) specificity, 19.7% (17.2% to 22.45%) PPV and 93.3% (90.8% to 95.1%) NPV. CONCLUSION: Neither MACS-ECG nor paramedic ECG interpretation had a sufficiently high PPV or NPV to 'rule in' or 'rule out' NSTEMI alone.

Diagnosis of an Acute Anterior Wall Infarction in Dual-Energy CT.

Due to its high morbidity and mortality, myocardial infarction is the leading cause of death worldwide. Against this background, rapid diagnosis is of immense importance. Especially in case of an atypical course, the correct diagnosis may be delayed and thus lead to increased mortality rates. In this report, we present a complex case of acute coronary syndrome. A triple-rule-out CT examination was performed in dual-energy CT (DECT) mode. While pulmonary artery embolism and aortic dissection could be ruled out with conventional CT series, the presence of anterior wall infarction was only detectable on DECT reconstructions. Subsequently, adequate and rapid therapy was then initiated leading to survival of the patient.