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-24±17%; P=0,28). CONCLUSION This study has shown that there is a systolic dysfunction late after a first episode of PE and this despite the absence of the symptoms and pulmonary hypertension. Direct oral anticoagulants, anti-IIa or anti-Xa, are widely used in the treatment and prevention of venous thromboembolic disease as well as in nonvalvular atrial fibrillation. Direct oral anticoagulants are characterized by a rapid onset of activity, a predictable response and a relatively wide therapeutic window. Nevertheless, theoretical drug interactions exist since direct oral anticoagulants are substrates of the transport protein P-glycoprotein and/or of isoforms of cytochromes P450 pathway. Direct oral anticoagulants do not have a marketing authorization for the treatment of cancer-associated thrombosis unlike low-molecular-weight heparins which remain the gold standard treatment today. However, recent studies have compared low-molecular-weight heparins to direct oral anticoagulants in the treatment of cancer-associated thrombosis. Results of these studies showed a non-inferiority of direct oral anticoagulants in the prevention of recurrent thromboembolic events but at the cost of an increased hemorrhagic risk, in particular for patients with gastrointestinal and urogenital cancers. Thus, international guidelines, unlike French guidelines, integrate them in first line of the therapeutic strategy of cancer patients. We are certainly entering an era of personalized therapy for cancer-associated thrombosis, considering cancer type and also the theoretical risk of drug interactions with anti-cancer treatments or supportive care. OBJECTIVE Menopausal transition has been associated with an increased risk of cardiovascular disease (CVD), mainly attributed to atherogenic dyslipidaemia, central obesity and insulin resistance. Whether arterial hypertension (AH) also contributes to menopause-associated CVD is currently unknown. The aim of this study was to systematically investigate and meta-analyze the best available evidence regarding the association between early menopause (EM) and AH risk. METHODS A comprehensive search was conducted in PubMed, CENTRAL and Scopus databases, up to January 20th, 2020. Data were expressed as odds ratio (OR) with 95 % confidence intervals (CI). The I2 index was employed for heterogeneity. RESULTS Ten studies were included in the quantitative analysis (273,994 postmenopausal women, 76853 cases with AH). Women with EM (age at menopause 45 years) (OR 1.10, 95 % CI 1.01-1.19, p = 0.03; I2 79 %). The direction or the magnitude of this association remained significant when the analysis was restricted to studies including groups matched for potential confounders, such as age, BMI, smoking or the use of menopausal hormone therapy or oral contraceptives. CONCLUSIONS Women with EM have an increased risk for AH compared with those of normal age at menopause. AIM Sex hormones have been suggested to have neuroprotective effects in the natural history of multiple sclerosis (MS), particularly in animal studies. The aim of the present review was to retrieve and systematically synthesize the evidence on the effect of menopause and hormonal replacement treatment (HRT) on the course of MS. METHODS A systematic literature search was conducted in the databases MEDLINE (accessed through PubMed), Scopus, clinicaltrials.gov and Cochrane Controlled Register of Trials (CENTRAL). Eligible studies were all those that included women with MS and reported on at least one of the following a) disability and MS relapse rate before and after menopause, b) serum sex hormone concentrations, c) sexual function, d) age at menopause onset. Effects of HRT on MS clinical outcomes were also assessed. see more RESULTS Of the 4,102 retrieved studies, 28 were included in the systematic review. Of these, one reported the age at menopause for both controls and women with MS and found no difference between the two groups. There was no difference in the rates of relapse before and after menopause (risk ratio 1.21, 95 % confidence interval 0.91-1.61, p = 0.218). Two intervention studies reported beneficial effects of estrogen therapy on women with MS; however, the majority of women were premenopausal. Three studies addressed the issue of sexual dysfunction in women with MS, but information on hormonal parameters was limited. CONCLUSIONS The age at menopause is not associated with the presence of MS. The evidence on a potential causal effect of estrogen depletion on disability is inconclusive; still, relapse rate seems not be associated with menopause. The effect of HRT on the natural course of the disease remains to be defined. V.Sex is a major determinant of cardiometabolic risk. DNA methylation (DNAm), an important epigenetic mechanism that differs between sexes, has been associated with cardiometabolic diseases. Therefore, we aimed to systematically review studies in adults investigating sex-specific associations of DNAm with intermediate cardiometabolic traits and incident cardiovascular disease including stroke, myocardial infarction (MI) and coronary heart disease (CHD). Five bibliographic databases were searched from inception to 15 July 2019. We selected 35 articles (based on 30 unique studies) from 17,023 references identified, with a total of 14,020 participants of European, North American or Asian ancestry. Four studies reported sex differences between global DNAm and blood lipid levels and stroke risk. In 25 studies that took a genome wide or candidate gene approach, DNAm at 31 gene sites was associated with sex differences in cardiometabolic diseases. The identified genes were PLA2G7, BCL11A, KDM6A, LIPC, ABCG1, PLTP, CETP, ADD1, CNN1B, HOOK2, GFBP-7,PTPN1, GCK, PTX3, ABCG1, GALNT2, CDKN2B, APOE, CTH, GNASAS, INS, PON1, TCN2, CBS, AMT, KDMA6A, FTO, MAP3K13, CCDC8, MMP-2 and ER-α. Prioritized pathway connectivity analysis associated these genes with biological pathways such as vitamin B12 metabolism, statin pathway, plasma lipoprotein, plasma lipoprotein assembly, remodeling and clearance and cholesterol metabolism. Our findings suggest that DNAm might be a promising molecular strategy for understanding sex differences in the pathophysiology of cardiometabolic diseases and that future studies should investigate the effects of sex on epigenetic mechanisms in cardiometabolic risk. In addition, we emphasize the gap between the translational potential and the clinical utilization of cardiometabolic epigenetics. V.