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The intensity and duration of the catabolic phase in COVID-19 patients can differ between survivors and non-survivors. The purpose of the study was to assess the determinants of, and association between, nitrogen balance trajectories and outcome in critically ill COVID-19 patients.This retrospective monocentric observational study involved patients admitted to the intensive care unit (ICU) of the University Hospital of Clermont Ferrand, France, from January 2020 to May 2021 for COVID-19 pneumonia. Patients were excluded if referred from another ICU, if their ICU length of stay was72 h, or if they were treated with renal replacement therapy during the first seven days after ICU admission. Data were collected prospectively at admission and during ICU stay. Death was recorded at the end of ICU stay. Comparisons of the time course of nitrogen balance according to outcome were analyzed using two-way ANOVA. At days 3, 5, 7, 10 and 14, uni- and multivariate logistic regression analyses were performed to assess the impact of a non-negative nitrogen-balance on ICU death. To investigate the relationships between nitrogen balance, inflammatory markers and protein intake, linear and non-nonlinear models were run at days 3, 5 and 7, and the amount of protein intake necessary to reach a neutral nitrogen balance was calculated. Subgroup analyses were carried out according to BMI, age, and sex.99 patients were included. At day 3, a similar negative nitrogen balance was observed in survivors and non-survivors: -16.4 g/d [-26.5, -3.3] and -17.3 g/d [-22.2, -3.8] (p = 0.54). The trajectories of nitrogen balance over time thus differed between survivors and non-survivors (p = 0.01). In survivors, nitrogen balance increased over time, but decreased from day 2 to day 6 in non-survivors, and thereafter increased slowly up to day 14. At days 5 and 7, a non-negative nitrogen-balance was protective from death. Administering higher protein amounts was associated with higher nitrogen balance.We report a prolonged catabolic state in COVID patients that seemed more pronounced in non-survivors than in survivors. Our study underlines the need for monitoring urinary nitrogen excretion to guide the amount of protein intake required by COVID-19 patients.

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Background SARS-CoV-2 has been responsible for considerable mortality worldwide, owing in particular to pulmonary failures such as ARDS, but also to other visceral failures and secondary infections. Recent progress in the characterization of the immunological mechanisms that result in severe organ injury led to the emergence of two successive hypotheses simultaneously tested here: hyperinflammation with cytokine storm syndrome or dysregulation of protective immunity resulting in immunosuppression and unrestrained viral dissemination. Methods In a prospective observational monocentric study of 134 patients, we analysed a panel of plasma inflammatory and anti-inflammatory cytokines and measured monocyte dysregulation via their membrane expression of HLA-DR. We first compared the results of patients with moderate forms hospitalized in an infectious disease unit with those of patients with severe forms hospitalized in an intensive care unit. In the latter group of patients, we then analysed the differences between the surviving and non-surviving groups and between the groups with or without secondary infections. Findings Higher blood IL-6 levels, lower quantitative expression of HLA-DR on blood monocytes and higher IL-6/mHLA-DR ratios were statistically associated with the risk of severe forms of the disease and among the latter with death and the early onset of secondary infections. Interpretation The unique immunological profile in patients with severe COVID-19 corresponds to a moderate cytokine inflammation associated with severe monocyte dysregulation. Individuals with major CSS were rare in our cohort of hospitalized patients, especially since the use of corticosteroids, but formed a very severe subgroup of the disease. Funding None.

Background Data regarding the use of direct oral anticoagulants (DOACs) for the treatment of acute pulmonary embolism (PE) are sparse. We conducted a prospective multicentre registry study to describe patterns of DOAC prescription for the treatment of acute PE, and the associated risk of 6-month adverse events in daily practice. Methods We included all PE patients discharged since the availability of DOACs for the dedicated indication of acute PE treatment. Clinical data and 6-month outcomes, including death, recurrent venous thromboembolism (VTE), bleeding, and chronic thromboembolic pulmonary hypertension (CTEPH) were recorded prospectively. Temporal trends in DOAC prescription were tested. Results Between 09/2012 and 04/2017, 1082 patients were included: 60.6% (n = 656) were treated with DOACs and 39.4% (n = 426) with another anticoagulant. The prescription rate of DOACs increased sharply just after their release on the market to reach a plateau over time, between 56% and 72% of the total prescription per year in PE patients (p for trend = 0.33). Active malignancy and renal function impairment were factors independently associated with non-prescription of DOACs. Overall, prescription of DOACs was appropriate in 95.3% of patients. The rate of use of non-recommended DOAC doses was 4.2% (n = 28). The rate of death, recurrent VTE, bleeding and CTEPH were 2.4%, 1.2%, 7.2%, and 1.9%, respectively in the DOAC group. Conclusion The choice to prescribe DOACs or not is related to patient characteristics. The overall appropriateness of prescription is high, while the rate of adverse events observed in patients treated with DOAC is low in our registry.

Background Renal dysfunction influences outcomes after pulmonary embolism (PE). We aimed to determine the incremental value of adding renal dysfunction, defined by estimated glomerular filtration rate (eGFR), on top of the European Society of Cardiology (ESC) prognostic model, for the prediction of 30-day mortality in acute PE patients, which in turn could lead to the optimization of acute PE management. Methods We performed a multicenter, non-interventional retrospective post hoc analysis based on a prospectively collected cohort including consecutive confirmed acute PE stratified per ESC guidelines. We first identified which of three eGFR formulae most accurately predicted death. Changes in global model fit, discrimination, calibration and reclassification parameters were evaluated with the addition of eGFR to the prognostic model. Results Among 1943 patients (mean age 67.3 (17.1), 50.4% women), 107 (5.5%) had died at 30 days. The 4-variable Modification of Diet in Renal Disease (eGFRMDRD4) formula predicted death most accurately. In total, 477 patients (24.5%) had eGFRMDRD4 MDRD4 information improved model fit, discriminatory capacity, and calibration of the ESC model. Reclassification parameters were significantly increased, yielding 18% reclassification of predicted mortality (p Conclusion The addition of eGFRMDRD4-derived renal dysfunction on top of the prognostic algorithm led to risk reclassification within the intermediate- and high-risk PE categories. The impact of risk stratification integrating renal dysfunction on therapeutic management for acute PE requires further studies.

Background Renal dysfunction may influence outcomes after pulmonary embolism (PE). We determined the incremental value of adding renal function impairment (estimated glomerular filtration rate, eGFR Methods and results We identified which of three eGFR formulae predicted death most accurately. Changes in global model fit, discrimination, calibration and net reclassification index (NRI) were evaluated with addition of eGFR. We prospectively included consecutive adult patients with acute PE diagnosed as per ESC guidelines. Among 1,943 patients, (mean age 67.3±17.1, 50.4% women), 107 (5.5% (95% CI 4.5–6.5%)) died during 30-day follow-up. The eGFRMDRD4 formula was the most accurate for prediction of death. The observed mortality rate was higher for intermediate-low risk (OR 1.8, 95% CI 1.1–3.4) and high-risk PE (OR 10.3, 95% CI 3.6–17.3), and 30-day bleeding was significantly higher (OR 2.1, 95% CI 1.3–3.5) in patients with vs without eGFRMDRD4 Conclusion Addition of eGFRMDRD4-derived renal dysfunction on top of the ESC prognostic algorithm yields significant reclassification of risk of death in intermediate and high-risk PE. Impact on therapy remains to be determined. Funding Acknowledgement Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): BMS-Pfizer Alliance, Bayer Healthcare

Background: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a common disease with an uncertain pathophysiology. It is characterized by polyps rich in eosinophils, with an activation status already investigated at the tissue level. In a group of CRSwNP patients, we assessed the activation status of circulating eosinophils in the blood before migration into tissues. Methods: Thirteen patients with CRSwNP and 16 healthy volunteers were enrolled. Several biologic parameters were studied: blood count of eosinophils; plasma eosinophil cationic protein; oxidative metabolism by chemiluminescence at baseline or when activated by phorbol 12-myristate 13-acetate or platelet-activating factor, with or without interleukin-5 (IL-5); percent of granulosar cells; and mean fluorescence intensity (MFI) by flow cytometry. Results: The mean number of eosinophils was significantly higher in patients with CRSwNP, whose eosinophils showed increased oxidative metabolism in the basal or activated state significantly decreasing in the presence of IL-5. There was also a higher percentage of CD49d(+), CD25(+), and CCR3(+) cells in patients, and a nonsignificant decrease in descending order in MFI between the control group, patients with normal eosinophil levels, patients with hyper-eosinophilia, and patients with aspirin-exacerbated respiratory disease. Conclusion: This study demonstrates a priming state of circulating eosinophils in CRSwNP patients when compared with healthy controls, as evidenced by the extent of oxidative metabolism, with increased sensitivity to IL-5 and by the observed variations of percent and MFI of CD49d, CCR3, and CD25. This priming is thus found at the peripheral level and occurs before the migration of eosinophils to polyps, reflecting the systemic and not just local nature of abnormalities in CRSwNP.

INTRODUCTION Left ventricular (LV) dysfunction is a major prognostic determinant in myotonic dystrophy type 1 (DM1). Therefore, markers of early-stage LV impairment may be useful. The aim of this study was to evaluate 2D echocardiographic LV strain in a cohort of DM1 patients with preserved left ventricular ejection fraction (LVEF) and to compare the results with matched controls. METHODS This prospective single-center study included 33 consecutive DM1 patients between February 2014 and February 2015. Mean age was 38.2±12.9 years, and 17 (52%) were males. Exclusion criteria were LVEF 120 milliseconds, history of atrial fibrillation, and presence of a pacemaker with ventricular pacing. DM1 patients were matched to healthy controls according to sex and age. RESULTS DM1 patients showed significant impairment of global longitudinal strain (GLS) as compared to controls (-18.0±1.9 vs -19.1±2.4; P=.03), characterized by a marked alteration at the apex (-20.0±3.3 vs -22.7±3.1; P

Background We explored the relation between adverse outcomes after acute pulmonary embolism (PE)and renal dysfunction classified by estimated glomerular filtration rate (eGFR) using the CKD-EPI equation. We assessed the incremental value of adding eGFR CKD-EPI to the ESC score for predicting 30d mortality. Methods Prospective, multicenter study of 1664 acute PE admitted from 01/2011 to 12/2017. Pts were categorized in 4 eGFR groups: Group 1 (eGFR ≥60 ml/min/1.73m2, n=1178), group 2 (45–59; n=257); group 3 (30–44; n=150), group 4 (≤29; n=79). Results All-cause and CV death at 30 days and 6 months were higher in group 3 (p=0.005 and p=0.03) and group 4 (p Without eGFR CKD-EPI OR (95% CI) With eGFR CKD-EPI OR (95% CI) ESC algorithm 2.59 (1.95–3.43) 2.30 (1.72–3.07) eGFR CKD-EPI – 2.60 (1.62–4.7) Measures of fit Bayes information criterion 607.30 599.32 Akaike information criterion 596.47 583.06 C-statistic 0.71* 0.77* P (Hosmer-Lemeshow) 0.057 0.43 Integrated discrimination improvement – 0.054 (0.052–0.056) Net reclassification improvement – 0.93 (0.90–0.95) Prognostic performance Sensitivity 62.5 (51.2–72.3) 76.2 (61.5–90.2) Specificity 64.2 (49.1–74.4) 69.9 (47.6–83.5) Positive predictive value 10.1 (8.2–11.3) 16.2 (14.2–18.2) Negative predictive value 0.97 (0.96–0.98) 98.1 (97.2–99.2) Positive likelihood ratio 1.96 (1.12–3.41) 2.12 (1.54–3.12) Negative likelihood ratio 0.50 (0.25–1.81) 0.54 (0.20–1.56) Youden index 0.31 (0.28–0.34) 0.39 (0.36–0.41) Difference in C-statistic: *p=0.04. Conclusion Renal function impairment increases the rate of adverse events after acute PE. Combined with the ESC early mortality risk score, eGFR improves risk classification.

Part of special issue:14ème Congrès Francophone d’Allergologie - 16-19 avril 2019 - Paris, Palais des Congrès; Le microbiote comme outil thérapeutique dans l’allergie alimentaire

Dose adjustment of direct oral anticoagulants (DOACs) is not required in the setting of acute PE treatment according to the manufacturer’s labelling, beyond the contraindication in severe renal insufficiency. We designed a prospective, multicenter cohort study to investigate the impact of prescription of non-recommended DOAC doses on 6-month adverse events. The primary endpoint was a composite of all-cause death, recurrent VTE, major bleeding, and chronic thromboembolic pulmonary hypertension (CTEPH). In total, among 656 patients discharged with DOACs between 09/2012 and 10/2016, 28 (4.3%) were not treated with a recommended DOAC dose. All the non-recommended DOAC dose prescriptions were under-dosed according to the drug labelling. After multivariate adjustment, age > 70 years, a history of coronary artery disease, creatinine clearance

Background Cats are the major source of indoor inhalant allergens after house dust mites. The global incidence of cat allergies is rising sharply, posing a major public health problem. Ten cat allergens have been identified. The major allergen responsible for symptoms is Fel d 1, a secretoglobin and not a lipocalin, making the cat a special case among mammals. Main body Given its clinical predominance, it is essential to have a good knowledge of this allergenic fraction, including its basic structure, to understand the new exciting diagnostic and therapeutic applications currently in development. The recent arrival of the component-resolved diagnosis, which uses molecular allergens, represents a unique opportunity to improve our understanding of the disease. Recombinant Fel d 1 is now available for in vitro diagnosis by the anti-Fel d 1 specific IgE assay. The first part of the review will seek to describe the recent advances related to Fel d 1 in terms of positive diagnosis and assessment of disease severity. In daily practice, anti-Fel d 1 IgE tend to replace those directed against the overall extract but is this attitude justified? We will look at the most recent arguments to try to answer this question. In parallel, a second revolution is taking place thanks to molecular engineering, which has allowed the development of various forms of recombinant Fel d 1 and which seeks to modify the immunomodulatory properties of the molecule and thus the clinical history of the disease via various modalities of anti-Fel d 1-specific immunotherapy. We will endeavor to give a clear and practical overview of all these trends.

T follicular helper (Tfh) and regulatory (Tfr) cells regulate B cell activation and ultimately antibody production. While concordant results show that Tfh cells are specific for the immunizing antigens, limited and even controversial results have been reported regarding the specificity of Tfr cells. Here we used high-throughput T cell receptor (TCR) sequencing to address this issue. We observed that although the Tfh- and Tfr-cell repertoires are less diverse than those of effector (Teff) and regulatory T (Treg) cells, they still represent thousands of clonotypes after immunization with a single antigen. T-cell receptor beta variable (TRBV) gene usage distinguishes both follicular T cells (Tfol) from non-Tfol cells, as well as helper (Teff and Tfh) vs. regulatory (Treg and Tfr) cells. Analysis of the sharing of clonotypes between samples revealed that a specific response to the immunizing antigen can only be detected in Tfh cells immunized with a non-self-antigen and Tfr cells immunized with a self-antigen. Finally, the Tfr TCR repertoire is more similar to that of Tregs than to that of Tfh or Teff cells. Altogether, our results highlight a bystander Tfol-cell activation during antigenic response in the germinal centres and support the Treg cell origin of Tfr cells.Significance StatementFollicular helper T (Tfh) cells promote high-affinity antibody production by B cells while follicular regulatory T (Tfr) cells represses it. The question of the specificity of follicular T (Tfol) cells is of utmost importance in the understanding of the antibody response specificity and our work is the first to analysed the global Tfol TCR repertoire in wild type mice. This allowed us not only to portray the overall global structure of these repertoires, but also to substantiate the fact that Tfr cells respond to self-antigen while Tfh cells respond to non self-antigen, a still controversial issue. Importantly, our work revealed an unexpected bystander activation of Tfol cells. We think and discuss that it has a general significance in immune responses and possibly immunopathologies.

End-systolic left ventricular (LV) elastance ( Ees) has been previously calculated and validated invasively using LV pressure-volume (P-V) loops. Noninvasive methods have been proposed, but clinical application remains complex. The aims of the present study were to 1) estimate Ees according to modeling of the LV P-V curve during ejection (“ejection P-V curve” method) and validate our method with existing published LV P-V loop data and 2) test the clinical applicability of noninvasively detecting a difference in Ees between normotensive and hypertensive subjects. On the basis of the ejection P-V curve and a linear relationship between elastance and time during ejection, we used a nonlinear least-squares method to fit the pressure waveform. We then computed the slope and intercept of time-varying elastance as well as the volume intercept (V0). As a validation, 22 P-V loops obtained from previous invasive studies were digitized and analyzed using the ejection P-V curve method. To test clinical applicability, ejection P-V curves were obtained from 33 hypertensive subjects and 32 normotensive subjects with carotid tonometry and real-time three-dimensional echocardiography during the same procedure. A good univariate relationship ( r2 = 0.92, P < 0.005) and good limits of agreement were found between the invasive calculation of Ees and our new proposed ejection P-V curve method. In hypertensive patients, an increase in arterial elastance ( Ea) was compensated by a parallel increase in Ees without change in Ea/ Ees. In addition, the clinical reproducibility of our method was similar to that of another noninvasive method. In conclusion, Ees and V0 can be estimated noninvasively from modeling of the P-V curve during ejection. This approach was found to be reproducible and sensitive enough to detect an expected increase in LV contractility in hypertensive patients. Because of its noninvasive nature, this methodology may have clinical implications in various disease states. NEW & NOTEWORTHY The use of real-time three-dimensional echocardiography-derived left ventricular volumes in conjunction with carotid tonometry was found to be reproducible and sensitive enough to detect expected differences in left ventricular elastance in arterial hypertension. Because of its noninvasive nature, this methodology may have clinical implications in various disease states.

International audience; Background: We hypothesized that dietary sodium may modulate the effect of systolic blood pressure and other nonhemodynamic factors, such as high uric acid and renal dysfunction, on changes in the left ventricular mass after renal transplantation. The objective of the present 3-year follow-up longitudinal study was to assess the concomitant influence of these factors on changes in the left ventricular mass after renal transplantation.Methods: Twenty-four-hour urinary sodium excretion, glomerular filtration rate (isotopic clearance), and left ventricular mass (echocardiography) assessment were done in 165 renal transplant patients during the first year and after a follow-up of 3 years after renal transplantation.Results: At follow-up, therapy of hypertension was associated with normalization of blood pressure in 64% and a decrease in the prevalence of left ventricular hypertrophy from 66% to 56%. At baseline and follow-up, systolic blood pressure, sodium intake, and serum uric acid emerged as independent and significant determinants of the final left ventricular mass index. When the population was divided according to sex-specific tertiles of the final 24-hr urinary sodium excretion, the relationship between change in serum uric acid during follow-up, final left ventricular mass index, and final glomerular filtration rate was significant only on the highest tertile of 24-hr urinary sodium excretion.Conclusion: The decrease in the prevalence of left ventricular hypertrophy after renal transplantation is blunted by high sodium intake. Persistence of the left ventricular hypertrophy may result from the combined adverse influences of excessive dietary sodium intake and increased serum uric acid during follow-up despite pharmacological control of blood pressure.

Because the functional interaction between the LV and arterial systems, termed ventricular-arterial coupling, is recognized as a key determinant of LV performance, the objective of the present study was to assess the impact of uncomplicated HT without LVH on LV performance using simultaneously echocardiography and carotid tonometry. LV maximal power (PmaxVG), cardiac power output (CPO), LV efficiency (CPO/PmaxVG), input aortic and output LV elastance (Ea and Ees) were assessed in 20 normotensive control subjects (NT) and 10 patients with untreated HT. PmaxVG was calculated according to the integral of the product of LV wall stress with strain rate (as an index of gradient velocity). Cyclic variation of wall thickness and SR were measured by speckel-tracking. Ea and Ees were derived and modelized from the pressure-volume curve. No difference in age, BMI and sex ratio was observed between NT and HT. Systolic BP (160±18 vs. 119±10mmHg), LV mass (99±15 vs. 76±12g/m(2)), PWV (9.7±2 vs. 6.9±1m/s) were significantly higher (P

Objective: Non invasive methods have been proposed to assess end systolic left ventricular (LV) elastance (Ees), but clinical application remains complex. The aim of the present study was to 1) estimate Ees according to modeling of LV pressure-volume (P-V) curve during ejection and validate our method with existing published LV P-V loop data 2) test clinical applicability to detect a difference in Ees between normotensive and hypertensive subjects. Methods: Based on P-V curve and a linear relationship between LV elastance and time during ejection, we fitted the systolic pressure curve (non linear least square method). We then computed slope and intercept of time varying elastance, and calculated Ees as LV elastance at the end of ejection. As a validation, 22 P-V loops obtained from previous invasive studies were digitized and analyzed with our method. To test clinical applicability, P-V curve was obtained from 32 normotensive and 33 hypertensive subjects, using carotid tonometry and real-time 3D echocardiography. Results: A strong univariate relationship (r2=0.92, p

Regulatory T cells (Tregs) are pivotal for maintenance of immune self-tolerance and also regulate immune responses to exogenous Ags, including allergens. Both decreased Treg number and function have been reported in allergic patients, offering new therapeutic perspectives. We previously demonstrated that Tregs can be selectively expanded and activated by low doses of IL-2 (ld-IL-2) inducing immunoregulation without immunosuppression and established its protective effect in autoimmune diseases. In this study, we evaluated the ability of ld-IL-2 to control allergy in an experimental model of food allergy. Ld-IL-2 induced Treg expansion and activation that elicited protection against clinical manifestations of food allergy in two mouse models with OVA and peanut. This clinical effect was lost in Treg-depleted mice, demonstrating the major contribution of Tregs in ld-IL-2 efficacy. Mechanistic studies further indicated that protection from allergy could be explained by a Treg-dependent local modification of the Th1/Th2 balance and an inhibition of mast cell recruitment and activation. Preventive and therapeutic effects of ld-IL-2 were observed over a 7-mo-period, highlighting its long-term efficacy. This study demonstrated that ld-IL-2 is efficient to prevent and to treat allergic immune responses, and thus represents a promising therapeutic strategy for managing allergic diseases.

BackgroundContrast induced nephrotoxicity (CIN) after coronary angiography or angioplasty (CA) has been shown to be related to mortality. The rate and predictors of CIN when preventive measures are applied are poorly documented.MethodsAll consecutive patients submitted to non-urgent CA in 2014 with low-osmolar contrast medium were stratified for CIN risk: patients with renal dysfunction (defined as eGFR44mmol/L in SCr. CIN rate was related to quartiles of eGFR before CA: 20% when eGFR87ml/min. The amount of contrast medium was not a predictor of CIN. In patients without renal dysfunction, a lower SCr was a predictor of CIN. Conversely, in patients with renal dysfunction, older age and diabetes were associated with CIN (figure).ConclusionsIn contemporary routine practice, CIN occurs in 20%, driven by a relative 25% increase in SCr, and irrespective of the amount of contrast medium. In patients with renal dysfunction, older age and diabetes were associated with CIN.

We aimed to evaluate the impact of thrombus burden as measured by Optical Coherence Tomography on the occurrence of peri-procedural myocardial infarction (type IVa MI) among patients undergoing percutaneous coronary intervention (PCI) in non ST elevation acute coronary syndrome (NSTE-ACS).

Introduction The therapeutic management of bypass failure has been little studied. Objectives Compare prognosis and the occurrence of cardiovascular events at 2 years in patients with venous bypass graft failure by differentiating between three patient groups: medical therapy, percutaneous coronary intervention (PCI) in native vessels (native PCI), and PCI in coronary artery bypass grafts (PCI-CABG). Methods Retrospective observational study in patients with bypass graft failure diagnosed between February 2009 and September 2013 at Poitiers University Hospital, France. Follow-up data at 1 year and at 2 years regarding major adverse cardiac events (MACEs), defined as death, acute coronary syndrome (ACS) or revascularization, were collected during patient visits to the department. Results From a series of 320 CABG patients examined using coronary angiography, all patients with bypass graft failure were included in the study (200 patients). Mean age was 69 years (+/- 11). Coronary angiography was performed a mean of 117 months after bypass surgery. Medical therapy alone was chosen in 88 patients, 75 patients underwent native PCI, and 37 patients underwent PCI-CABG. Patients in the PCI-CABG group were older (73.6 years; p = 0.027) and had significantly older bypass grafts (22% for a period of more than 10 years; p = 0.018), and their typical clinical presentation was one of ACS without ST-segment elevation (41%; p = 0.006). The groups were comparable in terms of hospital complications, except for vascular complications, which were more common in the PCI-CABG group (8%; p=0.01). At 1 year, no significant difference in terms of MACEs was found, but there was a trend towards an increase in ACS without ST-segment elevation (11%; p=0.06) in the PCI-CABG group, and towards an increase in ACS with STsegment elevation (7%; p = 0.06) in the medical therapy group. At 2 years, the medical therapy group stood out by virtue of a significant increase in MACEs compared with the other two groups (63%; p = 0.02). The native PCI group presented both fewer MACEs and fewer vascular complications. Conclusion MACEs were common and more severe in the medical therapy group. When coronary lesions are amenable to PCI, PCI in native vessels should be proposed as first-line treatment. PCI of CABG is performed in a riskier setting and has poorer prognosis.

Background: Catheter ablation is the treatment of choice for the management of atrial fibrillation (AF). The main limitation of this technique is the success rate, which is in the range of 70 to 80%. It is therefore critical to identify patients likely to benefit from this procedure, and who will