This 2023 statement updates clinical guidance for homozygous familial hypercholesterolaemia (HoFH), explains the genetic complexity, and provides pragmatic recommendations to address inequities in HoFH care worldwide. Key strengths include updated criteria for the clinical diagnosis of HoFH and the recommendation to prioritize phenotypic features over genotype. Thus, a low-density lipoprotein cholesterol (LDL-C) >10 mmol/L (>400 mg/dL) is suggestive of HoFH and warrants further evaluation. The statement also provides state-of-the art discussion and guidance to clinicians for interpreting the results of genetic testing and for family planning and pregnancy. Therapeutic decisions are based on the LDL-C level. Combination LDL-C-lowering therapy—both pharmacologic intervention and lipoprotein apheresis (LA)—is foundational. Addition of novel, efficacious therapies (i.e. inhibitors of proprotein convertase subtilisin/kexin type 9, followed by evinacumab and/or lomitapide) offers potential to attain LDL-C goal or reduce the need for LA. To improve HoFH care around the world, the statement recommends the creation of national screening programmes, education to improve awareness, and management guidelines that account for the local realities of care, including access to specialist centres, treatments, and cost. This updated statement provides guidance that is crucial to early diagnosis, better care, and improved cardiovascular health for patients with HoFH worldwide.

The purpose of this review was to assess the relationship between premature ovarian insufficiency (POI), defined as natural menopause 3 years, assessment of age menopause <40 years, and incident cases of fatal or nonfatal IHD, stroke, or overall CVD. Relative risks (RRs) and 95% confidence interval (CI) were pooled using a random-effect model. Overall, 10 observational studies were identified, comprising 190,588 women (follow-up 4–37 years) with 9440 events (2026 events for IHD (seven studies) and 6438 events for stroke (seven studies) and 976 for total CVD (two studies). POI was assessed by questionnaire and incident cases through certification and event registers. POI was related to an increased risk of developing or dying from IHD (hazard ratio (HR) 1.69, 95% CI 1.29–2.21, p = 0.0001) and total CVD (HR 1.61, 95% CI 1.22–2.12, p = 0.0007). No relation was found for stroke (HR 1.03, 0.88–1.19, p = 0.74). We found no evidence for heterogeneity. POI is an independent though modest risk factor of IHD and overall CVD but not of stroke. Because of the limited impact of POI on CVD risk compared to classical cardiovascular risk factors, it is unlikely that POI will be implemented as modifier of cardiovascular risk classification.

Cardiovascular disease is the leading cause of death in women and men globally, with most due to atherosclerotic cardiovascular disease (ASCVD). Despite progress during the last 30 years, ASCVD mortality is now increasing, with the fastest relative increase in middle-aged women. Missed or delayed diagnosis and undertreatment do not fully explain this burden of disease. Sex-specific factors, such as hypertensive disorders of pregnancy, premature menopause (especially primary ovarian insufficiency), and polycystic ovary syndrome are also relevant, with good evidence that these are associated with greater cardiovascular risk. This position statement from the European Atherosclerosis Society focuses on these factors, as well as sex-specific effects on lipids, including lipoprotein(a), over the life course in women which impact ASCVD risk. Women are also disproportionately impacted (in relative terms) by diabetes, chronic kidney disease, and auto-immune inflammatory disease. All these effects are compounded by sociocultural components related to gender. This panel stresses the need to identify and treat modifiable cardiovascular risk factors earlier in women, especially for those at risk due to sex-specific conditions, to reduce the unacceptably high burden of ASCVD in women.

Hypertensive disorders of pregnancy (HDP), such as gestational hypertension and pre-eclampsia, affect up to 10% of all pregnancies. These women have on average a twofold higher risk to develop cardiovascular disease (CVD) later in life as compared with women with normotensive pregnancies. This increased risk might result from an underlying predisposition to CVD, HDP itself or a combination of both. After pregnancy women with HDP show an increased risk of classical cardiovascular risk factors including chronic hypertension, renal dysfunction, dyslipidemia, diabetes and subclinical atherosclerosis. The prevalence and onset of cardiovascular risk factors depends on the severity of the HDP and the coexistence of other pregnancy complications. At present, guidelines addressing postpartum cardiovascular risk assessment for women with HDP show a wide variation in their recommendations. This makes cardiovascular follow-up of women with a previous HDP confusing and non-coherent. Some guidelines advise to initiate cardiovascular follow-up (blood pressure, weight and lifestyle assessment) 6–8 weeks after pregnancy, whereas others recommend to start 6–12 months after pregnancy. Concurrent blood pressure monitoring, lipid and glucose assessment is recommended to be repeated annually to every 5 years until the age of 50 years when women will qualify for cardiovascular risk assessment according to all international cardiovascular prevention guidelines.