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Background: The outcomes of real-world unstable angina (UA) in the high-sensitivity troponin era are unclear. We aimed to investigate the outcomes of UA referred to coronary angiography compared to stable angina (SA), non-ST-segment elevation myocardial infarction (NSTEMI), STEMI and a general population., Methods: We included the 9,694 patients with no prior coronary artery disease (CAD) referred to invasive or CT coronary angiography from 2013 to 2018 in Northern Norway (51% SA, 12% UA, 23% NSTEMI and 14% STEMI), and 11,959 asymptomatic individuals recruited from the Tromsø Study. We used Cox models to estimate the hazard ratios (HR) for all-cause mortality and major adverse cardiovascular events (MACE), defined as cardiovascular death, MI or obstructive CAD., Results: The median follow-up time was 2.8 years. The incidence rate of death was 8.5 per 1000 person-years (95 % confidence interval [CI] 8.0-9.0) in the general population, 9.7 (95 % CI 8.3-11.5) in SA, 14.9 (95 % CI 11.4-19.6) in UA, 29.7 (95 % CI 25.6-34.3) in NSTEMI and 36.5 (95 % CI 30.9-43.2) in STEMI. In multivariable adjusted analyses, compared with UA, SA had a 38 % lower risk of death and a non-significant lower risk of MACE (HR 0.62, 95 % CI 0.44-0.89; HR 0.86, 95 % CI 0.66-1.11). NSTEMI had a 2.4-fold higher risk of death (HR 2.39, 95 % CI 1.38-4.14) and a 1.6-fold higher risk of MACE (HR 1.62, 95 % CI 1.11-2.38) compared tox UA during the first year after coronary angiography, but a similar risk thereafter. There was no difference in the risk of death for UA with non-obstructive CAD and obstructive CAD (HR 0.78, 95 % CI 0.39-1.57)., Conclusion: UA had a higher risk of death but a similar risk of MACE compared to SA and a lower 1-year risk of death and MACE compared to NSTEMI., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors.)

Aims Patients presenting with non-ST-segment-elevation acute coronary syndrome represent a heterogeneous group with regard to the severity of coronary atherosclerosis and prognosis. The conventional approach to their treatment has involved admission to the hospital for pharmacologic stabilization, subsequent mobilization, and management by either a conservative or an invasive strategy. The choice of one approach over another is guided largely by local practice patterns and the availability of invasive facilities.Methods and results However, recent randomized trials comparing the strategies have demonstrated a superiority of the invasive strategy, particularly in patients at higher risk. Furthermore, randomized trials have provided information on refining risk stratification. On the basis of these data, we outline criteria for assessing risk and recommend that stratification be conducted at presentation using clinical features, the electrocardiogram, and biomarkers.Conclusion Higher-risk patients should be admitted for pharmacologic stabilization and assessed by coronary angiography within 48h with the aim of early revascularization, provided the risk of periprocedural complications is not prohibitive. Glycoprotein IIb/IIIa receptor inhibitors are indicated, particularly in patients requiring percutaneous coronary intervention. The conservative strategy remains appropriate for patients admitted to hospitals without invasive facilities. Patients not at highrisk may be observed in a facility with cardiac monitoring such as a chest pain unit and undergo subsequent stress testing. The adoption of such an early risk stratification and revascularization-based approach is likely to result in a reduction in recurrent myocardial infarction and ischaemia, duration of hospitalization, repeat hospitalization, and mortality. [ABSTRACT FROM PUBLISHER]

Objective: In the STEMI paradigm of Acute Myocardial Infarction (AMI), many NSTEMI patients have unrecognized acute coronary occlusion MI (OMI), may not receive emergent reperfusion, and have higher mortality than NSTEMI patients without occlusion. We have proposed a new OMI vs. Non-Occlusion MI (NOMI) paradigm shift. We sought to compare the diagnostic accuracy of OMI ECG findings vs. formal STEMI criteria for the diagnosis of OMI. We hypothesized that blinded interpretation for predefined OMI ECG findings would be more accurate than STEMI criteria for the diagnosis of OMI., Methods: We performed a retrospective case-control study of patients with suspected acute coronary syndrome. The primary definition of OMI was either 1) acute TIMI 0-2 flow culprit or 2) TIMI 3 flow culprit with peak troponin T ≥ 1.0 ng/mL or I ≥ 10.0 ng/mL., Results: 808 patients were included, of whom 49% had AMI (33% OMI; 16% NOMI). Sensitivity, specificity, and accuracy of STEMI criteria vs Interpreter 1 using OMI ECG findings among 808 patients were 41% vs 86%, 94% vs 91%, and 77% vs 89%, and for Interpreter 2 among 250 patients were 36% vs 80%, 91% vs 92%, and 76% vs 89%. STEMI(-) OMI patients had similar infarct size and mortality as STEMI(+) OMI patients, but greater delays to angiography., Conclusions: Blinded interpretation using predefined OMI ECG findings was superior to STEMI criteria for the ECG diagnosis of Occlusion MI. These data support further investigation into the OMI vs. NOMI paradigm and suggest that STEMI(-) OMI patients could be identified rapidly and noninvasively for emergent reperfusion using more accurate ECG interpretation., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2021 The Authors.)

There has been a reduction in the reported cases of acute myocardial infarction (MI) across the globe during the outbreak of coronavirus disease 2019 (COVID-19) (severe acute respiratory distress syndrome coronavirus 2). An attempt was made to find out the number of acute MI cases treated during the COVID-19 lockdown period (April 2020) and highlight the possible reasons for the changes in the occurrence. A multicentric retrospective observational study was performed to collect the selected data from 12 private hospitals distributed in 4 cities-Madurai, Trichy (Thiruchirapalli), Erode, and Salem-of the Tamil Nadu state in southern India. There was a significant ( P <.001) reduction in ST-segment elevation MI (STEMI), non-STEMI (NSTEMI), and total (STEMI and NSTEMI together) cases during the lockdown period (April 1 to 30, 2020) as compared with no-lockdown periods such as January and February 2020 and April 2019 and April 2018 in all cities, whereas the reduction was not significant for NSTEMI in Trichy when data for the lockdown period was compared with those for January and February 2020. Overall, there is a reduction in acute MI cases, which may be due to alterations in modifiable risk factors during the COVID-19 lockdown period. Hence, implementation of public education and polices on controlling modifiable risk factors is likely to pay dividends., (© 2020 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc.)

Objective: To assess the effects of weekend admission vs weekday admission on the management and outcomes of acute myocardial infarction (AMI)., Methods: Adult ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) hospital admissions were identified using the National (Nationwide) Inpatient Sample (2000-2016). Interhospital transfers were excluded. Timing of coronary angiography (CA) and percutaneous coronary intervention (PCI) relative to the day of admission was identified. Outcomes of interest included in-hospital mortality, receipt of early CA, timing of CA and PCI, resource utilization, and discharge disposition for weekend vs weekday admissions., Results: Of the 9,041,819 AMI admissions, 2,406,876 (26.6%) occurred on weekends. Compared with 2000, in 2016 there was an increase in weekend STEMI (adjusted odds ratio [aOR], 1.12; 95% CI, 1.08-1.16; P <.001) but not NSTEMI (aOR, 1.01; 95% CI, 0.98-1.02; P =.21) admissions. Compared with weekday admissions, weekend admissions received comparable CA (59.9% vs 58.8%) and PCI (38.4% vs 37.6%) and specifically lower rates of early CA (hospital day 0) (26.0% vs 20.8%; P <.001). There was a steady increase in CA and PCI use during the 17-year period. Mean ± SD time to CA was higher in the weekend group vs the weekday group (1.2±1.8 vs 1.0±1.8 days; P <.001). Weekend admission did not influence in-hospital mortality (aOR, 1.01; 95% CI, 1.00-1.01; P =.05) but had fewer discharges to home (58.7% vs 59.7%; P <.001)., Conclusion: Despite small differences in CA and PCI, there were no differences in in-hospital mortality of AMI admissions on weekdays vs weekends in the United States in the contemporary era., (© 2020 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc.)

Introduction: Thrombotic and inflammatory mechanisms are involved in the pathophysiology of acute coronary syndrome (ACS). The aim of the study was the evaluation of inflammation (white blood cells count/WBC, C-reactive protein/CRP, interleukin-6/IL-6) and platelet (platelet count/PLT, mean platelet volume/MPV, large platelet/LPLT, beta-thromboglobulin/β-TG) biomarkers in the groups of ACS patients depending on the severity of signs and symptoms and compared to controls without coronary artery disease., Materials and Methods: The study group included 93 patients categorized into 3 subgroups depending on the severity of signs and symptoms of ACS. PLT, MPV, LPLT, and WBC were determined on hematological analyzer, IL-6 and β-TG were measured using the ELISA method., Results: In the whole group of ACS patients WBC, CRP, IL-6, MPV, and β-TG were significantly higher as compared to controls. Analyzing the inflammation and platelet biomarkers depending on the severity of signs and symptoms in comparison to controls, statistically significant differences for above-mentioned parameters were also found. There were no significant differences between the advancement of coronary artery changes and inflammation as well as platelet parameters, except for CRP concentrations. The AUCs for all inflammation parameters tested were similar, however the highest AUCs showed WBC and CRP. Among platelet parameters the highest AUC revealed β-TG., Conclusion: Markers of inflammation and platelet activation may be associated to myocardial ischemia and myocardial injury. WBC, CRP and IL-6 as inflammation parameters and MPV and β-TG as platelet biomarkers may be useful indicators of the presence of coronary artery disease.

Objective: To assess the role of Copeptin in diagnosis of acute myocardial infarction in troponin-blind period., Subjects and Methods: This study was conducted on 40 patients who presented to emergency department complaining of chest pain and were highly suspicious to have acute cardiac ischemia, in addition to 10 subjects serving as a healthy control group. Blood samples were collected for determination of CK-MB, cTnI and Copeptin. These were measured twice (in patients' group); at 3 h and then at 6-9 h from admission time., Results: The first sample revealed a non-significant difference between UA group and AMI group as regards CKMB and troponin, however, high significant difference was found as regards Copeptin (Z = 5.29, P < 0.001). Moreover, ROC curve analysis of serum Copeptin for discriminating AMI group from UA group in the first sample showed diagnostic sensitivity and specificity of 100%., In Conclusion: Determination of copeptin in early diagnosis of AMI has diagnostic value being superior to a conventional cTn-I within the first three hours after acute chest pain.

Expression of the interleukin-1 receptor type I (IL-1RI) co-receptor Toll-like and interleukin-1 receptor regulator (TILRR) is significantly increased in blood monocytes following myocardial infarction and in the atherosclerotic plaque, whereas levels in healthy tissue are low. TILRR association with IL-1RI at these sites causes aberrant activation of inflammatory genes, which underlie progression of cardiovascular disease. The authors show that genetic deletion of TILRR or antibody blocking of TILRR function reduces development of atherosclerotic plaques. Lesions exhibit decreased levels of monocytes, with increases in collagen and smooth muscle cells, characteristic features of stable plaques. The results suggest that TILRR may constitute a rational target for site- and signal-specific inhibition of vascular disease.

Objectives: High sensitivity cardiac troponin T and I (hs-cTnT and hs-cTnI) assays show analytical, diagnostic and prognostic improvement over contemporary sensitive cTn assays. However, given the importance of troponin in the diagnosis of myocardial infarction, implementing this test requires rigorous analytical and clinical verification across the total testing pathway. This was the aim of this study., Design and Methods: Analytical verification included assessment of critical outlier frequency, for hs-cTnI and cTnI assays. Concordance for paired cTnI and hs-cTnI measurements ( n =1096) was verified using 99th percentiles for both genders (cTnI: 30 ng/L, hs-cTnI: 25 ng/L) and for men and women separately (hs-cTnI: M: 34;F: 16 ng/L). Discordant data was correlated with clinical and laboratory information. Diagnosis of Acute Coronary Syndrome (ACS) or Non-ACS was adjudicated by two cardiologists independently., Results: The hs-cTnI assay showed a lower (10-fold) critical outlier rate (0.091%) and more detectable results above the limit of detection (LOD) (23.4%) and 99th percentile (2.4%), compared to cTnI. Analytical concordance between the two assays was high (94.5%) but decreased (91.7%) when gender-specific hs-cTnI cut-offs were used. The hs-cTnI assay gave fewer false negatives (up to 1.0%) but disproportionately more false positives (up to 6.7%) overall, which improved (3.9%) for serial measurements., Conclusions: Laboratories should analytically and clinically verify hs-cTn assays before use, with attention to performance and the clinical and diagnostic algorithms that support appropriate testing and result interpretation. Work in the pre- and post-analytical phases is necessary to augment the analytical improvement in the new era of troponin testing.