Objective The aim of this study was to assess the impact of sex on the management and outcome of patients according to aortic stenosis (AS) severity. Introduction Sex differences in the management and outcome of AS are poorly understood. Methods Doppler echocardiography data of patients with at least mild-to-moderate AS [aortic valve area (AVA) ≤1.5 cm2 and peak jet velocity (VPeak) ≥2.5 m/s or mean gradient (MG) ≥25 mmHg] were prospectively collected between 2005 and 2015 and retrospectively analysed. Patients with reduced left ventricular ejection fraction (<50%), or mitral or aortic regurgitation >mild were excluded. Results Among 3632 patients, 42% were women. The mean indexed AVA (0.48 ± 0.17 cm2/m2), VPeak (3.74 ± 0.88 m/s), and MG (35.1 ± 18.2 mmHg) did not differ between sexes (all P ≥ 0.18). Women were older (72.9 ± 13.0 vs. 70.1 ± 11.8 years) and had more hypertension (75% vs. 70%; P = 0.0005) and less coronary artery disease (38% vs. 55%, P < 0.0001) compared to men. After inverse-propensity weighting (IPW), female sex was associated with higher mortality (IPW-HR: 1.91 [1.14–3.22]; P = 0.01) and less referral to valve intervention (competitive model IPW-HR: 0.88 [0.82–0.96]; P = 0.007) in the whole cohort. This excess mortality in women was blunted in concordant non-severe AS initially treated conservatively (IPW-HR = 1.03 [0.63–1.68]; P = 0.88) or in concordant severe AS initially treated by valve intervention (IPW-HR = 1.25 [0.71–2.21]; P = 0.43). Interestingly, the excess mortality in women was observed in discordant low-gradient AS patients (IPW-HR = 2.17 [1.19–3.95]; P = 0.01) where women were less referred to valve intervention (IPW-Sub-HR: 0.83 [0.73–0.95]; P = 0.009). Conclusion In this large series of patients, despite similar baseline hemodynamic AS severity, women were less referred to AVR and had higher mortality. This seemed mostly to occur in the patient subset with discordant markers of AS severity (i.e. low-gradient AS) where women were less referred to AVR.

Purpose of review Coronary artery bypass graft (CABG) surgery remains the gold-standard treatment for multivessel and left main coronary artery disease. Despite significant improvement in cardiovascular outcomes, patients undergoing CABG remain at risk for recurrent adverse ischemic events and other cardiovascular outcomes (coronary revascularisation, stroke, cardiac death, etc.). The purpose of this review is to summarize the most recent evidence in pharmacological preventive therapies addressing the residual cardiovascular risk in patients who have undergone CABG. Recent findings Novel cardiovascular pharmacological preventive strategies targeting inflammatory, metabolic and prothrombotic (antiplatelet and anticoagulation) pathways have been recently assessed, with promising results for secondary prevention after CABG. Summary Secondary prevention is an essential part of postoperative care after CABG. Novel lipid-lowering and glucose-controlling agents suggest a strong and consistent benefit on native coronary artery disease and overall cardiovascular outcomes. The role and the choice of enhanced antiplatelet/anticoagulation/lipid/glucose-modulating therapies following CABG should be better defined and deserves further investigation. Additional studies are required to identify new therapeutic target addressing the specific multifactorial nature of the graft CV disease and identifying the best preventive strategies for long-term graft patency.

Background Early vascular aging (EVA) is associated with higher risk of adverse cardiovascular events and can be estimated noninvasively by assessing arterial hemodynamics. Women with a history of preeclampsia have increased risk of cardiovascular disease, but underlying mechanisms are incompletely understood. We hypothesized that women with a history of preeclampsia display persistent arterial abnormalities and EVA in the postpartum period. Methods and Results We performed a comprehensive, noninvasive arterial hemodynamic evaluation in women with a history of preeclampsia (n=40) and age‐matched controls with previous normotensive pregnancies (n=40). We used validated methods integrating applanation tonometry with transthoracic echocardiography to obtain measures of aortic stiffness, steady and pulsatile arterial load, central blood pressure, and arterial wave reflections. Presence of EVA was defined as aortic stiffness higher than that predicted from reference values based on the participant's age and blood pressure. The association of preeclampsia with arterial hemodynamic variables was assessed with multivariable linear regression, and the association of severe preeclampsia with EVA was assessed with multivariable logistic regression, adjusted for confounders. We found that women with a history of preeclampsia had greater aortic stiffness, steady arterial load, central blood pressure, and arterial wave reflections when compared with controls. We observed a dose–response relationship, with the greatest abnormalities observed in subgroups with severe, preterm, or recurrent preeclampsia. Women with severe preeclampsia had 9.23 times greater odds of having EVA as compared with controls (95% CI, 1.67–51.06, P =0.011) and 7.87 greater odds of EVA as compared with women with nonsevere preeclampsia (95% CI, 1.29–47.77, P =0.025). Conclusions Our study comprehensively characterizes arterial hemodynamic abnormalities after preeclampsia and suggests that specific subgroups of women with a history of preeclampsia exhibit greater alterations in arterial hemodynamics related to arterial health. Our findings have important implications for understanding potential links between preeclampsia and cardiovascular events, and suggest women with severe, preterm, or recurrent preeclampsia as subgroups who may deserve intensification of efforts for prevention and early detection of cardiovascular disease.