PURPOSE. To evaluate the association between retinal microvasculature (vascular density) on optical coherence tomography-angiography (OCT-A) and the cardiovascular profile of patients hospitalized for acute coronary syndrome (ACS). METHODS. EYE-Myocardial Infarction (EYE-MI) study is a prospective cross-sectional study in the Cardiology Intensive Care Unit of Dijon University Hospital. Retinal OCT-A was performed for each patient within 2 days after admission. Superficial retinal capillary plexus (SCP) vascular density was measured. The population was divided into tertiles according to OCT-A data. RESULTS. Overall, 237 cases were retained for analysis. Patients in the tertile with the lowest retinal vascular density (RVD) were older, and more frequently had systemic hypertension and diabetes. Moreover, American Heart Association (AHA) risk and Global Registry of Acute Coronary Events (GRACE) scores were higher and left ventricular ejection fraction (LVEF) was lower in these patients. In multivariate analysis, the AHA risk score (odds ratio [OR], 1.06; 95% confidence interval [CI], 1.04-1.09; P < 0.001) and LVEF (OR, 0.95; 95% CI, 0.93-0.98; P ¼ 0.001) were significantly associated with the lowest tertile of RVD. The association between RVD and a high-risk cardiovascular profile was confirmed by a moderate correlation with the GRACE scores (Spearman r ¼ À0.33, P < 0.001). CONCLUSIONS. SCP density measured on OCT-A was associated with the cardiovascular risk profile and with impaired LVEF in patients with a high-risk cardiovascular status. In the future, quantitative retinal microvascular data could be considered a good surrogate of the cardiovascular risk profile and could improve cardiovascular risk assessments.

Background We aimed to evaluate the impact of coronavirus disease 2019 (COVID-19)-related lockdown on adherence to lifestyle and drug regimens in stay-at-home chronic coronary syndromes patients living in urban and rural areas. Methods A cross-sectional population-based study was perfomed in patients with chronic coronary syndromes. A sample of 205 patients was randomly drawn from the RICO (Observatoire des infarctus de Côte d'Or) cohort. Eight trained interviewers collected data by phone interview during week 16 (April 13 to April 19), i.e. 4 weeks after implementation of the French lockdown (start March 17, 2020). Results Among the 195 patients interviewed (of the 205, 3 had died, 1 declined, 6 lost), mean age was 65.5 ± 11.1 years. Only six patients (3%) reported drug discontinuation, mainly driven by media influence or family members. All 166 (85%) patients taking aspirin continued their prescribed daily intake. Lifestyle rules were less respected since almost half (45%) declared >25% reduction in physical activity, 26% of smokers increased their tobacco consumption by >25%, and 24% of patients increased their body weight > 2 kg. The decrease in physical activity and the increase in smoking were significantly greater in urban patients (P < .05). Conclusions The COVID-19-related lockdown had a negative impact on lifestyle in a representative sample of stay-at-home CCS patients.

IntroductionApoptosis can be induced in many cell types by engagement of the Fas (CD95/APO-1) receptor by its natural ligand (FasL) or agonistic antibodies (anti-Fas Ab). 1,2 Fas-mediated cell death was proposed to play a role in T-cell 3 and erythroid cell 4 homeostasis. Fas receptor was also suggested to be involved in the early phase of cytotoxic drugmediated leukemic cell apoptosis. 5,6 Signaling through Fas requires its aggregation and the formation of an intracellular protein complex referred to as the death-inducing signaling complex (DISC). 7,8 This complex consists of the cytoplasmic domain of Fas, the adaptor molecule FADD/MORT-1, and the cysteine aspartic acid-specific protease Mch5/Flice/Mach/procaspase-8. [9][10][11][12][13] This latter protein belongs to a family of structurally related cysteine proteases that currently includes 14 enzymes in mammals. 14 All are synthesized as inactive proenzymes that have to be cleaved at key aspartate residues to be activated. 15 Caspases can be divided into 2 groups according to the length of their prodomain, those with a short prodomain (procaspase-3, -6, and -7) and those with a long prodomain (the remainder). These enzymes were shown to function as a proteolytic cascade in which caspases with a long prodomain act upstream of those with a short prodomain. 16 In the Fasmediated cell death pathway, caspase-3 was suggested to play an important role in the cascade, downstream of caspase-8. 17 The binding of procaspase-8 to FADD/MORT-1 is mediated through tandem death effector domains (DED). The FLICEinhibitory protein, c-FLIP (Casper/I-Flice/Flame-1/Cash/Clarp/ Mrit/Usurpin) that contains similar DED but an inactive caspase domain, interferes with the formation of a functional DISC. [18][19][20][21][22][23][24][25] On recruitment to the DISC, procaspase-8 is processed into its active subunits, which are released from the complex to cleave intracellular substrates and to signal apoptosis. 26 The amount of active caspase-8 generated at the DISC and the level of expression of procaspase-3 could determine whether downstream pathways involve the mitochondria or not. 27 Type I cells in which caspase-8 directly activates downstream caspases to induce the cell demise were distinguished from type II cells in which caspases have to cleave the proapoptotic BH3 domainonly protein of the Bcl-2 family known as Bid to trigger cell death. 28,29 In this latter pathway, cleaved/activated Bid migrates from the cytosol to the mitochondria and induces the opening of the permeability transition pores, the loss of inner mitochondrial transmembrane potential, and the release of apoptogenic factors such as cytochrome c and apoptosis-inducing factor (AIF). [30][31][32][33] In the cytosol, cytochrome c triggers oligomerization of the adaptor molecule APAF-1 in the presence of adenosine triphosphate (ATP). Oligomerized APAF-1 recruits and activates caspase-9 For personal use only. on May 10, 2018. by guest www.bloodjournal.org From that, in turn, activates caspase-3 and other downstream casp...