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With the increasing burden of diabetes as a cause of macro- and microvascular disease linked to the epidemics of obesity, attention is being paid to dysglycaemic states that predict and precede the development of type 2 diabetes. Such conditions, termed pre-diabetes, are characterized by fasting plasma glucose, or plasma glucose levels on an oral glucose tolerance test, or values of glycated haemoglobin intermediate between 'normal' values and those characterizing diabetes. These last are by definition associated, in epidemiological terms, with a higher incidence of microvascular disease—mostly retinopathy. Pre-diabetes overlaps with the components of the 'metabolic syndrome'—among which are excess visceral adiposity; hypertension; hypertriglyceridaemia; high levels of small, dense low-density lipoproteins; and metabolic-associated fatty liver disease. There is little doubt that pre-diabetes has important prognostic implications, especially for the occurrence of myocardial infarction, ischaemic stroke, and peripheral arterial disease. It is disputed, however, whether pre-diabetes is itself an actionable disease entity, in addition to the risk factors characterizing it. Because of this uncertainty, the latest European Society of Cardiology guidelines chose not to include pre-diabetes as a treatment target for atherosclerotic cardiovascular disease, at variance from the three previous editions of such guidelines. This is spurring a debate, the Pro and Contra arguments featured in the present debate article. [ABSTRACT FROM AUTHOR]

Background and Aims Cardiogenic shock (CS) remains the primary cause of in-hospital death after acute coronary syndromes (ACS), with its plateauing mortality rates approaching 50%. To test novel interventions, personalized risk prediction is essential. The ORBI (Observatoire Régional Breton sur l'Infarctus) score represents the first-of-its-kind risk score to predict in-hospital CS in ACS patients undergoing percutaneous coronary intervention (PCI). However, its sex-specific performance remains unknown, and refined risk prediction strategies are warranted. Methods This multinational study included a total of 53 537 ACS patients without CS on admission undergoing PCI. Following sex-specific evaluation of ORBI, regression and machine-learning models were used for variable selection and risk prediction. By combining best-performing models with highest-ranked predictors, SEX-SHOCK was developed, and internally and externally validated. Results The ORBI score showed lower discriminative performance for the prediction of CS in females than males in Swiss (area under the receiver operating characteristic curve [95% confidence interval]: 0.78 [0.76–0.81] vs. 0.81 [0.79–0.83]; P =.048) and French ACS patients (0.77 [0.74–0.81] vs. 0.84 [0.81–0.86]; P =.002). The newly developed SEX-SHOCK score, now incorporating ST-segment elevation, creatinine, C-reactive protein, and left ventricular ejection fraction, outperformed ORBI in both sexes (females: 0.81 [0.78–0.83]; males: 0.83 [0.82–0.85]; P <.001), which prevailed following internal and external validation in RICO (females: 0.82 [0.79–0.85]; males: 0.88 [0.86–0.89]; P <.001) and SPUM-ACS (females: 0.83 [0.77–0.90], P =.004; males: 0.83 [0.80–0.87], P =.001). Conclusions The ORBI score showed modest sex-specific performance. The novel SEX-SHOCK score provides superior performance in females and males across the entire spectrum of ACS, thus providing a basis for future interventional trials and contemporary ACS management. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are the leading cause of death among women, and the incidence among younger women has shown the greatest increase over the last decades, in particular for acute myocardial infarction (AMI). Moreover, the prognosis of women post-AMI is poor when compared with men of similar ages. Since the 1990s, an abundant literature has highlighted the existing differences between sexes with regard to presentation, burden, and impact of traditional risk factors and of risk factors pertaining predominantly to women, the perception of risk by women and men, and the pathophysiological causations, their treatment, and prognosis. These data that have been accumulated over recent years highlight several targets for improvement. The objective of this collaborative work is to define the actions required to reverse the growing incidence of AMI in women and improve the patient pathway and care, as well as the prognosis. We aim to provide practical toolkits for different health professionals involved in the care of women, so that each step, from cardiovascular risk assessment to symptom recognition, to the AMI pathway and rehabilitation, thus facilitating that from prevention to intervention of AMI, can be optimized. [ABSTRACT FROM AUTHOR]

OBJECTIVES Extracorporeal cardiopulmonary resuscitation (ECPR) has emerged as a rescue for refractory cardiac arrest, of which acute coronary syndrome is a common cause. Data on the coronary revascularization strategy in patients receiving ECPR remain limited. METHODS The ECPR databases from two referral hospitals were screened for patients who underwent emergent revascularization. The baseline characteristics were matched 1:1 using propensity score between patients who underwent coronary artery bypass grafting (CABG) and those who received percutaneous coronary intervention (PCI). Outcomes, including success rate of weaning from extracorporeal membrane oxygenation (ECMO), hospital survival, and midterm survival in hospital survivors, were compared between CABG and PCI. RESULTS After matching, most of the patients (95%) had triple vessel disease. Compared with PCI (n  = 40), emergent CABG (n  = 40) had better early outcomes, in terms of the rates of successful ECMO weaning (71.1% vs 48.7%, P  = 0.05) and hospital survival (56.4% versus 32.4%, P  = 0.04). After a mean follow-up of 2 years, both revascularization strategies were associated with favourable midterm survival among hospital survivors (75.3% after CABG vs 88.9% after PCI, P  = 0.49), with a trend towards fewer reinterventions in patients who underwent CABG (P  = 0.07). CONCLUSIONS In patients who received ECPR because of triple vessel disease, the hospital outcomes were better after emergent CABG than after PCI. More evidence is required to determine the optimal revascularization strategy for patients who receive ECPR. [ABSTRACT FROM AUTHOR]

Cardiac emergencies in women, such as acute coronary syndromes, acute heart failure, and cardiac arrest, are associated with a high risk of adverse outcomes and mortality. Although women historically have been significantly underrepresented in clinical studies of these diseases, the guideline-recommended treatment for these emergencies is generally the same for both sexes. Still, women are less likely to receive evidence-based treatment compared to men. Furthermore, specific diseases affecting predominantly or exclusively women, such as spontaneous coronary dissection, myocardial infarction with non-obstructive coronary arteries, takotsubo cardiomyopathy, and peripartum cardiomyopathy, require specialized attention in terms of both diagnosis and management. In this clinical consensus statement, we summarize current knowledge on therapeutic management of these emergencies in women. Key statements and specific quality indicators are suggested to achieve equal and specific care for both sexes. Finally, we discuss several gaps in evidence and encourage further studies designed and powered with adequate attention for sex-specific analysis. [ABSTRACT FROM AUTHOR]

Background Data about the clinical benefit from initial low-density lipoprotein cholesterol (LDL-C) reduction with lipid lowering treatment for secondary prevention and risk of major vascular events amongst older as compared with younger individuals treated during routine clinical care are limited. We investigated this in a nationwide cohort. Methods Individuals aged ≥ 50 years with a first-time hospitalisation for a cardiovascular event (index event, including acute coronary syndrome, non-haemorrhagic stroke, transient ischaemic attack and coronary revascularisation), 1 January 2008 to 31 October 2018, who subsequently used lipid lowering treatment, and had an LDL-C measurement before and after the event were included. Hazard ratios (HRs) for major vascular events per 1 mmol/L reduction in LDL-C were estimated for the included 21,751 older and 22,681 younger individuals (≥/<70 years old) using Cox regression. Results LDL-C lowering was associated with a 12% lower risk of major vascular events in older individuals per 1 mmol/L reduction in LDL-C (HR 0.88, 95% confidence interval [CI] 0.84–0.93), with no significant difference compared with the risk reduction amongst younger individuals (HR 0.88, 95% CI 0.83–0.93; P -value for difference between age groups: 0.86). The risk reduction was more pronounced when post hoc restricting, as a proxy for compliance, to new users with an LDL-C reduction above the lowest decile for both older (0.81, 95% CI 0.73–0.90) and younger (0.81, 95% CI 0.72–0.91) individuals. Conclusions This study strongly supports a similar relative clinical benefit of LDL-C reduction with lipid lowering treatment for secondary prevention of major vascular events amongst individuals aged ≥70 and <70 years. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to investigate fatty acids, lipid mediator levels, and the desaturase index rates on different acute coronary syndrome types and their possible relationship with routine lipid parameters. Methods The study included 81 patients with myocardial infarction (MI), 20 patients with unstable angina pectoris, and 31 healthy people. Fatty acids, CD59, lipoxin A4, 8-isoprostane, serum lipids, albumin, C-reactive protein (CRP), and high sensitive troponin levels were measured in all participants. Results When the fatty acid groups were evaluated as a ratio of albumin, MUFA/albumin and SFA/albumin ratios were significantly higher in the MI group compared to the control group. Although CD59 and lipoxin A4 levels were higher in the control group, there was no significant differences between the groups. When lipoxin A4/CRP and CD59/CRP ratios were evaluated, the results were significantly lower than those in the control group.  Conclusion Lipid mediators may be useful in treating atherosclerosis by contributing to the resolution of inflammation. [ABSTRACT FROM AUTHOR]

Aims The functional capacity of the immune cells is strongly dependent on their metabolic state and inflammatory responses are characterized by a greater use of glucose in immune cells. This study is aimed to establish the role of glucose metabolism and its players [glucose transporter 1 (GLUT-1) and pyruvate kinase isozyme M2 (PKM2)] in the dysregulation of adaptive immunity and inflammation observed in patients with non-ST-segment elevation myocardial infarction (NSTEMI). Methods and results We enrolled 248 patients allocated to three groups: NSTEMI patients, chronic coronary syndromes (CCS) patients, healthy subjects (HSs). NSTEMI patients showed higher expression of GLUT-1 and an enhanced glucose uptake in T cells when compared with CCS patients (P < 0.0001; P = 0.0101, respectively) and HSs (P = 0.0071; P = 0.0122, respectively). PKM2 had a prevalent nuclear localization in T lymphocytes in NSTEMI (P = 0.0005 for nuclear vs. cytoplasm localization), while in CCS and HS, it was equally distributed in both compartments. In addition, the nuclear fraction of PKM2 was significantly higher in NSTEMI compared with HS (P = 0.0023). In NSTEMI patients, treatment with Shikonin and Fasentin, which inhibits PKM2 enzyme activity and GLUT-1-mediated glucose internalization, respectively, led to a significant reduction in GLUT-1 expression along with the down-regulation of pro-inflammatory cytokine expression. Conclusion NSTEMI patients exhibit dysregulation of the GLUT-1/PKM2 metabolic loop characterized by nuclear translocation of PKM2, where it acts as a transcription regulator of pro-inflammatory genes. This detrimental loop might represent a new therapeutic target for personalized medicine. [ABSTRACT FROM AUTHOR]

Background and Aims Dipeptidyl peptidase 3 (DPP3) is a protease involved in the degradation of angiotensin II which disturbs peripheral blood pressure regulation and compromises left ventricular function. This study examined the relationship of circulating DPP3 (cDPP3) with cardiogenic shock (CS) and mortality in patients presenting with acute coronary syndromes (ACS). Methods Plasma cDPP3 levels were assessed at baseline and 12–24 h after presentation in patients with ACS prospectively enrolled into the multi-centre SPUM-ACS study (n = 4787). Results Circulating DPP3 levels were associated with in-hospital CS when accounting for established risk factors including the ORBI risk score [per log-2 increase, hazard ratio (HR) 1.38, 95% confidence interval (CI) 1.05–1.82, P =.021]. High cDPP3 was an independent predictor of mortality at 30 days (HR 1.87, 95% CI 1.36–2.58, P <.001) and at one year (HR 1.61, 95% CI 1.28–2.02, P <.001) after adjustment for established risk factors and the GRACE 2.0 score. Compared to values within the normal range, persistently elevated cDPP3 levels at 12–24 h were associated with 13.4-fold increased 30-day mortality risk (HR 13.42, 95% CI 4.86–37.09, P <.001) and 5.8-fold increased 1-year mortality risk (HR 5.79, 95% CI 2.70–12.42, P <.001). Results were consistent across various patient subgroups. Conclusions This study identifies cDPP3 as a novel marker of CS and increased mortality in patients with ACS. Circulating DPP3 offers prognostic information beyond established risk factors and improves early risk assessment. [ABSTRACT FROM AUTHOR]

The article focuses on how illness perception mediates the relationship between disease severity and health-related quality of life (HRQL) in patients with acute coronary syndrome (ACS), including the impact of illness perception on HRQL, the role of psychological stress and disease severity.

Keywords: Air pollution; Plaque healing; Acute coronary syndromes; Thrombosis; Inflammation EN Air pollution Plaque healing Acute coronary syndromes Thrombosis Inflammation 2403 2405 3 07/11/23 20230707 NES 230707 Introduction Plaque healing plays a key role in coronary atherosclerosis[1] and represents "the second hit" required to cause an acute coronary syndrome (ACS) after plaque destabilization, this latter being the "first hit".[[1], [3]] Moreover, an impaired plaque healing has been found in patients with recurrent ACS, suggesting its importance in preventing repeated symptomatic coronary thrombosis.[3] Nonetheless, mechanisms modulating plaque healing are unknown. In first acute coronary syndrome patients, particulate matter 2.5 chronic exposure levels were similar between patients with and without healed plaques in the culprit lesion, while particulate matter 2.5 was higher in those with macrophage infiltration and thin-cap fibroatheroma at the culprit plaque. Among recurrent ACS patients, 6 patients (20.7%) had TCFA at the culprit lesion, and these patients had higher PM2.5 (17.9 ± 3.6 vs. 13.6 ± 3.4 I µ i g/m SP 3 sp , I P i = 0.030) and PM10 (28.8 ± 3.2 vs. 24.2 ± 3.9 I µ i g/m SP 3 sp , I P i = 0.014) exposure levels compared to those without TCFA. [Extracted from the article]

Aims Post-acute coronary syndrome (ACS) P2Y12 inhibitor non-adherence is common and associated with greater risk of major adverse cardiovascular events (MACEs). Non-adherence can follow different trajectories from an inability to initiate, implement, or continue therapy for the intended duration. We aimed to evaluate P2Y12 inhibitor adherence trajectories among ACS patients treated with percutaneous coronary intervention (PCI), their frequency, and association with MACE. Methods and results We conducted a cohort study of adults discharged alive after PCI for ACS (2012–16) using the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease registry linked with administrative data. The primary outcome was P2Y12 inhibitor adherence trajectory in the year after PCI assessed using group-based trajectory modelling. We used logistic regression and Cox proportional-hazards regression to assess associations of trajectories with risk factors and MACE, respectively. We included 12 844 patients (mean age 62.4 years, 23.6% female). Five trajectories were identified: early consistent non-adherence (11.0%), rapid decline (7.7%), delayed initiation (6.0%), gradual decline (20.5%), and persistent adherence (54.8%). Compared with persistent adherence, rapid decline [hazard ratio (HR) 1.23, 95% confidence interval (CI) 1.01–1.49] and delayed initiation (HR 1.41, 95% CI 1.12–1.78) were associated with higher MACE in the overall cohort, whereas early consistent non-adherence was associated with higher MACE only in the subgroup receiving a drug-eluting stent (HR 2.44, 95% CI 1.60–3.71). Conclusion After PCI for ACS, patients followed one of five distinct P2Y12 inhibitor adherence trajectories. Rapid decline and delayed initiation were associated with a higher risk of MACE, whereas early consistent non-adherence was only associated with higher MACE risk in patients with a drug-eluting stent. [ABSTRACT FROM AUTHOR]

Background Choosing antithrombotic therapy for patients at high bleeding risk, particularly those requiring long-term anticoagulant therapy, who have acute coronary syndromes (ACS) and/or undergoing percutaneous coronary intervention (PCI) is becoming increasingly complex. Case summary A 78-year-old women was hospitalized with chest pain and a diagnosis of non-ST-elevation ACS was made. It was decided that the patient should undergo coronary angiogram with a view for angioplasty. Subsequently, she underwent successful PCI to the left anterior descending artery. Shortly after PCI, she was noted to be in atrial fibrillation. Furthermore, she had per rectal bleeding and acute kidney injury, which were managed conservatively. Aspirin and ticagrelor were stopped and she was discharged on dual antithrombotic therapy with clopidogrel and apixaban. Discussion Available evidence, driven mainly from expert consensus documents, advocates a case-by-case comprehensive evaluation that integrates patient- and procedure-related factors to assess patients for thrombotic and bleeding tendencies to identify those who may gain most net clinical benefit of antithrombotic combination therapy. In general, if thrombotic drivers prevail, an augmented antithrombotic regime with a view for a longer duration should be planned, and if bleeding drivers prevail, a de-escalated regime with a view for a shorter duration should be sought. [ABSTRACT FROM AUTHOR]

Aims Since its emergence in early 2020, the novel severe acute respiratory syndrome coronavirus 2 causing coronavirus disease 2019 (COVID-19) has reached pandemic levels, and there have been repeated outbreaks across the globe. The aim of this two part series is to provide practical knowledge and guidance to aid clinicians in the diagnosis and management of cardiovascular (CV) disease in association with COVID-19. Methods and results A narrative literature review of the available evidence has been performed, and the resulting information has been organized into two parts. The first, which was reported previously, focused on the epidemiology, pathophysiology, and diagnosis of CV conditions that may be manifest in patients with COVID-19. This second part addresses the topics of: care pathways and triage systems and management and treatment pathways, both of the most commonly encountered CV conditions and of COVID-19; and information that may be considered useful to help patients with CV disease (CVD) to avoid exposure to COVID-19. Conclusion This comprehensive review is not a formal guideline but rather a document that provides a summary of current knowledge and guidance to practicing clinicians managing patients with CVD and COVID-19. The recommendations are mainly the result of observations and personal experience from healthcare providers. Therefore, the information provided here may be subject to change with increasing knowledge, evidence from prospective studies, and changes in the pandemic. Likewise, the guidance provided in the document should not interfere with recommendations provided by local and national healthcare authorities. [ABSTRACT FROM AUTHOR]

Aims The lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and its shedding product [soluble LOX-1 (sLOX-1)] are implicated in atherosclerotic cardiovascular disease (ASCVD) pathogenesis. Herein, we examined the relationship of sLOX-1 with both fatal events and plaque progression in patients with acute coronary syndromes (ACS). Methods and results Plasma sLOX-1 was assessed at baseline in ACS and chronic coronary syndrome (CCS) patients prospectively recruited in the multicentre SPUM-ACS study, with sex- and age-matched healthy subjects serving as additional controls (n = 2924). Compared with both CCS and controls, ACS patients showed markedly elevated sLOX-1 levels (median, 2.00 and 2.00 vs. 35.08 pg/mL; P < 0.0001) which were independently associated with increased mortality risk over 30-day [tertile (T)3: adjusted hazard ratio (HR), 3.11; 95% confidence interval (CI), 1.44–10.61; P = 0.0055] and 1-year intervals (T3: adjusted HR, 2.04; 95% CI, 1.19–3.92; P = 0.0098). Results remained consistent after adjustment for GRACE 2.0 (T3: adjusted HR, 1.86; 95% CI, 1.04–3.74; P = 0.0391) and were primarily driven by the pronounced relationship of sLOX-1 with cardiovascular mortality at 30 days (T3: adjusted HR, 3.81; 95% CI, 1.62–19.62; P = 0.0036) and at 1 year (T3: adjusted HR, 2.29; 95% CI, 1.19–5.34; P = 0.0148). In ACS patients undergoing serial intracoronary imaging and statin therapy, sLOX-1 dropped significantly in those with coronary plaque regression at 1 year (ΔsLOX-1: −4.64 ± 1.80; P = 0.0057), and showed a good discrimination for predicting plaque progression (area under the curve = 0.74; 95% CI, 0.59–0.86; P = 0.0031). Conclusion Plasma sLOX-1 levels are increased during ACS and predict fatal events beyond traditional and emerging risk factors. Persistently high sLOX-1 associates with coronary plaque progression in patients with established ASCVD. Clinical Trial Registration NCT01000701. [ABSTRACT FROM AUTHOR]

Aims Patients with heart failure (HF) have not been shown to benefit from statins. In a post hoc analysis, we evaluated outcomes in ODYSSEY OUTCOMES in patients with vs. without a history of HF randomized to the proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor alirocumab or placebo. Methods and results Among 18 924 patients with recent acute coronary syndrome (ACS) receiving intensive or maximum-tolerated statin treatment, the primary outcome of major adverse cardiovascular events (MACE) was compared in patients with or without a history of HF. The pre-specified secondary outcome of hospitalization for HF was also analysed. Overall, 2815 (14.9%) patients had a history of HF. Alirocumab reduced low-density lipoprotein cholesterol and lipoprotein(a) similarly in patients with or without HF. Overall, alirocumab reduced MACE compared with placebo [hazard ratio (HR): 0.85; 95% confidence interval (CI): 0.78–0.93; P = 0.0001]. This effect was observed among patients without a history of HF (HR: 0.78; 95% CI: 0.70–0.86; P < 0.0001), but not in those with a history of HF (HR: 1.17; 95% CI: 0.97–1.40; P = 0.10) (P interaction = 0.0001). Alirocumab did not reduce hospitalization for HF, overall or in patients with or without prior HF. Conclusion Alirocumab reduced MACE in patients without a history of HF but not in patients with a history of HF. Alirocumab did not reduce hospitalizations for HF in either group. Patients with a history of HF are a high-risk group that does not appear to benefit from PCSK9 inhibition after ACS. [ABSTRACT FROM AUTHOR]

The article presents the discussion on the impact of Covid-19 on cardiovascular disease in the acute and emergency settings. Topics include increasing late presentations of STEMI, infarct size, and complications, delaying in revascularization, and reduction in admissions for acute heart failure (AHF); and T-cell activation being a key step in the sequence leading to plaque erosion and thrombus formation.

Aims We assessed the impact of intravenous fentanyl and lignocaine on the pharmacokinetics and pharmacodynamics of ticagrelor in patients with unstable angina and non-ST-elevation myocardial infarction and their procedural analgesic efficacy and safety. Methods and results Seventy patients undergoing coronary angiography with ticagrelor loading were included in the pharmacokinetic and pharmacodynamic analyses of this randomized trial. Plasma ticagrelor levels 2 h post-loading dose were significantly lower in the fentanyl arm than in the lignocaine treatment arm (598 vs. 1008 ng/mL, P  = 0.014). The area under the plasma–time curves for ticagrelor (1228 vs. 2753 ng h/mL, P  < 0.001) and its active metabolite (201 vs. 447 ng h/mL, P  = 0.001) were both significantly lower in the fentanyl arm. Expression of activated platelet glycoprotein IIb/IIIa receptor (2829 vs. 1426 mean fluorescence intensity, P  = 0.006) and P-selectin (439 vs. 211 mean fluorescence intensity, P  = 0.001) was significantly higher at 60 min in the fentanyl arm. A higher proportion of patients had high on-treatment platelet reactivity in the fentanyl arm at 60 min using the Multiplate Analyzer (41% vs. 9%, P  = 0.002) and 120 min using the VerifyNow (30% vs. 3%, P  = 0.003) and VASP (37% vs. 6%, P  = 0.002) assays. Both drugs were well tolerated with a high level of patient satisfaction. Conclusions Unlike fentanyl, lignocaine does not impair the bioavailability or delay the antiplatelet effect of ticagrelor. Both drugs were well tolerated and effective with a high level of patient satisfaction for procedural analgesia. Routine procedural analgesia during percutaneous coronary intervention should be reconsidered and if performed, lignocaine is a beneficial alternative to fentanyl. [ABSTRACT FROM AUTHOR]

Acute coronary syndrome with cardiogenic shock is a life-threatening condition, but with planned staged treatment combined with coronary revascularization and mechanical circulatory supports its management is increasingly possible. Here, we present our successful life-saving case. A 76-year-old male patient was diagnosed with ST-elevation myocardial infarction with cardiogenic shock due to severe stenosis of the left main coronary artery based on the severe triple vessel disease. We initially introduced Impella CP and performed a percutaneous coronary intervention without stenting on the patient. We maintained hemodynamics with Impella CP and performed coronary artery bypass grafting after a week. Intraoperatively, Impella CP was left to function as a left ventricular vent. The patient required upgrading to Impella 5.5 plus veno-arterial extracorporeal membrane oxygenation postoperatively, but his condition gradually improved, all mechanical circulatory supports could be weaned off, and he eventually survived. [ABSTRACT FROM AUTHOR]

The article focuses on Percutaneous coronary interventions (PCI) constitute the most widely used revascularization modality in patients with coronary artery disease (CAD). Topics include COVID-19 had a striking and unexpected effect on PCI activity around the world; and primary PCI remains the therapy of choice for ST-segment elevation myocardial infarction (STEMI) during the pandemic.

Aims  To compare the safety and efficacy of edoxaban combined with P2Y12 inhibition following percutaneous coronary intervention (PCI) in patients with atrial fibrillation (AF) presenting with an acute coronary syndrome (ACS) or chronic coronary syndrome (CCS). Methods and results  In this pre-specified sub-analysis of the ENTRUST-AF PCI trial, participants were randomly assigned 1:1 to edoxaban- or vitamin K antagonist (VKA)-based strategy and randomization was stratified by ACS (edoxaban n  = 388, VKA n  = 389) vs. CCS (edoxaban n  = 363, VKA = 366). Participants received edoxaban 60 mg once-daily plus a P2Y12 inhibitor for 12 months, or VKA combined with a P2Y12 inhibitor and aspirin 100 mg (for 1–12 months). The primary bleeding endpoint at 12 months occurred in 59 (15.2%) vs. 79 (20.3%) ACS patients [hazard ratio (HR): 0.73, 95% confidence interval (CI): 0.59–1.02, P  = 0.063], and in 69 (19.0%) vs. 73 (19.9%) CCS patients (HR: 0.94, 95%CI: 0.68–1.31, P  = 0.708) with edoxaban- and VKA-based therapy, respectively [ P for interaction (P -int) = 0.2741]. The main secondary endpoint (composite of CV death, myocardial infarction, stroke, systemic embolic events, or definite stent thrombosis) in ACS patients was 33 (8.5%) vs. 28 (7.2%) (HR: 1.16, 95%CI: 0.70–1.92), compared with 16 (4.4%) vs. 18 (4.9%) (HR: 0.91, 95%CI: 0.47–1.78) CCS patients with edoxaban and VKA-based therapy, respectively (P -int = 0.5573). Conclusions  In patients with AF who underwent PCI, the edoxaban-based regimen, as compared with VKA-based regimen, provides consistent safety and similar efficacy for ischaemic events in patients with AF regardless of their clinical presentation. [ABSTRACT FROM AUTHOR]

Aims In a randomized, parallel, blinded study, we investigate the impact of clopidogrel, prasugrel, or ticagrelor on peripheral endothelial function in patients undergoing stenting for an acute coronary syndrome. Methods and results The primary endpoint of the study was the change in endothelium-dependent flow-mediated dilation (FMD) following stenting. A total of 90 patients (age 62 ± 9 years, 81 males, 22 diabetics, 49 non-ST elevation myocardial infarctions) were enrolled. There were no significant differences among groups in any clinical parameter. Acutely before stenting, all three drugs improved FMD without differences between groups (P  = 0.73). Stenting blunted FMD in the clopidogrel and ticagrelor group (both P  < 0.01), but not in the prasugrel group. During follow-up, prasugrel was superior to clopidogrel [mean difference 2.13, 95% confidence interval (CI) 0.68–3.58; P  = 0.0047] and ticagrelor (mean difference 1.57, 95% CI 0.31–2.83; P  = 0.0155), but this difference was limited to patients who received the study therapy 2 h before stenting. Ticagrelor was not significantly superior to clopidogrel (mean difference 0.55, 95% CI −0.73 to 1.82; P  = 0.39). No significant differences were seen among groups for low-flow-mediated dilation. Plasma interleukin (IL)-6 (P  = 0.02 and P  = 0.01, respectively) and platelet aggregation reactivity in response to adenosine diphosphate (P  = 0.002 and P  = 0.035) were lower in the prasugrel compared to clopidogrel and ticagrelor group. Conclusion As compared to ticagrelor and clopidogrel, therapy with prasugrel in patients undergoing stenting for an acute coronary syndrome is associated with improved endothelial function, stronger platelet inhibition, and reduced IL-6 levels, all of which may have prognostic implications. This effect was lost in patients who received the study medication immediately after stenting. EUDRACT-No 2011-005305-73 Open in new tab Download slide Open in new tab Download slide [ABSTRACT FROM AUTHOR]

Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term ‘vulnerable plaque’ was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of ‘vulnerability’ of a specific lesion to the more comprehensive goal of identifying patient ‘cardiovascular vulnerability’. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and ‘local’ diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of ‘high-risk’ plaques occurring in ‘vulnerable’ patients. [ABSTRACT FROM AUTHOR]

CD34+ cells are haematopoietic stem cells used therapeutically in patients undergoing radiation or chemotherapy due to their regenerative potential and ability to restore the haematopoietic system. In animal models, CD34+ cells have been associated with therapeutic angiogenesis in response to ischaemia. Several trials have shown the potential safety and efficacy of CD34+ cell delivery in various cardiovascular diseases. Moreover, Phase III trials have now begun to explore the potential role of CD34+ cells in treatment of both myocardial and peripheral ischaemia. CD34+ cells have been shown to be safe and well-tolerated in the acute myocardial infarction (AMI), heart failure, and angina models. Several studies have suggested potential benefit of CD34+ cell therapy in patients with coronary microvascular disease as well. In this review, we will discuss the therapeutic potential of CD34+ cells, and describe the pertinent trials that have used autologous CD34+ cells in no-options refractory angina, AMI, and heart failure. Lastly, we will review the potential utility of autologous CD34+ cells in coronary endothelial and microvascular dysfunction. [ABSTRACT FROM AUTHOR]

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In conclusion, this trial provides evidence that among patients with ACS and multivessel coronary artery disease, an immediate complete revascularization strategy is non-inferior to a staged complete revascularization, and is associated with a shorter in-hospital stay. Keywords: Acute coronary syndromes; Multivessel disease; Complete revascularization EN Acute coronary syndromes Multivessel disease Complete revascularization 2425 2426 2 07/18/23 20230714 NES 230714 Key points The percutaneous complete revascularization strategies using sirolimus-eluting biodegradable polymer-coated stents in patients presenting with acute coronary syndrome and multivessel disease (BIOVASC) is an investigator-initiated, multicentre, open-label, non-inferiority, randomized trial aimed at assessing whether percutaneous coronary intervention (PCI) for non-culprit lesions of patients with acute coronary syndromes (ACS) and multivessel coronary artery disease should be performed during the index procedure or staged.[1] The study enrolled a total of 1525 patients aged between 18 and 85 years in 29 sites across Belgium, the Netherlands, Spain, and Italy (mean patient age, 66 years; 22% female; 21% with diabetes), with a diagnosis of ST-segment elevation myocardial infarction (STEMI, 40%) and non-ST-segment elevation ACS (52% non-ST-elevation MI and 8% unstable angina). The primary outcome occurred in 57 patients (7.6%) of the immediate complete revascularization arm and 71 patients (9.4%) of the delayed complete revascularization arm [hazard ratio (HR), 0.78; 95% confidence interval (CI), 0.55-1.11; P = 0.001 for non-inferiority; P = 0.166 for superiority]. [Extracted from the article]

Broken heart syndrome, more commonly known as Takotsubo cardiomyopathy (TCM), is an acute cardiac condition. It is characterized by regional cardiac wall motion abnormalities triggered by physical or emotional stress or administration of catecholamines such as epinephrine. The initial clinical presentation is similar to an acute coronary syndrome and must be ruled out. Visualization of the characteristic wall motion will trigger the diagnosis of TCM. In this case report, we present a 50-year-old woman with additional liposuction and fat grafting after autologous breast reconstruction. Shortly after infiltration with a solution containing epinephrine to achieve vasoconstriction, hypotension and bradycardia was noticed. This escalated into full asystole for which cardiac resuscitation was required. ST-elevations and a decrease in systolic function were clear indicators for urgent coronarography and ventriculography. These confirmed the diagnosis of TCM. Infiltration with epinephrine-containing products to achieve local vasoconstriction is used routinely. Medical professionals should be aware that this can trigger a TCM with an estimated mortality rate of 5%. No evidence of a specific preventive measure currently exists. We know that women with a neurologic or psychiatric comorbidity and high levels of stress are more at risk. Reducing stress and anxiolytic medication prior to surgery could be useful. We also know that the cardiac wall motion abnormality is mainly related to β-adrenoreceptors. The use of a selective α-adrenoreceptor agonist could be considered. Further research in the pathophysiology and incidence of TCM could improve identification of patients at risk and lead to more effective prevention and treatment.Level Of Evidence:5: [ABSTRACT FROM AUTHOR]

Background Delayed discharge is a system level problem. It is prevalent internationally, expensive and associated with detrimental outcomes for both patients and health care staff. The aim of this study was to examine reasons for delayed discharges and investigate the relationship between it and clinical complications in a rehabilitation unit. Methods A retrospective study design of patients on delayed discharge list, from December 2017 to August 2018. Data collected from review of medical charts and electronic patient records (BlueSpier). Results 62 patients were identified as delayed discharges, representing 33.3% of the total 186 discharges from the ward, over a 9-month period. Data was obtained for 27 patients. Mean age was 82 years (66-96 years) with an equal male: female ratio. Mean bed days lost was 37 days (4-274 days). 63% of discharges were delayed due to home care packages (HCP), including 44.4% (n=12) awaiting approval of new HCP and the remaining 18.5% (n=5) awaiting an increase in hours. 25.5% (n=7) of delayed patients were awaiting suitable nursing home placements. Other reasons for delayed discharges included awaiting equipment for home (n=5), home adaptations (n=3) and ward of court proceedings (n=1). Morbidities and clinical complications were common among delayed patients. 26% (n=7) became more dependent in mobility at discharge and 51.9% (n=14) experienced clinical complications. These complications include infections (n=9), falls (n=3), acute delirium (n=2), exacerbation of heart failure (n=1), low mood (n=1), acute coronary syndrome (n=1) and pressure sore (n=1). Conclusion 1 in 3 discharges from our rehabilitation ward were delayed. These delays led to functional decline in our patients and exposed them to avoidable adverse outcomes by unnecessary prolonging hospitalisation. Resources need to be directed towards prompt delivery of community services to facilitate a safe and timely hospital discharge. [ABSTRACT FROM AUTHOR]

Aims  Trimethyllysine (TML) serves as a nutrient precursor of the gut microbiota-derived metabolite trimethylamine N-oxide (TMAO) and is associated with incident cardiovascular (CV) events in stable subjects. We examined the relationship between plasma TML levels and incident CV events in patients presenting with acute coronary syndromes (ACS). Methods and results  Plasma levels of TML were quantified in two independent cohorts using mass spectrometry, and its relationship with CV events was investigated. In a Cleveland Cohort (N  = 530), comprised of patients presenting to the emergency department with chest pain and suspected ACS, TML was associated with major adverse cardiac events (MACE, myocardial infarction, stroke, need for revascularization, or all-cause mortality) over both 30 days [3rd tertile (T3), adjusted odds ratio (OR) 1.77, 95% confidence interval (CI) 1.04–3.01; P  < 0.05] and 6 months (T3, adjusted OR 1.95, 95% CI 1.15–3.32; P  < 0.05) of follow-up independent of traditional CV risk factors and indices of renal function. Elevated TML levels were also associated with incident long-term (7-year) all-cause mortality [T3, adjusted hazard ratio (HR) 2.52, 95% CI 1.50–4.24; P  < 0.001], and MACE even amongst patients persistently negative for cardiac Troponin T at presentation (e.g. 30-day MACE, T3, adjusted OR 4.49, 95% CI 2.06–9.79; P  < 0.001). Trimethyllysine in combination with TMAO showed additive significance for near- and long-term CV events, including patients with 'negative' high-sensitivity Troponin T levels. In a multicentre Swiss Cohort (N  = 1683) comprised of ACS patients, similar associations between TML and incident 1-year adverse cardiac risks were observed (e.g. mortality, adjusted T3 HR 2.74, 95% CI 1.28–5.85; P  < 0.05; and MACE, adjusted T3 HR 1.55, 95% CI 1.04–2.31; P  < 0.05). Conclusion  Plasma TML levels, alone and together with TMAO, are associated with both near- and long-term CV events in patients with chest pain and ACS. Download slide Download slide [ABSTRACT FROM AUTHOR]

The article focuses on meta-analysis designed to assess the effect of the use of arterial conduits (ACs) versus great saphenous vein (GSV) grafts as a third conduit for revascularization of the right coronary artery system, in addition to the bilateral internal mammary artery on the left coronaryartery. The primary end point was the long-term mortality rate.

Background Takotsubo Syndrome (TTS) is an acute reversible left ventricular dysfunction. Recently published studies have highlighted a similar mortality rate as acute coronary syndrome (ACS). We compared the impact of gender differences on the outcome of TTS patients as compared to ACS patient. Design and methods We included a collective of 138 patients TTS between 2003 and 2016 at our institution. Patients were divided according to their gender into two groups (Males n =21, 15% and females, n =117, 85%). They were compared with a cohort of 300 patients with a diagnosis of ACS. Results On the acute phase, in male patients with TTS, a treatment with inotropic was more often required (33.3 vs. 11.5%, P <0.01), were more susceptible to cardiogenic shock (28.6 vs. 12.5%, P <0.04). Concerning the long-term prognosis after the acute event, male patients had higher all-cause mortality over long-term follow-up. A Kaplan–Meier analysis indicated that the mortality of male patients with TTS was significantly higher compared to male patients with ACS (log-rank <0.01), while there was no significant difference between female patients with TTS and ACS (log-rank =0.60, P =0.45). In a multivariate cox regression analysis, male gender (HR 2.7, 95% CI: 1.1–6.5, P =0.02) GFR <60 ml/min (HR 2.8, 95% CI: 1.2–6.0, P =0.01) and history of cancer (HR 3.6, 95% CI 1.4–9.3, P <0.01) were independent predictors of 5-year mortality. Conclusions Considerable evidence suggests that TTS compared to ACS implicates more significant clinical short-term events on male patients and it may be associated with poorer long-term prognosis. [ABSTRACT FROM AUTHOR]

Burn injuries generate multisystem physiological derangements. The authors present a case series of three patients developing acute coronary syndrome (ACS) stemming from coronary vasospasm (CVS) over a course of 5 months. This etiology of ACS is significant as it has previously not been described in burn patients and requires a different management algorithm than vaso-occlusive disease.All patients were admitted to a single accredited burn unit. Burn mechanisms were flash burn, chemical fire, and house fire. TBSA were 20%, 72%, and 31%, respectively. Ages were 67-, 41-, and 52-year-old men. All smoked tobacco, and one had diabetes and coronary artery disease. CVS presented with acute onset ST elevations, severe bradycardia, and cardiac arrest in all. Diagnosis was made via EKG and angiography. Treatment was undertaken with nitrates and calcium channel blockers. One of the patients died of refractory disease.The authors identified CVS in burn patients with an incidence of 2% of admissions and accounting for 17% of our burn mortality during this period. To date, there is no linkage between CVS and burns described in humans; however, there is a well-described animal model in rats. The risk factors for CVS are common among burn patients, particularly smoking and endothelial dysfunction. CVS may be a significant cause of ACS in burn patients, and it should be considered in the setting of ACS especially with a negative angiography. Knowledge of this disease state can change burn management to mitigate risk and accommodate specific cardiac treatments. [ABSTRACT FROM AUTHOR]

This study examined the impact of inpatient education on diabetes knowledge, acute coronary syndrome (ACS) symptom management and diabetes self-management on discharge for patients with ACS and type 2 diabetes mellitus (T2DM). A cross-sectional survey and patient health record review of 160 patients was conducted in a major hospital in Shanghai. Patient education received was measured using a visual analogue scale. The survey included valid and reliable measures of diabetes knowledge, self-efficacy, attitudes to ACS and clinical outcomes. Inpatient education contributed to improvements in fasting blood glucose on discharge (P < 0.05). ACS symptom management [Chinese language version of the ACS response index (C-ACSRI) scores] and self-management of T2DM [Chinese version of diabetes management self-efficacy scale (C-DMSES) scores] on discharge differed for the limited education group and sufficient education group (P < 0.001). Based on the multiple regression analyses, increasing scores for the C-ASCRI and C-DMSES could be explained by higher scores for perceived health education. Education relating to ACS and T2DM delivered during an acute admission was associated with improved scores in ACS symptom management and T2DM self-management, preparing some patients to manage both conditions on discharge. [ABSTRACT FROM AUTHOR]

Introduction: The acute coronary syndrome (ACS) patients who are not ready to quit smoking immediately have an extremely low rate of cessation. This study aims to investigate the efficacy of intensive personalized '5As+5Rs'intervention (IPANR intervention) on smoking cessation in this population.Methods: A parallel-group randomized controlled trial was carried out, which compared IPANR intervention with routine 5Rs (control) at Fu Xing Hospital, Capital Medical University, Bei Jing, China. Three hundred and twenty hospitalized ACS smokers who were not ready to quit were randomly distributed to IPANR intervention group comprising three individual counseling during hospitalization and 15 intensive follow-up sessions (weekly during months 1, 2, 3, and monthly thereafter until month 6) or 5Rs group in a 1:1 fashion by 8 cardiologists who were blinded to the allocation sequence. Primary end point was carbon monoxide-confirmed continuous abstinence rate (CAR) through week 9 to week 12. Secondary outcome included abstinence rate at 24 weeks.Results: Overall, 97.5% (312/320) participants completed the trial. An intention-to-treat analysis showed statistically significant advantage of IPANR compared with control group at 4 weeks CAR (27.5% vs. 17.5%, RR = 1.571, 95% CI = 1.032-2.392, p = 0.032, number needed to treat (NNT) = 10), and abstinence rate at 24 weeks (23.8% vs.15.0%, RR 1.583, 95% CI = 0.998-2.512, p = 0.048, NNT: 11.36). At 24 weeks, cigarettes smoked per day by the patients who failed to quit were significant lower in IPANR group than 5Rs group (13.21 ± 8.23 vs. 17.45 ± 10.71; p < 0.001).Conclusions: The IPANR initiated during hospitalization, is a feasible and effective approach for smoking cessation in ACS patients not ready to quit immediately.Implications: Smoking has a major impact on acute stages of ACS for recurrent ischemic events and long-term outcomes. However, there are few evidence-based treatments for smokers who are not ready to quit. This study described a cessation intervention initiated during hospitalization and included 15 intensive follow-up aimed at enabling ACS smokers who were not ready to quit immediately to deliver adequate motivational and behavior change counseling. Given its effectiveness demonstrated in this prospective study, this intervention in hospitalized ACS smokers might have the potential to substantially improve the cessation rate of ACS patients who are not ready to quit smoking immediately. [ABSTRACT FROM AUTHOR]

Aims Chronic pre-treatment with statins may reduce mortality and morbidity in patients experiencing acute coronary syndromes (ACS), but mechanisms accounting for these findings are not completely understood. Methods and results The optical coherence tomography (OCT)-Formidable registry retrospectively enrolled 285 consecutive patients with ACS undergoing OCT in 9 European centres. Mean age was 60.4 ° 12.8 years, 148 (51.9%) patients had hyperlipemia, 45 (15.8%) diabetes mellitus and 142 (49.8%) presented with ST Segment Elevation Myocardial Infarction (STEMI). Patients were stratified according to statin prescription: 150 (52.6%) were on chronic pretreatment with statins before ACS and were more likely to present with non-ST segment elevation acute coronary syndromes (NSTE-ACS) at admission (111, 74%) rather than STEMI, while the opposite was observed for patients not on statins. The primary end-point of ruptured plaque at OCT occurred significantly less frequently in the patients on chronic pre-treatment with statins [odds ratio (OR) 0.375, 95% confidence interval (CI) 0.185-0.759, P = 0.006]. The secondary end-point of thin-cap fibro-atheroma (TCFA) at any site was significantly less frequent in the statin group (OR 0.423, 95%CI 0.213-0.840, P = 0.014). No differences were observed for the secondary endpoint of not-ruptured TCFA as the culprit lesion. Pre-specified sensitivity analysis was conducted according to the pattern of ACS: the reported differences were confirmed for NSTE-ACS patients, with a trend towards less plaque rupture and a significant reduction of TCFA at any site with statins, but not for STEMI. Conclusions Chronic pre-treatment with statins is associated with a reduced prevalence of ruptured plaques in patients presenting with ACS, particularly in those with NSTE-ACS. Statins bear hence the potential to reduce morbidity during the acute phase of ACS. [ABSTRACT FROM AUTHOR]

Aims In patients with acute coronary syndrome (ACS), the higher activity of effector T-cells suggests that mechanisms involving adaptive immunity dysregulation might play a role in coronary instability. The shedding of the functional CD31 domain 1-5 leads to uncontrolled lymphocyte activation. In experimental models, matrix metalloproteinase- 9 (MMP-9) has been implicated in endothelial CD31 cleavage. Interestingly, higher serum levels of MMP-9 have been observed in ACS. We aim to investigate the mechanisms underlying CD31 dysregulation in ACS. Methods and results To assess CD31 cleavage on CD4þ T-cells, we analysed by flow cytometry CD4þ T-cells of 30 ACS, 25 stable angina (SA) patients and 28 controls (CTRL) using two different CD31 antibodies that specifically recognize domain 1-5 or the non-functional membrane-proximal domain 6. The ratio between the domains was significantly lower in ACS than in SA and CTRL (P = 0.002 ACS vs. SA; P = 0.002 ACS vs. CTRL). After stimulation with anti- CD3/CD28, the 1-5/6 domain ratio was significantly lower in ACS than in SA (P = 0.005). ELISA of supernatants obtained from T-cell receptor-stimulated CD4þ T-cells showed higher production of MMP-9 in ACS than in SA (P < 0.001). CD31 domain 1-5 expression in activated CD4þ T-cells from ACS patients increased after treatment with a specific MMP-9 inhibitor (P = 0.042). Conclusion Our study suggest that enhanced MMP-9 release plays a key role in determining the cleavage and shedding of the functional CD31 domain 1-5 in CD4þ T-cells of ACS patients. This mechanism might represent an important therapeutic target to modulate T-cell dysregulation in ACS. [ABSTRACT FROM AUTHOR]

The article offers update from the European Society of Cardiology (ESC) and European Association for Cardio-Thoracic Surgery (EACTS) on dual antiplatelet therapy in coronary artery disease. Topics discussed are efficacy and safety of dual antiplatelet therapy and risk stratification tools, dual antiplatelet therapy after percutaneous coronary intervention and dual antiplatelet therapy for patients treated with coronary artery bypass and those with medically managed acute coronary syndrome.

Aims We aimed to identify a novel biomarker involved in the early events leading to an acute coronary syndrome (ACS) and evaluate its role in diagnosis and risk stratification. Methods and results Biomarker identification was based on gene expression profiling. In coronary thrombi of ACS patients, cysteinerich angiogenic inducer 61 (Cyr61, CCN1) gene transcripts were highly up-regulated compared with peripheral mononuclear cells. In a murine ischaemia-reperfusion model (I/R), myocardial Cyr61 expression was markedly increased compared with the controls. Cyr61 levels were determined in human serum using an enzyme-linked immunosorbent assay. Cohorts of ACS (n = 2168) referred for coronary angiography, stable coronary artery disease (CAD) (n = 53), and hypertrophic obstructive cardiomyopathy (HOCM) patients (n = 15) served to identify and evaluate the diagnostic and prognostic performance of the biomarker. Cyr61 was markedly elevated in STelevation myocardial infarction patients compared with non-ST-elevation myocardial infarction/unstable angina or stable CAD patients, irrespective of whether coronary thrombi were present. Cyr61 was rapidly released after occlusion of a septal branch in HOCM patients undergoing transcoronary ablation of septal hypertrophy. Cyr61 improved risk stratification for all-cause mortality when added to the reference GRACE risk score at 30 days (C-statistic 0.88 to 0.89, P= 0.001) and 1 year (C-statistic 0.77 to 0.80, P< 0.001) comparable to high-sensitivity troponin T (30 days: 0.88 to 0.89, P < 0.001; 1 year: 0.77 to 0.79, P < 0.001). Similar results were obtained for the composite endpoint of all-cause mortality or myocardial infarction. Conversely, in a population-based case-control cohort (n = 362), Cyr61 was not associated with adverse outcome. Conclusion Cyr61 is a novel early biomarker reflecting myocardial injury that improves risk stratification in ACS patients. [ABSTRACT FROM AUTHOR]

Objective: To evaluate compliance with American Heart Association/American College of Cardiology (AHA/ACC) performance measures for adults with acute myocardial infarction (AMI) and to investigate the factors associated with compliance, in an AMI System of Care in Brazil.Design: Observational longitudinal study.Setting: A high-complexity University Hospital, part of the AMI System of Care implemented in Belo Horizonte, Brazil, in 2010.Participants: Of note, 1129 patients with ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) admitted to a single center over 36 months (between 2011 and 2014).Main Outcome Measures: Compliance with 13 pre-specified AHA/ACC AMI performance measures was evaluated for patients with AMI, observing exclusion criteria and appropriate numerators and denominators. Median compliance was calculated and variables independently associated with compliance rates were evaluated.Results: Median age was 60 (51/68) years, 67.7% male, 69.8% presented with STEMI and hospital mortality was 8.7%. Median compliance with performance measures was 83% (75/88). Among patients with STEMI, 56% received reperfusion therapy. Overall, 67.3% of patients complied with ≥80% of quality measures. Factors independently associated with better compliance were later date of presentation (semester), likely reflecting ongoing training (OR = 1.19, 95% CI: 1.10-1.28, P < 0.001), male gender (OR = 1.33, 95% CI: 1.00-1.76, P < 0.046), Killip I/II on admission (OR = 1.95, 95% CI: 1.36-2.80, P < 0.001) and diagnosis of NSTEMI (OR = 5.0, 95% CI: 3.51-7.11, P < 0.001).Conclusion: Compliance with AHA/ACC AMI performance measures remains below target in Brazil, but the time trends observed suggest improvement. Continuing education, reduction of system delays and prioritizing high-risk groups are needed to optimize AMI systems of care and improve patient outcomes. [ABSTRACT FROM AUTHOR]

Aim To explore platelet reactivity on dual antiplatelet therapy (DAPT) of acute coronary syndrome (ACS) patients infected with HIV. Methods and results Acute coronary syndrome patients infected with HIV (n = 80) were matched to ACS patients without HIV (n = 160) on age, sex, diabetes, and DAPT (aspirin 100%, clopidogrel 68%, prasugrel 31%, ticagrelor 1%). Platelet reactivity was evaluated after ACS (>30 days) by measuring residual platelet aggregation (RPA) to aspirin and to P2Y12 inhibitors with light transmission aggregometry (LTA), Verify Now aspirin assay (ARU), and P2Y12 assay (PRU) and with the VASP platelet reactivity index (VASP-PRI). Proportion of patients with high residual platelet reactivity (HPR) was evaluated. HIV-infected ACS patients had higher levels of platelet reactivity in response to P2Y12 inhibitors (RPA: 23.8 ± 2.7% vs. 15.3 ± 1.3%; P = 0.001; PRU: 132 ± 10 vs. 107.4 ± 6.6; P = 0.04; and VASP-PRI: 45.2 ± 2.6% vs. 32.0 ± 2.0%; P < 0.001) and to aspirin (RPA: 3.6 ± 1.5% vs. 0.4 ± 0.1%; P = 0.004 and ARU: 442 ± 11 vs. 407 ± 5; P = 0.002) compared with non-HIV. HIV-infection was independently associated with increased platelet reactivity regardless of the test used (RPA: P = 0.005; PRU: P < 0.001 and VASP-PRI: P < 0.001) and a higher proportion of HPR (OR = 7.6; P < 0.001; OR= 2.06; P = 0.06; OR= 2.91; P = 0.004, respectively) in response to P2Y12 inhibitors. Similar results were found with aspirin. Protease inhibitors use was associated with increased platelet reactivity and higher rate of HPR. Conclusions Acute coronary syndrome patients infected with HIV have increased levels of platelet reactivity and higher prevalence of HPR to P2Y12 inhibitors and aspirin than non-HIV patients. These results could provide potential explanations for the observed increase risk of recurrent ischemic events in the HIV-infected population. [ABSTRACT FROM AUTHOR]