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Introduction Serum cholesterol efflux capacity, a biomarker of the early step of the reverse cholesterol transport, has been associated with atherosclerosis independently of high-density lipoprotein (HDL) cholesterol level. Objective To evaluate the prognostic impact of serum cholesterol efflux capacity on mortality in a large cohort of patients hospitalized for an acute myocardial infarction (MI). Method Serum cholesterol efflux capacity was measured in 1,609 consecutive patients admitted with an acute MI. Results In a fully adjusted model that included age, sex, traditional cardiovascular risk factors including lipid levels, and prognostic factors of MI, serum cholesterol efflux capacity was a strong predictor of survival (adjusted hazard ratio for mortality per 1-SD increase in serum cholesterol efflux capacity, 0.79; 95% confidence interval: 0.66 to 0.95; P = 0.0132). Patients displaying an elevated serum cholesterol efflux capacity had a marked lower rate of mortality at 6 years (adjusted hazard ratio: 0.54 [0.32 to 0.89]; P = 0.0165) as compared with patients with reduced serum cholesterol efflux capacity. Conclusion Serum cholesterol efflux capacity, an integrative marker of reverse cholesterol transport pathway and efficacy, was inversely associated with all-cause mortality in MI patients independently of HDL cholesterol level and other risk factors.

Background The optimal management of left ventricular thrombus (LVT) is unknown, particularly with the emergence of the non-vitamin K antagonist anticoagulants (NOACs). Purpose To identify the independent correlates of LVT regression and clinical outcomes. Methods A computerized case sensitive search on 90 065 consecutive echocardiograms performed between January 2011 and December 2017 identified patients with a LVT. Repeated echocardiographic data, treatment and major adverse cardiac events (MACE), including death, stroke, myocardial infarction or acute peripheral artery emboli were analyzed as well as major bleeding events (BARC ≥ 3) and all-cause mortality. Results We included 159 patients with an LVT confirmed by two independent experts. Patients were treated by vitamin K antagonists (48.4%), parenteral heparins (27.7%) and NOACs (22.6%) with additional antiplatelet therapy in 67.9% of the population. Total LVT regression was reached in 62.3% of the patients in a median time of 103 [32–392] days. The independent correlates associated with LVT regression were a non-ischemic cardiomyopathy (HR 0.36; 95%CI [0.19–0.69], P = 0.002) and a smaller baseline thrombus area (HR 0.66; 95%CI [0.45–0.96], P = 0.031). Cardiovascular events were frequent with 37.1% of MACE, 18.9% of major bleeding and 13.2% of all-cause mortality during a median follow-up of 632 [187–1126] days. A left ventricular ejection fraction >35% (HR 0.46; 95%CI [0.23–0.93], P = 0.029) and an anticoagulation therapy > 3 months (HR 0.42; 95%CI [0.20–0.88], P = 0.021) were independently associated with less MACE. A reduced risk of mortality was observed among patients that obtained a total LVT regression (HR 0.48; 95%CI [0.23–0.98]; P = 0.039) ( Fig. 1 ). Conclusions The presence of LVT was associated with a very high risk of MACE and mortality. Total thrombus regression, obtained with either vitamin K antagonists or NOACs, led to a better prognosis.

Introduction Recent studies have emphasized the prognostic value of mild left ventricular ejection fraction (LVEF) impairment in severe aortic stenosis. However, despite adaptive mechanisms to pressure overload, subtle impaired systolic function could be worsened by increased after load and partly reversible immediately after its correction. The aim was to evaluate the short terms effects of transcatheter aortic valve replacement (TAVR) on LV systolic function assessed by global longitudinal strain (GLS). We hypothesized that abrupt decrease of LV after load after TAVR could lead to immediate improvement of LV systolic function. Method Patients referred to our Department for TAVR were included from January 2018 to July 2018 in this observational prospective single center study. Transthoracic echocardiography (TTE) was performed immediately before and 1–5 days after TAVR by the same operator and reviewed in a blind fashion. Results Thirty-five symptomatic patients with severe aortic stenosis referred for TAVR (age 84 ± 5 y, 18 male, NYHA 2-3, orifice area 0.7 ± 0.2 cm2, LVEF 66 ± 13%, GLS - 15.1 ± 4.7%) were included. Only 9/35 (26%) had a LVEF ≤ 60%. Overall, no significant change in LVEF (65 ± 14%; P = 0.55) or GLS (−16.1 ± 4.8%; P = 0.11) occurred immediately after TAVR despite a dramatic decrease in transoartic mean pressure gradient (44 ± 15 mm Hg versus 6 ± 3 mmHg; P Conclusion Following TAVR, an early improvement in LV systolic function assessed by GLS was observed only in patients with pre-existing mild LV systolic dysfunction. Further studies should evaluate whether this improvement is associated with better long term outcome.

RésuméLa variabilité interindividuelle de réponse au clopidogrel est un phénomène fréquent, bien établi et observé chez une proportion non négligeable de patients. Une avancée rapide des connaissances a permis de comprendre que cette variabilité est principalement liée à la variabilité de production de métabolite actif à partir de la prodrogue qu’est le clopidogrel. Les patients présentant une résistance biologique déterminée par la réalisation de tests fonctionnels plaquettaires ou par des tests génétiques prédisant l’existence d’un faible métabolisme ont un risque accru d’accidents cardiovasculaires permettant de parler de résistance au clopidogrel. À l’inverse, il a été récemment montré que des variants génétiques activateurs du métabolisme hépatique sont associés à une réponse accrue au clopidogrel. Avec l’arrivée de nouvelles thiénopyridines de métabolisme différent et l’accès croissant aux tests fonctionnels ou génétiques, la prise en charge optimale de ces patients reste une question ouverte.AbstractInter-individual variability in the response to clopidogrel is frequent, well established and observed in a fairly large proportion of patients. A rapid advance in the knowledge of this phenomenon has shown that this variability is related mainly to differences in active metabolite production from the prodrug, clopidogrel. Patients presenting biological resistance, determined through platelet function tests or genetic tests predicting the existence of low metabolism, have a higher risk of cardiovascular accidents. In contrast, genetic variants that activate hepatic metabolism are associated with an increased response to clopidogrel. With the arrival of new thienopyridines, with different metabolism, and the growing access to functional and genetic tests, optimal management of these patients remains an open question.

Background Heterozygous Familial Hypercholesterolemia (HeFH) is an underdiagnosed form of dyslipidemia associated with higher risk of myocardial infarction (MI). Identifying patients with possible HeFH would allow family screening and more aggressive treatment. The aim of this study was to assess the prevalence and impact on outcomes of possible HeFH in ST segment Elevation MI (STEMI) patients. Methods Lipid profiling was performed in consecutive STEMI patients admitted at the Pitie-Salpetriere Center, with two measurements, one performed on the arterial blood on arrival in the cath-lab and the second after a fasting period during hospitalization. A possible HEFH was defined by a Dutch Lipid Clinic Score ≥ 3, calculated from medical history and LDL-cholesterol. Major ischemic events and mortality were assessed at one-year. Results Among 1788 consecutive MI patients, the diagnosis of possible HeFH was reached in 12% of patients. There was no significant difference between LDL-cholesterol measured on admission on anticoagulated arterial blood and non-anticoagulated venous blood after a fasting period (1.18 ± 0.41 g/dL vs. 1.17 ± 0.48 g/dL; P = 0.76). HeFH patients were younger (50.6 ± 10.1 vs. 65.5 ± 13.2 years; P Fig. 1 ). Conclusion Possible HeFH is frequent in STEMI patients when screened with the Dutch Lipid Clinic Score that allows characterization of a potentially higher risk population. The better prognosis of these patients may be related to their young age and more aggressive treatment.

Background Elderly patients are at high-risk of bleedings, particularly in the setting of acute coronary syndrome treated with an invasive strategy. Treatment adjustment by platelet function testing (PFT) failed to improve clinical outcomes in the randomized ANTARCTIC trial. Purpose This prespecified substudy aims at determining the predictive value of PFT on occurrence of bleedings. Methods We analyzed the 877 patients over the age of 75 years included in the ANTARCTIC trial and randomized to a strategy of dose or drug antiplatelet therapy adjustment or a conventional “one size fits all” strategy without PFT. In the monitoring group, patients received prasugrel 5 mg daily after coronary stenting and PFT was done 14 days after randomization and repeated 14 days after treatment adjustment. Occurrence of bleedings was collected up to one year and correlated with PFT. Results Clinically relevant bleedings (Bleeding Academic Research Consortium types 2, 3 or 5) were frequently observed (20.6%, n = 181 patients) with one third occurring in the first month. Cutaneous and gastro-intestinal bleedings were the two predominant complications. There was no significant difference in the final treatment between patients with or without clinically relevant bleedings (respectively, clopidogrel 75 mg: 19.9% and 19.6%, prasugrel 5 mg: 77.3% and 77.9%, prasugrel 10 mg: 2.6% and 2.8%; P = 0.91) The main predictive factors of major bleedings in multivariate model were age > 85 years [adj.HR(95% CI): 2.48(1.25;4.91); P = 0.0093] and hemoglobin level (per gram of decrease) [adj.HR(95% CI): 1.45(1.18;1.79); P = 0.0004]. The last PFT was an independent predictive factor of clinically relevant bleedings (adj.HR(95% CI): 0.95(0.90;0.99); P = 0.017). Conclusion Clinically relevant bleedings were frequent in elderly patients in the setting of acute coronary syndrome. PFT did not improve clinical outcomes but identified the bleeding risk of these patients when the chronic treatment was installed.

Background Platelet function testing offers the possibility to individualize antiplatelet therapy in coronary artery disease patients but failed to improve clinical outcomes in randomized trials. However, high-on-treatment platelet reactivity (HPR) remains a risk factor for recurrent ischemic events and low-on-treatment platelet reactivity (LPR) is a risk factor for bleedings. Methods We collected data of patients assigned to the monitoring arm of the randomized ARCTIC and ANTARCTIC trials that evaluated the platelet reactivity by the VerifyNow P2Y12 test two weeks after coronary stenting. HPR was defined by PRU ≥ 208, LPR by PRU ≤ 85 and optimal platelet reactivity (OPR) by 85. Results Among the 1418 patients included, HPR was present in 269 patients (18.9%), OPR was reached in 681 patients (48.0%) and LPR in 468 patients (33.0%). The primary composite endpoint occurred in 9.7%, 11.5% and 14.3% respectively. There was no significant difference in the net clinical benefit between HPR and OPR patients (adjusted HR: 0.91(0.48–1.72); P = 0.77) and between LPR and OPR patients (adjusted HR: 1.13 (0.67–1.90); P = 0.64). There were no difference in the individual clinical endpoints between the three groups. ROC curve analysis demonstrated that PRU when used for treatment adjustment has a limited ability to discriminate net clinical benefit, ischemic or bleeding complications (curve–c index = 0.55, 0.51 or 0.59, respectively). Conclusion Two weeks after stenting, an optimal platelet reactivity was obtained in less than half of the population. The net clinical benefit of these patients was not different from that of patients with HPR and LPR who had treatment adjustment.