The 2024 ESC Guidelines recommend a target systolic blood pressure of 120-129 mmHg for adults on BP-lowering medications, while highlighted research shows semaglutide reduces systolic BP by 4.95 mmHg.
For the podcast associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts. This Focus Issue on hypertension and epidemiology, prevention, and healthcare policies contains the ‘2024 ESC Guidelines for the management of elevated blood pressure and hypertension: Developed by the task force on the management of elevated blood pressure and hypertension of the European Society of Cardiology (ESC) and endorsed by the European Society of Endocrinology (ESE) and the European Stroke Organisation (ESO)’.1 This 2024 document updates the 2018 ESC/European Society of Hypertension (ESH) Guidelines on the management of arterial hypertension. While the current document builds on prior guidelines, it also incorporates important updates and new recommendations based on current evidence. A major, evidence-based change in the 2024 Guidelines is the recommendation to pursue a target systolic blood pressure (BP) of 120–129 mmHg among adults receiving BP-lowering medications. There are several important caveats to this recommendation, including: (i) the requirement that treatment to this BP target is well tolerated by the patient; (ii) the fact that more lenient BP targets can be considered in persons with symptomatic orthostatic hypotension, those aged ≥85 years, or those with moderate-to-severe frailty or limited life expectancy; and (iii) a strong emphasis on out-of-office BP measurement to confirm that the systolic BP target of 120–129 mmHg is achieved. For those selected individual cases where a target systolic BP of 120–129 mmHg is not pursued, due to either intolerance or the existence of conditions that favour a more lenient BP target, the authors recommend targeting a BP that is as low as reasonably achievable. Personalized clinical decision-making and shared decisions with the patient are also emphasized. This issue also contains the Special Article entitled ‘European Society of Cardiology: the 2023 Atlas of Cardiovascular Disease Statistics’ by Adam Timmis from the Queen Mary University London in the UK, and colleagues. This report from the European Society of Cardiology (ESC) Atlas Project updates and expands upon the 2021 report in presenting cardiovascular disease (CVD) statistics for the ESC member countries.2 This paper examines inequalities in cardiovascular healthcare and outcomes in ESC member countries utilizing mortality and risk factor data from the World Health Organization and the Global Burden of Disease study, with additional economic data from the World Bank. Cardiovascular healthcare data were collected by questionnaire circulated to the national cardiac societies of ESC member countries. Statistics pertaining to 2022, or the latest available year, are presented. New material in this report includes contemporary estimates of the economic burden of CVD and mortality statistics for a range of CVD phenotypes. Main causal factors and cardiovascular consequences of obesity. CV, cardiovascular; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; SCD, sudden cardiac death.7 The global prevalence of obesity has more than doubled over the past four decades, currently affecting more than a billion individuals.3–6 In a Special Article entitled ‘Obesity and cardiovascular disease: an ESC clinical consensus statement’, Konstantinos C. Koskinas from the University of Bern in Switzerland, and colleagues indicate that beyond its recognition as a high-risk condition that is causally linked to many chronic illnesses, obesity has been declared a disease per se that results in impaired quality of life and reduced life expectancy.7 Notably, two-thirds of obesity-related excess mortality is attributable to CVD. Despite the increasingly appreciated link between obesity and a broad range of CVD manifestations including atherosclerotic disease, heart failure, thromboembolic disease, arrhythmias, and sudden cardiac death, obesity has been under-recognized and suboptimally addressed compared with other modifiable cardiovascular risk factors (Figure 1). In the view of major repercussions of the obesity epidemic on public health, attention has focused on population-based and personalized approaches to prevent excess weight gain and maintain a healthy body weight from early childhood and throughout adult life, as well as on comprehensive weight loss interventions for persons with established obesity. This clinical consensus statement by the ESC discusses current evidence on the epidemiology and aetiology of obesity; the interplay between obesity, cardiovascular risk factors, and cardiac conditions; the clinical management of patients with cardiac disease and obesity; and weight loss strategies including lifestyle changes, interventional procedures, and antiobesity medications, with particular focus on their impact on cardiometabolic risk and cardiac outcomes. The document aims to raise awareness on obesity as a major risk factor and to provide guidance for implementing evidence-based practices for its prevention and optimal management within the context of primary and secondary CVD prevention. Emerging evidence indicates that chemical exposures in the environment are overlooked drivers of CVD.8,9 In a State of the Art Review article entitled ‘Micro-nanoplastics and cardiovascular diseases: evidence and perspectives’, Francesco Prattichizzo from the Polo Scientifico e Tecnologico in Milan, Italy, and colleagues suggest that micro- and nanoplastic (MNP) particles derived largely from the chemical or mechanical degradation of plastics might represent a novel CVD risk factor.10 Experimental data in pre-clinical models suggest that MNPs can foster oxidative stress, platelet aggregation, cell senescence, and inflammatory responses in endothelial and immune cells while promoting a range of cardiovascular and metabolic alterations that can lead to disease and premature death. In humans, MNPs derived from various plastics, including polyethylene and polyvinylchloride, have been detected in atherosclerotic plaques and other cardiovascular tissues, including pericardium epicardial adipose tissue pericardial adipose tissue myocardium and left atrial appendage. MNPs have measurable levels within thrombi, and seem to accumulate preferentially within areas of vascular lesions. Their presence within carotid plaques is associated with subsequent increased incidence of cardiovascular events. To further investigate the possible causal role of MNPs in CVD, future studies should focus on large, prospective cohorts assessing the exposure of individuals to plastic-related pollution, the possible routes of absorption, the existence of a putative safety limit, the correspondence between exposure and accumulation in tissues, the timing between accumulation and CVD development, and the pathophysiological mechanisms instigated by pertinent concentrations of MNPs. Data from such studies would allow the design of preventive, or even therapeutic, strategies. Meanwhile, existing evidence suggests that reducing plastic production and use will produce benefits for the environment and for human health. This goal could be achieved through the UN Global Plastics Treaty that is currently in negotiation. A variety of maternal heart conditions are associated with abnormal placentation and reduced foetal growth.11–16 However, their impact on offspring’s long-term cardiovascular health is poorly studied. In a Fast Track Clinical Research article entitled ‘Pre-existing maternal cardiovascular disease and the risk of offspring cardiovascular disease from infancy to early adulthood’, Muhammad Zakir Hossin from the Karolinska Institutet in Stockholm, Sweden, and colleagues aim to investigate the association between intrauterine exposure to pre-existing maternal CVD and offspring CVD occurring from infancy to early adulthood, using paternal CVD as a negative control.17 This nationwide cohort study used register data of live singletons without major malformations or congenital heart disease born between 1992 and 2019 in Sweden. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models, adjusted for essential maternal characteristics. Paternal CVD served as a negative control for assessment of unmeasured genetic and environmental confounding. Of the ∼2 600 000 offspring analysed (49% female), 1% were born to mothers with pre-existing CVD. During a median follow-up of 14 years (range 1–29 years), 17 382 offspring were diagnosed with CVD. Offspring of mothers with CVD had a 2.09 times higher adjusted HR of CVD compared with offspring of mothers without CVD. Compared with maternal CVD, paternal CVD showed an association of smaller magnitude. Increased hazards of offspring CVD were also found when stratifying maternal CVD into maternal arrhythmia (HR 2.94), vascular (HR 1.59), and structural heart diseases (HR 1.48). The authors conclude that maternal CVD is associated with an increased risk of CVD in offspring during childhood and young adulthood. Paternal comparison suggests that genetic or shared familial factors do not explain this association. Difference in systolic blood pressure (SBP) change and alterations of antihypertensive medications for semaglutide and placebo arms using individual participant data (IPD) from three randomized controlled trials examining the effect of semaglutide 2.4 mg on body weight over 68 weeks. ANCOVA, analysis of covariance; BP, blood pressure; CI, confidence interval.22 Hypertension is an important and highly prevalent risk factor.18–21 Randomized clinical trials (RCTs) assessing semaglutide reported reductions of systolic BP in trial populations with baseline BP in the normotensive range. In another Fast Track Clinical Research article entitled ‘Semaglutide and blood pressure: an individual patient data meta-analysis’, Cormac Kennedy from Trinity College Dublin in Ireland, and colleagues aimed to determine whether this systolic BP reduction is greater in hypertensive groups.22 Individual patient data (IPD) from three RCTs examining the effect of semaglutide 2.4 mg on body weight over 68 weeks were included. Trial participants were categorized according to a hypertension diagnosis, treatment or baseline measurement (HTN), baseline systolic BP >130 mmHg (HTN130), or >140 mmHg (HTN140), and those with apparent resistant hypertension (RH). The primary analysis compared the in-trial change in systolic BP in the semaglutide and placebo arms. Alterations of antihypertensive medications were quantified by treatment intensity score and compared between arms. These analyses were performed using analysis of covariance. Overall, ∼3100 participants were included. The difference in systolic BP change between the treatment groups was –4.95 mmHg overall. This difference was –4.78 mmHg for HTN, –4.93 mmHg for HTN130, –4.09 mmHg for HTN140, and –3.16 mmHg for RH. Reduction in SBP was mediated substantially by weight loss. The antihypertensive treatment intensity score decreased for those on semaglutide compared with placebo (Figure 2). The authors conclude that this IPD analysis of three large RCTs shows BP reductions with semaglutide in participants with hypertension that are similar to those seen in all trial participants. These results suggest that semaglutide is a useful adjunctive treatment for patients with hypertension and obesity. The manuscript is accompanied by an Editorial by Jordana B. Cohen from the University of Pennsylvania, PA, USA and Adam P. Bress from the University of Utah in Salt Lake City, UT, USA.23 The authors conclude that a 5 mmHg reduction in systolic BP has significant implications for population health, particularly given the high prevalence of both obesity and hypertension. Meta-analyses of RCTs consistently demonstrate that a 5 mmHg reduction in systolic BP is associated with a 10% relative decrease in the risk of major cardiovascular events. The findings of the current study suggest that BP lowering may be an important mediator of the protective target organ effects of glucagon-like peptide-1 (GLP-1) receptor agonists, which merits closer investigation. The editors hope that this issue of the European Heart Journal will be of interest to its readers. Dr. Crea reports speaker fees from Abbott, Amgen, Astra Zeneca, BMS, Chiesi, Daiichi Sankyo, enarini outside the submitted work. With thanks to Amelia Meier-Batschelet, Johanna Huggler, and Martin Meyer for help with compilation of this article.
Filippo Crea (Mon,) conducted a editorial in Hypertension, obesity, and cardiovascular disease. The 2024 ESC Guidelines recommend a target systolic blood pressure of 120-129 mmHg for adults on BP-lowering medications, while highlighted research shows semaglutide reduces systolic BP by 4.95 mmHg.