Search

Although a reduction in hospital admissions of acute coronary syndromes (ACS) patients has been observed globally during the coronavirus disease 2019 (COVID-19) pandemic, clinical features of those patients have not been fully investigated. The aim of the present analysis is to investigate the incidence, clinical presentation, and outcomes of patients with ACS during the COVID-19 pandemic. We performed a retrospective analysis of consecutive patients who were admitted for ACS at our institution between March 1 and April 20, 2020 and compared with the equivalent period in 2019. Admissions for acute myocardial infarction (AMI) reduced by 39.5% in 2020 compared with the equivalent period in 2019. Owing to the emergency medical services (EMS) of our region, all time components of ST-elevated myocardial infarction care were similar during the COVID-19 outbreak as compared with the previous year's dataset. Among the 106 ACS patients in 2020, 7 patients tested positive for COVID-19. Higher incidence of type 2 myocardial infarction (29% vs. 4%, p = 0.0497) and elevated D-dimer levels (5650 μg/l [interquartile range (IQR) 1905-13,625 μg/l] vs. 400 μg/l [IQR 270-1050 μg/l], p = 0.02) were observed in COVID-19 patients. In sum, a significant reduction in admission for AMI was observed during the COVID-19 pandemic. COVID-19 patients were characterized by elevated D-dimer levels on admission, reflecting enhanced COVID-19 related thrombogenicity. The prehospital evaluation by EMS may have played an important role for the timely revascularization for STEMI patients., (© 2020. Springer Science+Business Media, LLC, part of Springer Nature.)

Aim: In percutaneous coronary intervention (PCI)-treated acute coronary syndrome (ACS) patients on clopidogrel therapy, high on-treatment platelet adenosine diphosphate (ADP) reactivity was observed in numerous studies, with significant increases in non-fatal myocardial infarction, definite/probable stent thrombosis, or cardiovascular mortality. Compared to clopidogrel, prasugrel and ticagrelor provide more potent platelet inhibition. Whether new P2Y12 inhibitors reduce thrombotic events in a similar manner compared to the rate observed with appropriate P2Y12 inhibition by clopidogrel must still be determined. This study sought to compare long-term outcomes between clopidogrel responders (platelet reactivity index [PRI] vasodilator-stimulated phosphoprotein [VASP] ＜61%) and patients under prasugrel or ticagrelor therapy following PCI-treated ACS., Methods: 730 ACS patients undergoing urgent PCI were prospectively enrolled into two groups: clopidogrel responders (n=448) and those under ticagrelor or prasugrel therapy (n=282). The primary endpoint was a composite of cardiovascular death, myocardial infarction, stent thrombosis, and stroke; the secondary endpoint comprised major hemorrhagic events., Results: The median follow-up was 260±186 days. Clopidogrel patients were older and more likely to present non-ST segment elevation myocardial infarction, cardiovascular risk factors, atrial fibrillation, or prior vascular disease. After propensity score matching, the primary endpoint was met in 7.1% of the clopidogrel group and 4.1% of the prasugrel/ticagrelor group (p=0.43). Minor bleeding events were significantly reduced in the clopidogrel group (1.1% vs. 3%; p=0.03). In a multivariate analysis, the antiplatelet treatment strategy was not an independent primary endpoint predictor., Conclusion: In PCI-treated ACS patients, clopidogrel therapy and PRI VASP ＜61% were not associated with increased risks of thrombotic events compared to prasugrel or ticagrelor therapy.

Background: Microparticles (MPs) have emerged as a surrogate marker of endothelial dysfunction and cardiovascular risk. This study examined the potential of MPs from senescent endothelial cells (ECs) or from patients with acute coronary syndrome (ACS) to promote premature EC aging and thrombogenicity., Methods: Primary porcine coronary ECs were isolated from the left circumflex coronary artery. MPs were prepared from ECs and venous blood from patients with ACS (n=30) and from healthy volunteers (n=4) by sequential centrifugation. The level of endothelial senescence was assessed as senescence-associated β-galactosidase activity using flow cytometry, oxidative stress using the redox-sensitive probe dihydroethidium, tissue factor activity using an enzymatic Tenase assay, the level of target protein expression by Western blot analysis, platelet aggregation using an aggregometer, and shear stress using a cone-and-plate viscometer., Results: Senescence, as assessed by senescence-associated β-galactosidase activity, was induced by the passaging of porcine coronary artery ECs from passage P1 to P4, and was associated with a progressive shedding of procoagulant MPs. Exposure of P1 ECs to MPs shed from senescent P3 cells or circulating MPs from ACS patients induced increased senescence-associated β-galactosidase activity, oxidative stress, early phosphorylation of mitogen-activated protein kinases and Akt, and upregulation of p53, p21, and p16. Ex vivo, the prosenescent effect of circulating MPs from ACS patients was evidenced only under conditions of low shear stress. Depletion of endothelial-derived MPs from ACS patients reduced the induction of senescence. Prosenescent MPs promoted EC thrombogenicity through tissue factor upregulation, shedding of procoagulant MPs, endothelial nitric oxide synthase downregulation, and reduced nitric oxide-mediated inhibition of platelet aggregation. These MPs exhibited angiotensin-converting enzyme activity and upregulated AT1 receptors and angiotensin-converting enzyme in P1 ECs. Losartan, an AT1 receptor antagonist, and inhibitors of either mitogen-activated protein kinases or phosphoinositide 3-kinase prevented the MP-induced endothelial senescence., Conclusions: These findings indicate that endothelial-derived MPs from ACS patients induce premature endothelial senescence under atheroprone low shear stress and thrombogenicity through angiotensin II-induced redox-sensitive activation of mitogen-activated protein kinases and phosphoinositide 3-kinase/Akt. They further suggest that targeting endothelial-derived MP shedding and their bioactivity may be a promising therapeutic strategy to limit the development of an endothelial dysfunction post-ACS., (© 2016 American Heart Association, Inc.)

It was the study objective to determine whether glycaemic control affects the extent of platelet inhibition by thienopyridines as assessed by vasodilator-stimulated phosphoprotein flow cytometry (VASP-FCT) in patients with diabetes mellitus (DM) undergoing percutaneous coronary intervention (PCI) during acute coronary syndrome (ACS). Although the proportion of high on-treatment residual platelet reactivity is higher in DM, the contributions of glycaemic control and other factors associated with DM, such as excess body weight and inflammation, to this impaired platelet inhibition by thienopyridines have not yet been fully characterised. In this study, the extent of P2Y12 ADP receptor pathway inhibition was evaluated by the VASP-FCT. Platelet activation was expressed as the platelet reactivity index (PRI). Low response to clopidogrel (LR) was defined as a PRI of >61%. Four hundred forty-five consecutive ACS patients (DM = 160, NDM = 285) were enrolled. The proportion of LR was higher in DM patients (50 vs. 37.5%). In DM, PRI was not correlated with glycosylated haemoglobin (HbA1c) or glycaemia. In a univariate analysis, LR was associated with age, male sex, overweight, and white blood cell count (WBC). In a multivariate analysis, WBC >10,000 and body weight >80 kg were the sole independent predictors of LR to clopidogrel (hazard ratio (HR) 3.02 [1.36-6.68], p=0.006 and HR 2.47 [1.14-5.35], p = 0.021, respectively). Conversely, in non-DM patients, ST-elevation myocardial infarction was the sole independent predictor of LR. In conclusion, in ACS DM patients undergoing PCI, the extent of P2Y12 inhibition by clopidogrel is not related to glycaemic control but is related to body weight and inflammatory status as assessed by the WBC.

Objectives: We sought to determine whether low platelet response to the P2Y(12) receptor antagonist clopidogrel as assessed by vasodilator-stimulated phosphoprotein flow cytometry test (VASP-FCT) differentially affects outcomes in patients with or without chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI)., Background: Although both CKD and impaired platelet responsiveness to clopidogrel are strong predictors of unfavorable outcome after PCI, the impact of their association is unknown. The platelet VASP-FCT assay is specific for the P2Y(12) ADP receptor pathway. In this test, platelet activation is expressed as the platelet reactivity index (PRI)., Methods: Four-hundred forty unselected patients (CKD: 126, estimated glomerular filtration rate [eGFR] <60 ml/min/1.73 m(2)), no-CKD: 314 eGFR >60 ml/min/1.73 m(2)) undergoing urgent (n = 336) or planned (n = 104) PCI were prospectively enrolled. In each subgroup, patients were classified as low-responders (LR: PRI ≥ 61%) or responders (R: PRI <61%) to clopidogrel., Results: At a mean follow-up of 9 ± 2 months, all-cause mortality, cardiac death, and possible stent thrombosis were higher in CKD than in no-CKD patients. Within the CKD group, the LR status was associated with higher rates of all-cause mortality (25.5% vs. 2.8%, p < 0.001), cardiac death (23.5% vs. 2.8%, p < 0.001), all stent thrombosis (19.6% vs. 2.7%, p = 0.003), and MACE (33.3% vs. 12.3%, p = 0.007). Conversely, in no-CKD patients, the LR status did not affect outcomes. Multivariate analysis identified Killip class ≥ 3, drug-eluting stent implantation, and the interaction between LR and CKD (hazard ratio: 11.96, 95% confidence interval: 1.22 to 116.82; p = 0.033) as independent predictors of cardiac death., Conclusions: In CKD patients, the presence of low platelet response to clopidogrel is associated with worse outcomes after PCI., (Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Aims: Cardiovascular disease has been recognized as a major determinant of coronavirus disease 2019 (COVID‐19) vulnerability and severity. Angiotensin‐converting enzyme (ACE) 2 is a functional receptor for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and is up‐regulated in patients with heart failure. We sought to examine the potential association between reduced left ventricular ejection fraction (LVEF) and the susceptibility to SARS‐CoV‐2 infection. Methods and results: Of the 1162 patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention between February 2014 and October 2018, we enrolled 889 patients with available clinical follow‐up data. Follow‐up was conducted by telephone interviews 1 month after the start of the French lockdown which began on 17 March 2020. Patients were divided into two groups according to LVEF <40% (reduced LVEF) (n = 91) or ≥40% (moderately reduced + preserved LVEF) (n = 798). The incidence of COVID‐19‐related hospitalization or death was significantly higher in the reduced LVEF group as compared with the moderately reduced + preserved LVEF group (9% vs. 1%, P < 0.001). No association was found between discontinuation of ACE‐inhibitor or angiotensin‐receptor blockers and COVID‐19 test positivity. By multivariate logistic regression analysis, reduced LVEF was an independent predictor of COVID‐19 hospitalization or death (odds ratio: 6.91, 95% confidence interval: 2.60 to 18.35, P < 0.001). Conclusions: In a large cohort of patients with previous ACS, reduced LVEF was associated with increased susceptibility to COVID‐19. Aggressive COVID‐19 testing and therapeutic strategies may be considered for patient with impaired heart function. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Cardiovascular Diseases is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of this study, is to investigate the effects of a short-term exposure to air pollutants, as assessed by Nitrogen dioxide (NO2), Particulate Matter PM2,5 and PM10 concentrations, on coronary event onsets in Strasbourg, France. An observational, analytical, retrospective, epidemiological study was conducted in Strasbourg between 1 January 2012 and 31 December 2014. Higher daily coronary events rates were evidenced when NO2 concentrations were measured above 40 µg/m3 (1.258 (95% CI 1.142–1.374) vs. 1.110 (95% CI 1.033–1.186); p = 0.015). The NO2 concentration was higher than 30 µg/m3 for 677 days (61.8%). Higher daily coronary events rates were evidenced when NO2 concentrations were measured above 30 µg/m3 (1.208 (95% CI 1.128–1.289) vs. 1.067 (95% CI 0.961–1.172) p = 0.009). A marked seasonality of NO2, PM2.5, and PM10 concentrations characterized by an increase during winter and a decrease during the summer could be established. The seasonality of coronary events was evidenced simultaneously. After adjustments were made to account for the time and the month, no independent impact of NO2, PM2.5 or PM10 on daily coronary events could be demonstrated. [ABSTRACT FROM AUTHOR]

Background: Bedside diagnosis between Takotsubo syndrome (TTS) and ST elevation (STEMI) and non-ST elevation (NSTEMI) myocardial infarction remains challenging. We sought to determine a cardiac biomarker profile to enable their early distinction. Methods: 1100 patients (TTS n = 314, STEMI n = 452, NSTEMI n = 334) were enrolled in two centers. Baseline clinical and biological characteristics were compared between groups. Results: At admission, cut-off values of BNP (B-type natriuretic peptide)/TnI (Troponin I) ratio of 54 and 329 distinguished respectively STEMI from NSTEMI, and NSTEMI from TTS. Best differentiation was obtained by the use of BNP/TnI ratio at peak (cut-of values of 6 and 115 discriminated respectively STEMI from NSTEMI, and NSTEMI from TTS). We developed a score including five parameters (age, gender, history of psychiatric disorders, LVEF, and BNP/TnI ratio at admission) enabling good distinction between TTS and STEMI (77% specificity and 92% sensitivity, AUC 0.93). For the distinction between TTS and NSTEMI, a four variables score (gender, history of psychiatric disorders, LVEF, and BNP at admission) achieved a good diagnostic performance (89% sensitivity, 85% specificity, AUC 0.94). Conclusion: A distinctive cardiac biomarker profile enables at an early stage a differentiation between TTS and ACS. A four (NSTEMI) or five variables score (STEMI) permitted a better discrimination. [ABSTRACT FROM AUTHOR]

Background: Residual coronary artery disease (CAD) has been associated with worsened prognosis in patients undergoing percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS). The residual SYNTAX Score (rSS) aims to assess residual CAD after PCI. The association between kidney function and rSS has not been investigated in ACS patients. In this study, we sought to determine whether chronic kidney disease (CKD) patients exhibit more incomplete revascularization following stage revascularization procedures by PCI. We evaluated the impact of incomplete revascularization on the occurrence of major cardiovascular events (MACE) at one-year follow-up. Methods: A total of 831 ACS patients undergoing PCI were divided into 3 subgroups according to their estimated Glomerular Filtration Rate (eGFR): 695 with eGFR ≥ 60 mL/min/1.73 m², 108 with eGFR 60–30 mL/min/1.73 m², 28 with eGFR < 30 mL/min/1.73 m². Initial SYNTAX score (SS) and rSS were calculated for all patients. Incomplete revascularization was defined by rSS > 8. The primary endpoint was the occurrence of MACE (all-cause mortality, myocardial infarction (MI), repeated revascularization except from planned revascularization, stroke and definite or probable recurrent stent thrombosis) one year after the index procedure. Results: Severe CKD patients had significantly higher MACE (12.0% vs. 25.9% vs. 35.7%; p < 0.001), all-cause mortality, cardiovascular mortality and heart failure events. Patients with rSS > 8 had higher MACE, all-cause and cardiovascular mortality. CKD was an independent predictive factor of rSS > 8 (HR: 1.65, 95% CI: 1.01 to 2.71; p = 0.048). Multivariate analysis identified rSS > 8, but not CKD, as an independent predictor of cardiac death and MACE. Conclusion: In ACS, CKD is predictive of incomplete revascularization, which stands out as a strong predictor of adverse cardiovascular outcomes including cardiac death and MACE. [ABSTRACT FROM AUTHOR]

Objectives: We sought to determine whether low platelet response to the P2Y12 receptor antagonist clopidogrel as assessed by vasodilator-stimulated phosphoprotein flow cytometry test (VASP-FCT) differentially affects outcomes in patients with or without chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI). Background: Although both CKD and impaired platelet responsiveness to clopidogrel are strong predictors of unfavorable outcome after PCI, the impact of their association is unknown. The platelet VASP-FCT assay is specific for the P2Y12 ADP receptor pathway. In this test, platelet activation is expressed as the platelet reactivity index (PRI). Methods: Four-hundred forty unselected patients (CKD: 126, estimated glomerular filtration rate [eGFR] <60 ml/min/1.73 m2), no-CKD: 314 eGFR >60 ml/min/1.73 m2) undergoing urgent (n = 336) or planned (n = 104) PCI were prospectively enrolled. In each subgroup, patients were classified as low-responders (LR: PRI ≥61%) or responders (R: PRI <61%) to clopidogrel. Results: At a mean follow-up of 9 ± 2 months, all-cause mortality, cardiac death, and possible stent thrombosis were higher in CKD than in no-CKD patients. Within the CKD group, the LR status was associated with higher rates of all-cause mortality (25.5% vs. 2.8%, p < 0.001), cardiac death (23.5% vs. 2.8%, p < 0.001), all stent thrombosis (19.6% vs. 2.7%, p = 0.003), and MACE (33.3% vs. 12.3%, p = 0.007). Conversely, in no-CKD patients, the LR status did not affect outcomes. Multivariate analysis identified Killip class ≥3, drug-eluting stent implantation, and the interaction between LR and CKD (hazard ratio: 11.96, 95% confidence interval: 1.22 to 116.82; p = 0.033) as independent predictors of cardiac death. Conclusions: In CKD patients, the presence of low platelet response to clopidogrel is associated with worse outcomes after PCI. [ABSTRACT FROM AUTHOR]