ce the precision of ablative therapy and may support a greater role for adjunctive strategies and technology to address arrhythmogenic tissue harbored in the mid-myocardium and subepicardium. BACKGROUND Arterial stiffening is central in the vascular aging process. Traditionally, vascular research has focused on atherosclerotic vascular disease, whereas arterial stiffness has not attracted similar attention. OBJECTIVES The purpose of this study was to assess lifetime trajectories of arterial stiffening in Chinese populations facing a high burden of cardiovascular disease, with a particular focus on age-sex interactions and potential determinants. METHODS This large-scale observational study comprised 2 independent cross-sectional population samples and 1 prospective cohort totaling 80,415 healthy subjects with brachial-ankle pulse wave velocity (baPWV) measurements available. Associations with potential risk conditions were analyzed using linear regression, linear random intercepts mixed models, and L1-regularized linear models. RESULTS The dynamics of age-dependent arterial stiffening differed in sexes, with stiffer vessel observed in men from adolescence to age 58 years and in women thereafter. see more The steeper increase in baPWV in women after menopause is partly explained by the fact that vascular risk factors are more strongly associated with arterial stiffness in women than in men. Age and systolic blood pressures were the strongest determinants of baPWV, whereas other vascular and metabolic risk factors, except low-density lipoprotein cholesterol, showed consistent associations of moderate strength. CONCLUSIONS The significant age-sex interaction in arterial stiffening provides an important clue of explanation for the heightened cardiovascular disease risk in postmenopausal women. Detailed knowledge on lifetime trajectories of arterial stiffening, and its potential risk factors is a prerequisite for the development of new prevention strategies counteracting vascular aging. BACKGROUND Early in the prevention and treatment of bioprosthetic valve thrombosis (BPVT), anticoagulation is effective, but the long-term outcome after BPVT is unknown. OBJECTIVES The goal of this study was to assess the long-term outcomes of patients with BPVT treated with anticoagulation. METHODS This analysis was a matched cohort study of patients treated with warfarin for suspected BPVT at the Mayo Clinic between 1999 and 2017. RESULTS A total of 83 patients treated with warfarin for suspected BPVT (age 57 ± 18 years; 45 men [54%]) were matched to 166 control subjects; matching was performed according to age, sex, year of implantation, and prosthesis type and position. Echocardiography normalized in 62 patients (75%) within 3 months (interquartile range [IQR] 1.5 to 6 months) of anticoagulation; 21 patients (25%) did not respond to warfarin. Median follow-up after diagnosis was 34 months (IQR 17 to 54 months). There was no difference in the primary composite endpoint between the patients with BPVT and the matched control subjects (log-rank test, p = 0.79), but the former did have a significantly higher rate of major bleeding (12% vs. 2%; p  less then  0.0001). BPVT recurred (re-BPVT) in 14 (23%) responders after a median of 23 months (IQR 11 to 39 months); all but one re-BPVT patient responded to anticoagulant therapy. Patients with BPVT had a higher probability of valve re-replacement (68% vs. 24% at 10 years' post-BPVT; log-rank test, p  less then  0.001). CONCLUSIONS BPVT was associated with re-BPVT and early prosthetic degeneration in a significant number of patients. Indefinite warfarin anticoagulation should be considered after a confirmed BPVT episode, but this strategy must be balanced against an increased risk of bleeding. BACKGROUND Aortic risk has not been evaluated in patients with Marfan syndrome and documented pathogenic variants in the FBN1 gene. OBJECTIVES This study sought to describe aortic risk in a population with Marfan syndrome with pathogenic variants in the FBN1 gene as a function of aortic root diameter. METHODS Patients carrying an FBN1 pathogenic variant who visited our reference center at least twice were included, provided they had not undergone aortic surgery or had an aortic dissection before their first visit. Aortic events (aortic surgery or aortic dissection) and deaths were evaluated during the 2 years following each patient visit. The risk was calculated as the number of events divided by the number of years of follow-up. RESULTS A total of 954 patients were included (54% women; mean age 23 years). During follow-up (9.1 years), 142 patients underwent prophylactic aortic root surgery, 5 experienced type A aortic dissection, and 12 died (noncardiovascular causes in 3, unknown etiology in 3, post-operative in 6). When aortic root diameter was  less then 50 mm, risk for proven type A dissection (0.4 events/1,000 patient-years) and risk for possible aortic dissection (proven aortic dissection plus death of unknown cause, 0.7 events/1,000 patients-years) remained low in this population that was treated according to guidelines. Three type A aortic dissections occurred in this population during the 8,594 years of follow-up, including 1 in a patient with a tubular aortic diameter of 50 mm, but none in patients with a family history of aortic dissection. The risk for type B aortic dissection in the same population was 0.5 events/1,000 patient-years. CONCLUSIONS In patients with FBN1 pathogenic variants who receive beta-blocker therapy and who limit strenuous exercise, aortic risk remains low when maximal aortic diameter is  less then 50 mm. The risk of type B aortic dissection is close to the remaining risk of type A aortic dissection in this population, which underlines the global aortic risk. Biofluids contain various circulating cell-free RNAs (ccfRNAs). The composition of these ccfRNAs varies among biofluids. They constitute tantalizing biomarker candidates for several pathologies and have been demonstrated to be mediators of cellular communication. Little is known about their function in physiological and developmental settings, and most works are limited to in vitro studies. Here, we develop iTAG-RNA, a method for the unbiased tagging of RNA transcripts in mice in vivo. We use iTAG-RNA to isolate hepatocytes and kidney proximal epithelial cell-specific transcriptional responses to a dietary challenge without interfering with the tissue architecture and to identify multiple hepatocyte-secreted ccfRNAs in plasma. We also identify specific transfer of liver-derived ccfRNAs to adipose tissue and skeletal muscle, where they likely constitute a buffering system to maintain lipid homeostasis under acute high-fat-diet feeding. Our findings directly demonstrate in vivo transfer of RNAs between tissues and highlight its implications for endocrine signaling and homeostasis.