Search

Background: Acute Coronary Syndrome (ACS) stands as a significant contributor to cardiovascular mortality, necessitating improved diagnostic tools for early detection and tailored therapeutic interventions. Current diagnostic modalities, exhibit limitations in sensitivity and specificity, urging the quest for novel biomarkers to enhance discrimination of the different stages of ACS including unstable angina, Non-ST-segment Elevation Myocardial Infarction (NSTEMI), and ST-segment Elevation Myocardial Infarction (STEMI)., Methods: This study investigated the potential of a plasma-circulating multi-noncoding RNA (ncRNA) panel, comprising four miRNAs (miR-182-5p, miR-23a-3p, miR-146a-5p, and miR-183-5p) and three lncRNAs (SNHG15, SNHG5, and RMRP), selected based on their intricate involvement in ACS pathogenesis and signaling pathways regulating post-myocardial infarction (MI) processes. The differential expression of these ncRNAs was validated in sera of ACS patients and healthy controls via real-time polymerase chain reaction (RT-PCR)., Results: Analysis revealed a marked upregulation of the multi-ncRNAs panel in ACS patients. Notably, miRNA-182-5p and lncRNA-RMRP exhibited exceptional discriminatory power, indicated by the high area under the curve (AUC) values (0.990 and 0.980, respectively). Importantly, this panel displayed superior efficacy in discriminating between STEMI and NSTEMI, outperforming conventional biomarkers like creatine kinase-MB and cardiac troponins. Additionally, the four miRNAs and lncRNA RMRP showcased remarkable proficiency in distinguishing between STEMI and unstable angina., Conclusion: The findings underscore the promising potential of the multi-ncRNA panel as a robust tool for early ACS detection, and precise differentiation among ACS subtypes, and as a potential therapeutic target., Competing Interests: Declaration of Competing Interest The authors report no declarations of interest., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

The concept that the culprit lesion in non-ST segment elevation myocardial infarction (NSTEMI) is caused by sudden plaque rupture with acute thrombus formation has recently been challenged. While angiography is an old gold-standard for culprit identification it merely visualizes the lumen contour. Optical coherence tomography (OCT) provides a detailed view of culprit features. Combined with myocardial edema on cardiac magnetic resonance (CMR), indicating acute ischemia and thus culprit location, we aimed to characterize culprit lesions using OCT. Patients with NSTEMI referred for angiography were prospectively enrolled. OCT was performed on angiographic stenoses ≥50% and on operator-suspected culprit lesions. Hierarchical OCT-culprit identifiers were defined in case of multiple unstable lesions, including OCT-defined thrombus age. An OCT-based definition of an organizing thrombus as corresponding to histological early healing stage was introduced. Lesions were classified as OCT-culprit or non-culprit, and characteristics compared. CMR was performed in a subset of patients. We included 65 patients with 97 lesions, of which 49 patients (75%) had 53 (54%) OCT-culprit lesions. The most common OCT-culprit identifiers were the presence of acute (66%) and organizing thrombus (19%). Plaque rupture was visible in 45% of OCT-culprit lesions. CMR performed in 38 patients revealed myocardial oedema in the corresponding territories of 67% of acute thrombi and 50% of organizing thrombi. A culprit lesion was identified by OCT in 75% patients with NSTEMI. Acute thrombus was the most frequent feature followed by organizing thrombus. Applying specific OCT-criteria to identify the culprit could prove valuable in ambiguous cases., (© 2023. The Author(s).)

Objectives: Parametric cardiac magnetic resonance (CMR) techniques have improved the diagnosis of pathologies. However, the primary tool for differentiating non-ST elevation myocardial infarction (NSTEMI) from myocarditis is still a visual assessment of conventional signal-intensity-based images. This study aimed at analyzing the ability of parametric compared to conventional techniques to visually differentiate ischemic from non-ischemic myocardial injury patterns., Methods: Twenty NSTEMI patients, twenty infarct-like myocarditis patients, and twenty controls were examined using cine, T2-weighted CMR (T2w) and late gadolinium enhancement (LGE) imaging and T1/T2 mapping on a 1.5 T scanner. CMR images were presented in random order to two experienced fully blinded observers, who had to assign them to three categories by a visual analysis: NSTEMI, myocarditis, or healthy., Results: The conventional approach (cine, T2w and LGE combined) had the best diagnostic accuracy with 92% (95%CI: 81-97) for NSTEMI and 86% (95%CI: 71-94) for myocarditis. The diagnostic accuracies using T1 maps were 88% (95%CI: 74-95) and 80% (95%CI: 62-91), 84% (95%CI: 67-93) and 74% (95%CI: 54-87) for LGE, and 83% (95%CI: 66-92) and 73% (95%CI: 53-87) for T2w. The accuracies for cine (72% (95%CI: 52-86) and 60% (95%CI: 38-78)) and T2 maps (62% (95%CI: 40-79) and 47% (95%CI: 28-68)) were significantly lower compared to the conventional approach (p < 0.001 and p < 0.0001)., Conclusions: The conventional approach provided a reliable visual discrimination between NSTEMI, myocarditis, and controls. The diagnostic accuracy of a visual pattern analysis of T1 maps was not significantly inferior, whereas the diagnostic accuracy of T2 maps was not sufficient in this context., Clinical Relevance Statement: The ability of parametric compared to conventional CMR techniques to visually differentiate ischemic from non-ischemic myocardial injury patterns can avoid potentially unnecessary invasive coronary angiography and help to shorten CMR protocols and to reduce the need of gadolinium contrast agents., Key Points: • A visual differentiation of ischemic from non-ischemic patterns of myocardial injury is reliably achieved by a combination of conventional CMR techniques (cine, T2-weighted and LGE imaging). • There is no significant difference in accuracies between visual pattern analysis on native T1 maps without providing quantitative values and a conventional combined approach for differentiating non-ST elevation myocardial infarction, infarct-like myocarditis, and controls. • T2 maps do not provide a sufficient diagnostic accuracy for visual pattern analysis for differentiating non-ST elevation myocardial infarction, infarct-like myocarditis, and controls., (© 2023. The Author(s).)

The aim of the study is to evaluate the dependence of associations of ST2, and Troponin I level on the nature of the anatomical lesion of the coronary arteries. We examined 200 patients with NSTEMI aged 38 to 80 years, who were urgently hospitalized in the Vinnytsya Regional Clinical Center of Cardiovascular Pathology. All patients underwent laboratory testing of ST2, and Troponin I level in plasma by enzyme-linked immunosorbent assay on the first day of hospitalization before coronary angiography. In the association of relatively high levels of ST2 and relatively high levels of Troponin I, there is a positive correlation between the degree of coronary arteries damage, while in the association of relatively low levels of ST2 and Troponin I, severe stenotic coronary arteries lesions can be ruled out. Determining the associations of ST2 and Troponin I before coronary angiography allows to predict the degree of stenotic lesions of the coronary arteries and to determine the expected intervention strategy in patients with NSTEMI.

Aims: Coronary artery disease (CAD) is described as a range of clinical conditions including myocardial infarction (MI) and unstable angina. Lipid and apolipoprotein profiles together with the study of cholesterol deposit and efflux serve to identify novel pre and post infarct scenarios for the treatment of these patients. In (non-ST elevation myocardial infarction) NSTEMI patients, we analysed both systemic and intracoronary serum ability to accept cholesterol as well as cholesterol efflux capacity (CEC) of monocytes in terms of expression of genes involved in the reverse cholesterol transport (RCT)., Methods and Results: While HDL-C quantity was similar between systemic and coronary arterial blood, in 21 NSTEMI patients we observed a significant reduction of the preβ-HDL fraction and the levels of Apolipoproteins AI, AII, B and E in coronary versus systemic serum. These data are complemented with the observed reduction of CEC. On the contrary, compared to systemic arterial monocytes, in coronary microenvironment of NSTEMI patients after myocardial infarction, the monocytes exhibited a higher mRNA expression of nuclear receptor LXRα and its targets ABCA1 and APOE, which drive cholesterol efflux capacity., Conclusion: In this cross-sectional study we observe that in the immediate post infarction period, there is a spontaneous bona fide ligand-induced activation of the LXR driven cholesterol efflux capacity of intracoronary monocytes to overcome the reduced serum ability to accept cholesterol and to inhibit the post-infarction pro-inflammatory local microenvironment., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) studies have demonstrated that lipid core plaque (LCP) is frequently observed in the culprit segment of myocardial infarction (MI). However, little is known about the impact of clinical presentations such as chronic coronary syndrome (CCS) and acute coronary syndrome (ACS) including unstable angina (UA), non ST-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI) on LCP. The present prospective single-center registry included a total of 178 patients who underwent percutaneous coronary intervention under NIRS-IVUS guidance. Patients were divided into CCS and ACS groups, and ACS patients were further sub-divided into the 3 groups according to the clinical presentation. The primary endpoint was coronary LCP in the target lesion assessed by NIRS-IVUS with maximal lipid core burden index over any 4 mm segment (maxLCBI 4mm ). The study population included 124 and 54 patients with CCS and ACS. MaxLCBI 4mm in the target lesion was significantly higher in the ACS group than in the CCS group (503 [284-672] vs. 406 [250-557], p = 0.046). Among ACS patients, MaxLCBI 4mm in the target lesion was also significantly different in those with UA (n = 18), NSTEMI (n = 21), and STEMI (n = 15) (288 [162-524] vs. 518 [358-745] vs. 646 [394-848], p = 0.021). In conclusion, LCP assessed by NIRS-IVUS, a surrogate of coronary plaque vulnerability, was significantly different according to the clinical presentations such as CCS, UA, NSTEMI, and STEMI.

Background: In intermediate- and high-risk non-ST elevated acute coronary syndrome (NSTE-ACS) patients, a routine invasive approach is recommended. The timing of coronary angiography remains controversial. To assess whether an immediate (<3 hours) invasive treatment strategy would reduce infarct size and is safe, compared with an early strategy (12-24 hours), for patients admitted with NSTE-ACS while preferably treated with ticagrelor., Methods: In this single-center, prospective, randomized trial an immediate or early invasive strategy was randomly assigned to patients with NSTE-ACS. At admission, the patients were preferably treated with a combination of aspirin, ticagrelor and fondaparinux. The primary endpoint was the infarct size as measured by area under the curve (AUC) of CK-MB in 48 hours. Secondary endpoints were bleeding outcomes and major adverse cardiac events (MACE): composite of all-cause death, MI and unplanned revascularization. Interim analysis showed futility regarding the primary endpoint and trial inclusion was terminated., Results: In total 249 patients (71% of planned) were included. The primary endpoint of in-hospital infarct size was a median AUC of CK-MB 186.2 ng/mL in the immediate group (IQR 112-618) and 201.3 ng/mL in the early group (IQR 119-479). Clinical follow-up was 1-year. The MACE-rate was 10% in the immediate and 10% in the early group (hazard ratio [HR] 1.13, 95% CI: 0.52-2.49)., Conclusions: In NSTE-ACS patients randomized to either an immediate or an early-invasive strategy the observed median difference in the primary endpoint was about half the magnitude of the expected difference. The trial was terminated early for futility after 71% of the projected enrollment had been randomized into the trial., Competing Interests: Declaration of interest FWAV has received honoraria for consulting and presentations from AstraZeneca. All other authors have no conflicts of interest to declare., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Contrast-enhanced (CE) steady-state free precession (SSFP) CMR at 1.5T has been shown to be a valuable alternative to T2-based methods for the detection and quantifications of area-at-risk (AAR) in acute myocardial infarction (AMI) patients. However, CE-SSFP's capacity for assessment of AAR at 3T has not been investigated. We examined the clinical utility of CE-SSFP and T2-STIR for the retrospective assessment of AAR at 3T with single-photon-emission-computed tomography (SPECT) validation., Materials and Methods: A total of 60 AMI patients (ST-elevation AMI, n = 44;  non-ST-elevation AMI, n = 16) were recruited into the CMR study between 3 and 7 days post revascularization. All patients underwent T2-STIR, CE-bSSFP and late-gadolinium-enhancement CMR. For validation, SPECT images were acquired in a subgroup of patients (n = 30)., Results: In 53 of 60 patients (88 %), T2-STIR was of diagnostic quality compared with 54 of 60 (90 %) with CE-SSFP. In a head-to-head per-slice comparison (n = 365), there was no difference in AAR quantified using T2-STIR and CE-SSFP (R 2  = 0.92, p < 0.001; bias:-0.4 ± 0.8 cm 2 , p = 0.46). On a per-patient basis, there was good agreement between CE-SSFP (n = 29) and SPECT (R 2  = 0.86, p < 0.001; bias: - 1.3 ± 7.8 %LV, p = 0.39) for AAR determination. T2-STIR also showed good agreement with SPECT for AAR measurement (R 2  = 0.81, p < 0.001, bias: 0.5 ± 11.1 %LV, p = 0.81). There was also a strong agreement between CE-SSFP and T2-STIR with respect to the assessment of AAR on per-patient analysis (R 2  = 0.84, p < 0.001, bias: - 2.1 ± 10.1 %LV, p = 0.31)., Conclusions: At 3T, both CE-SSFP and T2-STIR can retrospectively quantify the at-risk myocardium with high accuracy.

Background: Myocardial infarction with nonobstructive coronary arteries (MINOCA) can be clinically categorized as ST-segment elevation (STE) and non-ST-segment elevation (NSTE), whose clinical prognosis are poorly understood. The aim of this study was to compare the clinical outcome and their predictors of patients with STE and NSTE in MINOCA population., Methods: A total of 265 patients with MINOCA (102 with STE, and 163 with NSTE) were consecutively collected. Clinical profile, prognosis, and predictors of all patients were assessed., Results: The proportion of patients with NSTE was greater than patients with STE in MINOCA population. Patients with NSTE were older and more likely to be female and had a higher incidence of atrial fibrillation. Both high density lipoprotein (HDL) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were higher in the NSTE group. Patients with STE were more likely to have a history of smoking and a higher diastolic blood pressure. During the 1-year follow up, there were no differences in the outcomes between the STE and NSTE groups, with no significant differences in mortality and a similar rate of major adverse cardiovascular events (MACE) (20.9% vs 19.3%, P = 0.767). The multivariable predictors of MACE in the NSTE groups were age, lower level of total cholesterol, hypertension, and smoking history, whereas reduced left ventricular ejection fraction, and diabetes mellitus were the multivariable predictors of major adverse cardiac events in the STE group., Conclusions: There were differences in the clinical profile between STE and NSTE in the MINOCA population, whereas the outcomes during the 1-year follow up were similar. The STE and NSTE groups had different predictive factors for major adverse cardiac events., (Copyright © 2020 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Aims: To investigate in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) the prevalence and the features of optical coherence tomography (OCT)-detected macrophages accumulation in culprit plaques as compared with nonculprit plaques (NCP)., Methods: The study is a post-hoc analysis of a prospective study aimed at evaluating the relationship between aortic inflammation as assessed by F-fluorodeoxyglucose-PET and features of coronary plaque vulnerability as assessed by OCT. We enrolled 32 patients with first NSTE-ACS who successfully underwent three-vessel OCT., Results: The median age was 65 (54-72) years and 27 patients (84%) were men. Culprit plaques were clinically defined. Overall, the rate of lipid plaques and lipid plaques containing macrophages were 6.4 and 4.2 per patient, respectively. Culprit plaques had a smaller minimal luminal area, a higher extension of lipid component and a thinner fibrous cap than NCPs. Macrophages accumulations were more likely found in culprit plaque (84 vs. 61%, P = 0.015) in which they had also a higher circumferential extension. On univariable analysis, macrophages accumulation extension had a higher association with culprit plaques (odds ratio = 4.42; 95% confidence interval; 2.54-9.15, P < 0.001) than the mere presence of macrophages accumulation (odds ratio = 3.36; 95% confidence interval; 1.30-8.66, P = 0.012). Culprit plaques with thrombus had a lower distance between macrophages accumulation and the luminal surface than culprit plaque with no thrombus (0.06 vs. 0.1 mm; P = 0.04)., Conclusion: In patients with NSTE-ACS, macrophages accumulations are more likely present in culprit plaque in which they disclose also a greater extension compared with those observed in NCP. The distance between macrophages accumulation and the luminal surface is lower in thrombotic culprit plaque than that in nonthrombotic culprit plaque.

Background Muscle wasting is an important predictor of long-term outcome in patients with cardiovascular disease, but the prognostic value of muscle wasting in patients with non‒ST-segment‒elevation myocardial infarction is not established. The aim of this study is to investigate the prognostic value of muscle wasting, defined by psoas muscle mass index (PMI), in patients with non‒ST-segment‒elevation myocardial infarction. Methods and Results A total of 132 consecutive patients with non‒ST-segment‒elevation myocardial infarction were prospectively enrolled between 2015 and 2018. Primary end point was incidence of cardiovascular events including cardiovascular deaths, non-fatal myocardial infarction, or non-fatal stroke. Cross-sectional area of the psoas muscle at the L3 vertebral level was obtained by computed tomography and PMI was calculated. The median follow-up period was 2.4 years (interquartile range, 1.1-4.0 years). There were 45 cardiovascular events (34%) during the study periods. The optimal cutoff value of PMI to predict cardiovascular events was 772 mm 2 /m 2 , as assessed by receiver operating curve analysis. Patients with reduced PMI (PMI<772 mm 2 /m 2 ) had significantly higher cardiovascular events than those with preserved PMI (PMI≥772 mm 2 /m 2 ) (48% versus 21%; log-rank test P <0.001). Multivariate Cox proportional hazards model revealed that reduced PMI was a statistically significant predictor of cardiovascular events (hazard ratio, 3.30; 95% CI, 1.70-6.40; P <0.001). Conclusions Muscle wasting defined as PMI is a simple and useful objective marker to predict future cardiovascular outcome in patients with non‒ST-segment‒elevation myocardial infarction. Registration Information URL: https://www.umin.ac.jp/ctr/; Unique identifier: UMIN000013445.

Concentrations of different circulating microparticles (MPs) may have clinical and physiological relevance to cardiovascular disease pathologies., Purpose: To quantify plasma concentrations of CD31+/CD42b-, CD62E+, and CD34+ MPs across healthy individuals and those with coronary artery disease (CAD) or acute cardiovascular events (non-ST elevation myocardial infarction (NSTEMI)). Fasted blood was obtained from CAD patients (n = 10), NSTEMI patients (n = 13), and healthy older men (n = 15) 60-75 years old., Methods: CD31+/CD42b-, CD62E+, and CD34+ MPs were isolated from plasma and quantified using flow cytometry. Relationships between MP subtypes, fasting blood lipids, blood glucose, blood pressure, body mass index, and total number of medications were assessed., Results: Concentrations of CD31+/CD42b- MPs were significantly lower in CAD and NSTEMI subjects compared with healthy individuals (p = .02 and .003, respectively). No differences between groups were found for CD62E+ or CD34+ MPs (p > .05 for both). Surprisingly, among all variables assessed, only CD62E+ MP concentrations were positively correlated with triglyceride levels (p = .012) and inversely correlated with SBP (p = .03)., Conclusions: Our findings provide support for the use of different MP subtypes, specifically CD31+/CD42b- MPs, as a potential biomarker of cardiovascular disease. Importantly, results from this study should be looked at in adjunct to previous MP work in CVD conditions as a way of highlighting the complex interactions of variables such as comorbid conditions and medications on MP concentrations., (© 2020 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Importance: Thyroid hormones play a key role in modulating myocardial contractility. Subclinical hypothyroidism in patients with acute myocardial infarction is associated with poor prognosis., Objective: To evaluate the effect of levothyroxine treatment on left ventricular function in patients with acute myocardial infarction and subclinical hypothyroidism., Design, Setting, and Participants: A double-blind, randomized clinical trial conducted in 6 hospitals in the United Kingdom. Patients with acute myocardial infarction including ST-segment elevation and non-ST-segment elevation were recruited between February 2015 and December 2016, with the last participant being followed up in December 2017., Interventions: Levothyroxine treatment (n = 46) commencing at 25 µg titrated to aim for serum thyrotropin levels between 0.4 and 2.5 mU/L or identical placebo (n = 49), both provided in capsule form, once daily for 52 weeks., Main Outcomes and Measures: The primary outcome measure was left ventricular ejection fraction at 52 weeks, assessed by magnetic resonance imaging, adjusted for age, sex, type of acute myocardial infarction, affected coronary artery territory, and baseline left ventricular ejection fraction. Secondary measures were left ventricular volumes, infarct size (assessed in a subgroup [n = 60]), adverse events, and patient-reported outcome measures of health status, health-related quality of life, and depression., Results: Among the 95 participants randomized, the mean (SD) age was 63.5 (9.5) years, 72 (76.6%) were men, and 65 (69.1%) had ST-segment elevation myocardial infarction. The median serum thyrotropin level was 5.7 mU/L (interquartile range, 4.8-7.3 mU/L) and the mean (SD) free thyroxine level was 1.14 (0.16) ng/dL. The primary outcome measurements at 52 weeks were available in 85 patients (89.5%). The mean left ventricular ejection fraction at baseline and at 52 weeks was 51.3% and 53.8%, respectively, in the levothyroxine group compared with 54.0% and 56.1%, respectively, in the placebo group (adjusted difference in groups, 0.76% [95% CI, -0.93% to 2.46%]; P = .37). None of the 6 secondary outcomes showed a significant difference between the levothyroxine and placebo treatment groups. There were 15 (33.3%) and 18 (36.7%) cardiovascular adverse events in the levothyroxine and placebo groups, respectively., Conclusions and Relevance: In this preliminary study involving patients with subclinical hypothyroidism and acute myocardial infarction, treatment with levothyroxine, compared with placebo, did not significantly improve left ventricular ejection fraction after 52 weeks. These findings do not support treatment of subclinical hypothyroidism in patients with acute myocardial infarction., Trial Registration: isrctn.org Identifier: http://www.isrctn.com/ISRCTN52505169.

Background: Recently, trimethylamine N-oxide (TMAO) unexplained gut microbe has been proposed as a promising risk factor for atherosclerotic cardiovascular disease (CVD) pathogenesis and adverse events. The relationship of TMAO with coronary atherosclerotic burden has been evaluated in patients with stable coronary artery disease and ST-segment elevation myocardial infarction, but still needs to be explored in newly diagnosed non-ST-segment elevation myocardial infarction (NSTEMI) patients., Material and Methods: A prospective, single-center, SZ-NSTEMI trial (ChiCTR1900022366) is underway to investigate the relationship of TMAO with the severity and prognosis of coronary atherosclerosis in newly diagnosed NSTEMI patients who will undergo coronary angiography with primary percutaneous coronary intervention (pPCI). The primary endpoint of the study will be assessed the association of TMAO with coronary atherosclerotic severity quantify by the number of diseased coronary arteries and SYNTAX score after the coronary angiography. The secondary endpoints will be identified the TMAO as a prognostic biomarker for the short (1 month) and long-term (12 months) major cardiovascular and cerebrovascular events (MACCEs) rate including myocardial infarction, target vessel revascularization, stroke, heart failure, all-cause rehospitalization, and all-cause mortality after the pPCI. The blood samples will be collected from each patient before the procedure to measure the TMAO by isotope dilution high-performance liquid chromatography. In conclusion, SZ-NSTEMI will be the first cohort that will be investigated the association of TMAO with the severity and prognosis of coronary atherosclerotic burden in NSTEMI patients, aiming to identify TMAO as a predictor and a prognostic biomarker.

Rationale: The De Winter ST/T-wave complex is a rare and special electrocardiogram (ECG) manifestation in some patients with a total or subtotal occlusion in the proximal left anterior descending (LAD) coronary artery. It mainly appears as an ST-segment superior oblique depression instead of an ST elevation. However, a transitory change of the De Winter ST/T-wave complex has not been reported previously., Patient Concerns: A 40-year-old man developed sudden precordial dull and unrelieved pain. One hour later, he suddenly lost consciousness when he arrived at the emergency department. After successful cardiopulmonary resuscitation (CPR), 2 ECGs were taken at 22-minute interval, which showed completely different manifestations. The first ECG showed acute inferior-wall ST elevation myocardial infarction (STEMI), while the second ECG showed a De Winter ST/T-wave complex, which indicated acute anterior-wall myocardial infarction., Diagnosis: The patient was diagnosed with acute myocardial infarction., Interventions: The patient responded to urgent treatment by percutaneous coronary intervention (PCI)., Outcomes: It was confirmed that the case was consistent with the main characteristics of a De Winter ST/T-wave complex after PCI. The first ECG was a rare transitory change of the De Winter ST/T-wave complex. The patient was well recovered and discharged., Lessons: The De Winter ST/T-wave complex is an extremely dangerous and rare ECG manifestation that is not widely recognized at present. Although the mechanism is not very clear, it should be considered as indicating an equivalent risk of STEMI because it may suggest total or subtotal occlusion in the proximal LAD coronary artery. It is believed that in the near future, the mechanism of ECG including its transitory changes, will be fully revealed.

Background: Strain has shown a promising diagnostic and prognostic value in acute coronary syndromes. With, however, less data in non-ST elevation myocardial infarction (NSEMI)., Aim: to evaluate in NSTEMI patients, the ability of strain to predict the severity of the disease, by assessing correlations to established prognostic parameters, and to predict culprit and occluded coronary arteries (CA). Secondary, to determine factors associated to strain changes during follow-up., Methods: The study was prospective, NSTEMI patients with significant coronary lesion and without significant non-ischaemic disease were included. Angiographic and echocardiographic investigation including global (GLS) and territorial (TLS) longitudinal strain were performed within 24h from admission. Syntax I score was calculated. Severe coronary artery disease (CAD) was defined by left main of three-vessel disease., Results: Seventy NSTEMI patients aged 60.2±10.1 years were enrolled; 61% were smokers, 54% diabetics and 46% hypertensive. 34% had a severe CAD, 7% had an acute coronary occlusion (ACO) and 14% a chronic coronary total occlusion (CTO). GLS >-15.3% predicted a left ventricular ejection fraction (LVEF) <50% with 80% Sensitivity (Se) and 78% Specificity (Sp). GLS was associated to CAD complexity and severity. GLS > -14.1% detected severe CAD with 83% Se and 80%Sp. TLS determined the culprit artery in 74% of cases and TLS > -9.2% predicted ACO with 85% Se and 85% Sp. TLS was also associated to CTO. At a 10 months median follow-up [3-12months], GLS significantly improved, baseline LVEF, GLS, wall motion score index and revascularization were the predictors of this improvement., Conclusion: In NSTEMI patients, GLS detected severe CAD and poor myocardial function. TLS predicted the culprit vessel and its occlusion. GLS improvement at midterm was predicted by baseline systolic LV function parameters and myocardial revascularization.

Background: Endothelial microvesicles (EMVs) have emerged as markers of endothelial injury. However, little is known about their levels in the coronary circulation of acute coronary syndrome (ACS) and stable coronary artery disease (CAD). We hypothesized that ACS patients exhibit a more pronounced increase of EMVs both in the peripheral and coronary circulation when compared with CAD. We also investigated possible associations of EMVs with markers preclinical target organ damage., Methods: We enrolled consecutive eligible patients undergoing coronary angiography. Blood samples were collected from the stem of the left coronary artery and the femoral artery. ΕMVs were measured by a standardized flow cytometry protocol. Central systolic blood pressure (cSBP) was measured invasively and patients' history was recorded., Results: CAD patients exhibited increased levels of EMVs compared with controls. When patients with ACS and stable CAD were compared, the former had significantly increased EMVs in both coronary and peripheral circulation. Importantly, both ACS and CAD patients exhibited increased levels of EMVs in the coronary circulation compared with periphery. In addition, EMVs were associated with cSBP., Conclusions: EMVs emerge as novel markers of ongoing underlying vascular damage, further augmenting the vicious cycle of inflammation and thrombosis mainly in ACS but also in stable CAD., (© American Journal of Hypertension, Ltd 2019. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Objective: The aim of this study was to examine DNA ligase activity and expression of DNA damage response pathway (DDR) genes in patients with stable angina (SA) and non-ST elevation myocardial infarction (NSTEMI) and determine whether they correlate with plaque morphology., Background: Patients with coronary artery disease (CAD) have evidence of deoxyribonucleic acid (DNA) damage in peripheral blood mononuclear cells (PBMCs). It is unclear whether this represents excess damage or defective DNA repair activity., Methods: DNA ligase activity and the expression of 22 DDR genes were measured in PBMCs of patients (both SA (n = 47) and NSTEMI (n = 42)) and in age and gender-matched controls (n = 35). Target lesion anatomical assessment was undertaken with frequency domain optical coherent tomography., Results: DNA ligase activity was different across the three groups of patients (control = 119 ± 53, NSTEMI = 115.6 ± 85.1, SA = 81 ± 55.7 units/g of nuclear protein; ANOVA p = 0.023). Pair wise comparison demonstrated that this significance is due to differences between the control and SA patients (p = 0.046). Genes involved in double strand break repair and nucleotide excision repair pathways were differentially expressed in patients with SA and NSTEMI. In SA patients, fibrocalcific plaques were strongly associated with GTSE1, DDB1, MLH3 and ERCC1 expression. By contrast, in NSTEMI patients the strongest association was observed between fibrous plaques and ATM and XPA expression., Conclusion: PBMCs from patients with CAD exhibit differences in DNA ligase activity and expression of DDR genes. Expression levels of certain DDR genes are strongly associated with plaque morphology and may play a role in plaque development and progression. Trial Registration Number URL: www.Clinicaltrials.gov; NCT02335086., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: The association between mean platelet volume (MPV) and coronary plaque vulnerability in patients with non-ST-elevation ACS (NSTE-ACS) has not been investigated. We performed a retrospective study to evaluate the association between MPV and plaque vulnerability using optical coherence tomography (OCT)., Methods: Consecutive NSTE-ACS patients who underwent pre-intervention OCT examination in our center were included in this study. Features of coronary plaques in the culprit arteries were classified as rupture, nonrupture with thin-cap fibroatheroma (TCFA), and nonrupture and non-TCFA. ROC analyses were used to determine the predictive efficacy of MPV for plaque rupture, and multivariate logistic regression analysis was performed to evaluate the potential independent predictors of plaque vulnerability., Results: Overall, 94 patients were included in this study. We identified 17 patients with plaque rupture, 10 with nonrupture with TCFA, and 67 with nonrupture and non-TCFA. ROC analyses showed that MPV ≥ 10.5 fL was predictive of plaque rupture in NSTE-ACS patients. Univariate analyses indicated that patients with higher MPV (≥ 10.5 fL) had higher body mass index and poorer lipid profiles compared to those with lower MPV. Moreover, those with higher MPV had higher incidences of plaque rupture and thrombosis (both P < 0.05). Results of multivariate analyses showed that diabetes and higher platelet distribution width (PDW) were independent risk factors of TCFA (P = 0.032 and 0.046, respectively), while diabetes, higher BMI, higher PDW, and higher MPV were independent determinants of plaque rupture in our cohorts (P all < 0.05)., Conclusions: Higher MPV is independently associated with higher risk of plaque rupture as evidenced by OCT in our cohort of NSTE-ACS patients.

We present the first reported case showing metastatic giant bone cell tumor being treated successfully with pembrolizumab after failing prior tyrosine kinase inhibitor therapy. Of note, the patient developed multiple systemic effects associated with checkpoint inhibitor use. One year after starting the checkpoint inhibitor (ICI), the patient also developed hepatitis that was confirmed by liver biopsy and pathology to be, in part, due to drug-mediated toxicity similar to prior ICI toxicity cases that have been reported. Additionally, although the patient had vascular risk factors (hypertension, diabetes and smoking), it was notable from a cardiology perspective that the patient developed 2 subsequent non-ST-elevation myocardial infarctions, with rapid progression of stenosis of the left circumflex artery 2 months apart. The first left heart catheterization showing minimal disease of the left circumflex, but 2 months later, presenting with chest pain, a repeat left heart catheterization showed significant stenosis of the left proximal circumflex, raising the possibilities that either ICI can promote plaque rupture and/or accelerated atherosclerosis; both phenomena have been shown to occur in animal models. The patient also developed thyroiditis with subsequent hypothyroidism, now on thyroid replacement from checkpoint inhibitor use. This case demonstrates the multiorgan adverse effects this new antioncologic agent can have and yet also its promising antitumor effects. Awareness of the side effects among primary care doctors and all specialists will be helpful in managing these potential side effects and research will help elucidate ways to prevent the adverse effects., (Copyright © 2019. Published by Elsevier Inc.)

Objective: This study aimed to assess the pathophysiological differences between saphenous vein grafts (SVG) and native coronary arteries (NCA) following presentation with non-ST elevated myocardial infarction (NSTEMI)., Background: There is accelerated pathogenesis of de novo coronary disease in harvested SVG following coronary artery bypass (CABG) surgery, which contributes to both early and late graft failure, and is also causal in adverse outcomes following vein graft PCI. However in vivo assessment, with OCT imaging, comparing the differences between vein grafts and NCAs has not previously been performed., Methods: We performed a retrospective, observational, analysis in patients who underwent PCI with adjunctive OCT imaging following presentation with NSTEMI, where the infarct-related artery (IRA) was either in an SVG or NCA., Results: A total of 1550 OCT segments was analysed from thirty patients with a mean age of 66.3 (±9.0) years were included. The mean graft age of 13.9 (±5.6) years in the SVG group. OCT imaging showed that the SVG group had evidence of increased lipid pool burden (lipid pool quadrants, 2.1 vs 2.7; p = 0.021), with a reduced fibro-atheroma cap-thickness in the SVG group (45.0 μm vs 38.5 μm; p = 0.05) and increased burden of calcification (calcified lesion length = 0.4 mm vs 1.8 mm; p = 0.007; calcified quadrants = 0.2 vs 0.9; p = 0.001; arc of superficial calcium deposits = 11.6° vs 50.9°; p = 0.007) when compared to NCA., Conclusion: This OCT study has demonstrated that vein grafts have a uniquely atherogenic environment which leads to the development of calcified, lipogenic, thin-capped fibro-atheroma's, which may be pivotal in the increased, acute and chronic graft failure rate, and may underpin the increased adverse outcomes following vein graft PCI., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Aims: To test T1 and T2 mapping in the assessment of acute myocardial injury in patients with non-ST-segment elevation myocardial infarction (NSTEMI), evaluated before revascularization., Methods: Forty-seven patients with acute NSTEMI underwent cardiac magnetic resonance (CMR) at 1.5 T, including T1 and T2 mapping., Results: Coronary angiography (CA) evidenced an obstructive coronary artery disease (CAD) in 36 patients (80%) and a non-obstructive CAD in 11 patients (20%). Edema was detected in 51.1/65.9% of patients in T1/T2 maps, respectively. This difference was due to artifacts in T1 maps. T1/T2 values were significantly higher in the infarcted myocardium (IM) compared with the remote myocardium (RM) (in T1: 1151.6 ± 53.5 ms vs. 958.2 ± 38.6 ms, respectively; in T2: 69 ± 6 ms vs. 51.9 ± 2.9 ms, respectively; p < 0.0001 for both). We found both an obstructive CAD at CA and myocardial edema at CMR in 53.2% of patients, while 8.5% of patients had a non-obstructive CAD and no edema. However, 25.5% of patients had an obstructive CAD without edema, while 12.8% of patients showed edema despite a non-obstructive CAD. Furthermore, in 6 of the edema-positive patients with multi-vessels obstructive CAD, CMR identified myocardial edema in a vascular territory different from that of the lesion supposed to be the culprit at CA., Conclusions: In a non-negligible percentage of NSTEMI patients, T1 and T2 mapping detect myocardial edema without significant stenosis at CA and vice versa. Therefore, CA and CMR edema imaging might provide complementary information in the evaluation of NSTEMI.

Circulating microRNAs (miRNAs) hold great potential as novel diagnostic markers for acute coronary syndrome (ACS). This study sought to identify plasma miRNAs that are differentially expressed in young ACS patients (mean age of 38.5 ± 4.3 years) and evaluate their diagnostic potentials. Small RNA sequencing (sRNA-seq) was used to profile plasma miRNAs. Discriminatory power of the miRNAs was determined using receiver operating characteristic (ROC) analysis. Thirteen up-regulated and 16 down-regulated miRNAs were identified in young ACS patients. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) validation showed miR-183-5p was significantly up-regulated (8-fold) in ACS patients with non-ST-segment elevated myocardial infarction (NSTEMI) whereas miR-134-5p, miR-15a-5p, and let-7i-5p were significantly down-regulated (5-fold, 7-fold and 3.5-fold, respectively) in patients with ST-segment elevated myocardial infarction (STEMI), compared to the healthy controls. MiR-183-5p had a high discriminatory power to differentiate NSTEMI patients from healthy controls (area under the curve (AUC) of ROC = 0.917). The discriminatory power for STEMI patients was highest with let-7i-5p (AUC = 0.833) followed by miR-134-5p and miR-15a-5p and this further improved (AUC = 0.935) with the three miRNAs combination. Plasma miR-183-5p, miR-134-5p, miR-15a-5p and let-7i-5p are deregulated in STEMI and NSTEMI and could be potentially used to discriminate the two ACS forms., Competing Interests: The authors have no competing interests associated with the manuscript.

Atherosclerosis is a chronic inflammatory disease characterized by a complex interplay between innate and adaptive immunity. Dendritic cells (DCs) play a key role in T-cell activation and regulation by promoting a tolerogenic environment through the expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (IDO), an intracellular enzyme involved in tryptophan catabolism. IDO expression and activity was analyzed in monocytes derived DCs (MDDCs) from non-ST segment elevation myocardial infarction (NSTEMI) patients, stable angina (SA) patients and healthy controls (HC) by real-time quantitative polymerase chain reaction (RT-qPCR) before and after in vitro maturation with lipopolysaccharide (LPS). The amount of tryptophan catabolite; kynurenine; was evaluated in the culture supernatants of mature-MDDCs by ELISA assay. Autologous mixed lymphocyte reaction (MLR) between mature-MDDCs and naïve T-cells was carried out to study the differentiation towards T-helper 1 (Th1) and induced regulatory T-cells (iTreg). Analysis of IDO mRNA transcripts in mature-MDDCs revealed a significant reduction in cells isolated from NSTEMI (625.0 ± 128.2; mean ± SEM) as compared with those from SA (958.5 ± 218.3; p = 0.041) and from HC (1183.6 ± 231.6; p = 0.034). Furthermore; the concentration of kynurenine was lower in NSTEMI patients (2.78 ± 0.2) and SA (2.98 ± 0.25) as compared with HC (5.1 ± 0.69 ng/mL; p = 0.002 and p = 0.016; respectively). When IDO-competent mature-MDDCs were co-cultured with allogeneic naïve T-cells, the ratio between the percentage of generated Th1 and iTreg was higher in NSTEMI (4.4 ± 2.9) than in SA (1.8 ± 0.6; p = 0.056) and HC (0.9 ± 0.3; p = 0.008). In NSTEMI, the tolerogenic mechanism of the immune response related to IDO production by activated MDDCs is altered, supporting their role in T-cell dysregulation., Competing Interests: The authors declare no conflicts of interest.

Objectives: We sought to assess a new modality of radiofrequency intravascular ultrasound (IVUS) called iMAP-IVUS (Boston Scientific, Santa Clara, California) during the evaluation of patients presenting with high-risk acute coronary syndromes., Background: There are limited data on plaque tissue characterization and phenotype classification using iMAP-IVUS., Methods: In the iWonder study patients presenting with ST-elevation myocardial infarction (STEMI) or non-STEMI underwent three-vessel grayscale IVUS and iMAP-IVUS tissue characterization prior to percutaneous intervention. In total 385 lesions from 100 patients were divided into culprit (n = 100) and nonculprit (n = 285) lesions. Lesion phenotype was classified as (i) thin-cap fibroatheroma (iMAP-derived TCFA); (ii) thick-cap fibroatheroma; (iii) pathological intimal thickening; (iv) fibrotic plaque; and (v) fibrocalcific plaque., Results: Culprit lesions had smaller minimum lumen cross-sectional area (MLA) with greater plaque burden compared to non-culprit lesions. Volumetric analysis showed that culprit lesions had longer length and larger vessel and plaque volumes compared to non-culprit lesions. iMAP-IVUS revealed that culprit lesions presented more NC and fibrofatty volume, both at lesion level and at the MLA site (all P < 0.001). Any fibroatheroma was more frequently identified in culprit lesions compared with non-culprit lesions (93% vs. 78.9%, P = 0.001), anywhere within the lesion 19.0%, P < 0.001) as well as at the MLA site (18.0% vs. 9.5%, P = 0.07)., Conclusions: Three-vessel radiofrequency iMAP-IVUS demonstrated a greater plaque burden and higher prevalence of any fibroatheroma as well as iMAP-derived TCFAs in culprit versus non-culprit lesions in patients presenting with STEMI or non-STEMI undergoing percutaneous coronary intervention. © 2017 Wiley Periodicals, Inc., (© 2017 Wiley Periodicals, Inc.)

Increased galectin-3 plasma concentration has been linked to an unfavorable outcome in patients with heart failure or atrial fibrillation (AF). There are no published data about the prognostic utility of galectin-3 and high-sensitivity C-reactive protein (hs-CRP) for long-term clinical outcome in the Non-ST elevation acute myocardial infarction (NSTEMI) patients with preexisting AF. Thirty-two patients with the first acute NSTEMI and preexisting AF and 22 patients without preexisting AF, were prospectively followed for fifteen months. Patients with AF had significantly higher galectin-3 plasma levels (p < 0.05) and hs-CRP concentration (p < 0.01), compared with patients without AF. Galectin-3 plasma concentration was not a significant covariate of the composite outcomes (p = 0.913). Patients with high hs-CRP (above 4.55 mg/L) showed 2.5 times increased risk (p < 0.05) of the composite outcome occurrence (p < 0.05). Besides, three-vessel coronary artery disease, creatinine serum level, and creatinine clearance were significant covariates (p < 0.05; p < 0.05; p < 0.01) of the composite outcome, respectively. Creatinine clearance, solely, has been shown to be an independent predictor of unfavorable prognosis after a 15-month follow-up. Galectin-3 and hs-CRP plasma levels were elevated in NSTEMI patients with AF, but with differential predictive value for an unfavorable clinical outcome. Only hs-CRP was associated with increased risk of composite outcome occurrence.

This study was performed to gain further insight in the heterogeneity of monocytes in the different categories of acute coronary syndrome (ACS), especially between patients with unstable angina pectoris, ST-elevation myocardial infarction (STEMI), and non-ST-elevation myocardial infarction (NSTEMI). For this purpose, blood samples were collected in the acute phase from patients presenting with an ACS. These samples were examined with multiparameter flow cytometry to identify the different monocyte subsets and to analyze the expression of monocyte-associated molecules. Leukocytes, as well as an absolute number of monocytes, showed a clear and significant increase in patients with STEMI. This increase was seen in all subtypes of monocytes. The classical monocytes (CD14++CD16-) of patients with an NSTEMI had a significantly increased CD11b expression when compared to the control group, while these cells showed a decreased expression pattern in STEMI patients. This increased CD11b-expression was also seen in the intermediate monocytes of NSTEMI, while it was almost completely downregulated on the intermediate monocytes of STEMI. Finally, CX3CR1, which is almost exclusively expressed on intermediate and nonclassical monocytes, showed a significant decrease in expression in patients with STEMI. In conclusion, intermediate and nonclassical monocytes have a different immunophenotypic pattern in patients with STEMI versus NSTEMI. These differences reflect the pro-inflammatory state of the monocytes in NSTEMI and can be used as target molecules for novel therapeutic strategies to diminish the migration of proinflammatory monocytes into the myocardial tissue. © 2017 International Society for Advancement of Cytometry., (© 2017 International Society for Advancement of Cytometry.)

The pharmacokinetics after a 180-mg loading dose (LD) of ticagrelor has not been thoroughly investigated in NSTEMI patients. We aimed to compare the ticagrelor uptake and on-treatment platelet reactivity between non-ST-segment elevation myocardial infarction (NSTEMI) patients and a control group of patients with stable coronary artery disease (SCAD) undergoing elective percutaneous coronary intervention. We performed an observational, prospective, single-center study including 40 NSTEMI patients and 20 SCAD controls. Key exclusion criteria included ongoing opioid treatment. Both groups received a 180-mg ticagrelor LD, and blood samples were taken pre-dose and 1, 2, 3, 4, 5, and 6 hours post-LD. Plasma concentrations of ticagrelor and its active metabolite AR-C124910XX were determined by validated methods. Platelet aggregation was tested using ADP-induced multiple electrode aggregometry. The primary endpoint was the time to maximal ticagrelor concentration (T max ). Clinical trial registration identifier number: NCT02292277. None of the pharmacokinetic variables differed significantly between the groups, including the T max of ticagrelor (2.0h [1.0-3.0] versus 2.0h [2.0-3.0], p = 0.393) and the active metabolite AR-C124910XX (3.0 [2.0-4.0] versus 3.0 [2.5-4.0], p = 0.289). High on-treatment platelet reactivity (HPR) was defined as > 46 aggregation units and was at one hour seen in 15% of the NSTEMI patients versus 10% of the controls (p = 1.0). At two hours post the 180-mg ticagrelor LD, 3% of the NSTEMI patients had HPR compared with none of the controls (p = 1.0). In conclusion, the uptake of ticagrelor was not significantly slower in NSTEMI patients not receiving opioids compared with the SCAD controls, leading to adequate onset of platelet inhibition in both groups.

Introduction: The prevalence of total coronary occlusion of an infarct‑related artery (IRA) and its impact on the outcome can differ between patients with non‑ST‑elevation myocardial infarction (NSTEMI) and those with ST‑segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI)., Objectives: We evaluated the impact of IRA occlusion on the outcome of myocardial infarction according to the presence or absence of ST‑segment elevation and the location of the culprit lesion., Patients and Methods: We analyzed 4581 patients with STEMI and 2717 patients with NSTEMI who underwent PCI and were enrolled in the Polish Registry of Acute Coronary Syndromes. Patients were divided into 3 cohorts depending on the IRA: left anterior descending artery (LAD), left circumflex artery (LCx), or right coronary artery (RCA). Patients were further divided according to preprocedural Thrombolysis in Myocardial Infarction (TIMI) flow to either a subgroup with total occlusion (TO; TIMI flow grade, 0) or a subgroup with incomplete occlusion (nTO; TIMI flow grade ≥1)., Results: TO was observed in 2949 patients (64.4%) with STEMI and 723 patients (26.6%) with NSTEMI. The most common IRAs were the RCA (49.4%) and LCx (48.4%) in the STEMI and NSTEMI groups, respectively. STEMI patients with TO of the LAD showed higher mortality during the 36‑month follow‑up; mortality in the NSTEMI group was comparable between patients with TO and nTO. STEMI and NSTEMI groups with TO of the LCx showed higher in‑hospital mortality. No differences were observed between patients with TO and nTO of the RCA., Conclusions: Totally occluded IRA (TIMI flow grade 0) on baseline angiogram was not associated with higher 36‑month mortality rates after both NSTEMI and STEMI treated with PCI in comparison with patients with patent IRA except for totally occluded LAD in STEMI.

Introduction: Near-infrared spectroscopy (NIRS) is a new method to identify lipid core plaque (LCP). The LCP and vascular response were assessed with NIRS to examine whether LCP was compressed or redistributed during percutaneous coronary intervention with stent implantation., Methods: In 25 patients with non-ST segment elevation myocardial infarction (NSTEMI) NIRS acquisition was performed after predilation, stent implantation with nominal pressure and high-pressure post-dilation with a non-compliant balloon. The intravascular ultrasound (IVUS) measures included volumes of external elastic membrane (EEM), lumen and plaque+media. The NIRS measures included lipid core burden index (LCBI) and maximum value of LCBI for any of the 4-mm segment (maxLCBI 4mm )., Results: From predilation to stent implantation and post-dilation EEM volume increased from 337±124mm 3 to 369±136mm 3 and to 397±144mm 3 (p<0.001), while plaque volume decreased from 225±84mm 3 to 202±85mm 3 and to 192±81mm 3 (p<0.001). Plaque shift to the proximal reference segment was found in 40% of the lesions. The maxLCBI 4mm decreased significantly from predilation to stent implantation (492±235 to 208±193 (p<0.001), whereas post dilation did not cause any further significant reduction. Also LCBI decreased significantly from predilation to stent implantation (173±103 to 68±67, p<0.001), without any further significant reduction during post-dilation. The LCBI did neither in the proximal nor in the distal reference segments change significantly during stent implantation or post-dilation., Conclusion: Lumen enlargement was caused by vessel expansion, plaque compression and longitudinally plaque redistribution. Lipid-core burden at the stented segment was decreased., (Copyright © 2016 Elsevier Inc. All rights reserved.)

INTRODUCTION    The modification of arterial stiffness and intima-media thickness (IMT) is controversial in patients with clinically significant atherosclerosis. OBJECTIVES    We evaluated the effects of 1‑year pharmacological therapy on arterial stiffness and IMT in survivors of non‑ST‑segment elevation myocardial infarction (NSTEMI) who were treated according to current clinical guidelines. PATIENTS AND METHODS    A total of 298 patients with NSTEMI (median age, 64 years; 85 women) were enrolled to this study. Local (carotid) arterial stiffness and IMT were measured noninvasively before discharge and after 12 months of contemporary pharmacological treatment according to current clinical guidelines. The study group was divided into patients with normal systolic blood pressure (BP) (<140 mm Hg) and those with increased systolic BP (≥140 mm Hg) at 12 months. The results were presented as median (25th-75th percentile). RESULTS    There were no significant changes in local arterial stiffness between patients with normal and those with increased systolic BP (8.9 m/s [7.9-10.9 m/s] vs 8.7 m/s [7.8-10.1 m/s] at baseline and 9.6 m/s [8.3-11.0 m/s] vs 10.4 m/s [9.1-12.4 m/s] at 12 months, P = 0.67 and P = 0.05, respectively); however, a significant reduction in IMT was found in both groups (777 μm [664-896 μm] vs 715 μm [619-841 μm] at baseline and 818 μm [720-962 μm] vs 760 μm [674-897 μm] at 12 months, P = 0.0003 and P = 0.001, respectively). Arterial stiffness and IMT were affected by age and mean BP; however, adjustment for these variables did not affect the obtained results in multivariate models. CONCLUSIONS    The 1‑year pharmacological treatment of patients after NSTEMI was associated with a significant reduction in IMT but had no effect on the properties of the arterial structure.

In clinical practice, there is still a need for novel biomarkers, which can reliably rule in or rule out acute coronary syndrome (ACS) immediately on admission. This is of particular interest in patients with unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI) in whom diagnostic uncertainty is high. The aim of the present study is to evaluate the potential role of miRNA-499 and miRNA-210 as novel molecular biomarkers for early diagnosis of UA and NSTEMI suspected patients presented at the emergency unit. A total of 110 patients presenting to the intensive care unit (ICU) within 24 h of onset of chest pain suggestive of ACS were enrolled in the study. They included 37 UA, 48 NSTEMI and 25 noncardiac chest pain (NCCP) patients. Immediately at enrollment, blood samples were taken for estimation of serum miRNA-499 and miRNA-210 expression levels by real time PCR. miRNA-499 and miRNA-210 expression levels were significantly increased in UA and NSTEMI patients compared with NCCP patients (P < 0.001). Receiver operating characteristic (ROC) curve analysis revealed that the area under curve (AUC) of miR-499 for the diagnosis of UA and NSTEMI was 0.98 and 0.97, respectively; while the AUC of miRNA-210 was 0.84 and 0.90, respectively. The important finding of our study was that the AUC of miRNA-499 for the diagnosis of ACS patients with symptoms onset <3 h was 0.89, while the AUC of miRNA-210 was 0.86. Interestingly, combining miRNA-499 and miRNA-210 significantly improved the diagnostic value by increasing the AUC to 0.96, P < 0.001. In conclusion, serum miRNA-499 and miRNA-210 are associated with UA and NSTEMI and with those presenting within 3 h of symptom onset. Both miRNAs might be potentially novel biomarkers for accelerating the diagnosis of ACS patients in emergency unit. © 2016 IUBMB Life, 68(8):673-682, 2016., (© 2016 International Union of Biochemistry and Molecular Biology.)

Background: Although napkin-ring sign (NRS) plaques assessed by multidetector computed tomography (MDCT) is identified as a high-risk feature, the detailed morphological features are still unknown. The purpose of this study was to elucidate the morphological features of the MDCT-assessed NRS using intravascular ultrasound (IVUS)., Methods: We evaluated 204 plaques in 193 patients with non-ST-elevation acute coronary syndrome who were diagnosed using 128-slice MDCT and were assessed using IVUS prior to coronary intervention. Morphology was compared between plaques with and without MDCT-assessed NRS. Severe IVUS-assessed attenuation was defined as an attenuation angle >180°., Results: NRS was detected in 49 lesions. MDCT-assessed plaque attenuation was lower (p<0.0001), and cross-sectional plaque areas at lesion sites, remodeling index, and the prevalence of positive remodeling were greater, in lesions with NRS (p<0.005, p<0.0001, and p<0.0001, respectively). Furthermore, the IVUS-assessed remodeling index and prevalence of severe attenuation and speckled echo appearance were significantly greater in lesions with NRS (p<0.01, p<0.0001, and p<0.0001, respectively). Using multivariate analysis, IVUS-assessed speckled echo appearance was identified as an independent predictor of MDCT-assessed NRS (odds ratio, 3.59; 95% confidence interval, 1.49-8.66; p<0.005)., Conclusion: MDCT assessment of NRS may be associated with larger heterogeneous necrotic cores and greater positive remodeling., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Introduction: Coronary angiography is commonly performed following non-ST segment elevation myocardial infarction (NSTEMI) to assess the need for revascularization. Some of these patients have myocardial infarction (MI) with no obstructive coronary atherosclerosis (MINOCA). Patients without severe obstructive lesions are usually treated conservatively. However, coronary angiography has known limitations in the assessment of lesion severity. We report our experience of using coronary Optical Coherence Tomography (OCT) in a series of patients without severe obstructive coronary lesions., Methods: 165 patients underwent coronary OCT at Vancouver General Hospital. NSTEMI was the clinical presentation in 70 patients and 26 had angiographically intermediate lesions with 40%-69% diameter stenosis. Prior to OCT image acquisition, intracoronary nitroglycerin 100-200μg was administered. Blood in the vessel was displaced using contrast media by manual injections., Results: OCT of the angiographically intermediate lesions showed larger minimal luminal area (MLA) than the angiographically severe lesions (MLA 3.3mm(2)±1.8mm(2) vs. 1.6mm(2)±0.6mm(2), p<0.001) and less severe % lumen area stenosis (54.2%±11.4% vs. 70.9%±6.8%, p=0.001). Plaque rupture or intracoronary thrombus was detected in 8/26 (31%) patients. PCI with stent deployment was performed in 16 patients (62%)., Conclusion: In stabilized patients with NSTEMI and angiographically intermediate disease, OCT examination confirmed the lack of severe anatomical stenosis in most patients. However, OCT also identified coronary lesions with unstable features. Further research is needed to help guide management of this subgroup of patients., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: In patients with non-ST elevation acute coronary syndrome (NSTE-ACS), identification of the patients with high-risk coronary anatomy (HRCA) who are most likely to require coronary artery bypass grafting (CABG) is crucial. The SYNTAX score (SXscore) is an angiographic grading tool designed to determine the complexity of coronary artery disease. It appears that CABG offers significantly better outcomes in patients with SXscore ≥ 33, which shows severe HRCA., Aim: We sought to assess the accuracy of the GRACE score in predicting HRCA in terms of SXscore in patients with NSTE-ACS., Methods: Patients admitted to our coronary unit with a diagnosis of NSTE-ACS and undergoing coronary angiography during hospitalisation were recruited to this study. Patients were categorised into two groups based on SXscore: HRCA (SXscore ≥ 33) and low-risk coronary anatomy (LRCA, SXscore < 33). The cut-off level of GRACE score for HRCA was established by receiver operator characteristic (ROC) analysis., Results: We studied 207 consecutive patients (mean age: 59 ± 11 years, 27.5% female). The GRACE score was 139 ± 34 in the HRCA group and 114 ± 33 in the LRCA group (p = 0.001). There was a significant positive correlation between SXscore and GRACE score (r = 0.338, p < 0.001). The area under ROC curve for GRACE score was 0.71 (95% CI 0.60-0.81, p = 0.001). A GRACE score of 123 was identified as the optimal cut-off to predict HRCA with a sensitivity of 71% and a specificity of 60%. In multivariate regression analysis, GRACE score ≥ 123 was the only variable that identified HRCA (OR 2.8, 95% CI 1.18-6.6, p = 0.019).Conclusions: Our study demonstrates that, in the setting of NSTE-ACS, patients with HRCA, who are most likely to require CABG, have higher GRACE scores at presentation. However, the ability of GRACE score to predict HRCA was modest.