Cardiovascular prevention guidelines are based on robust evidence, yet their implementation in primary healthcare remains inconsistent due to systemic barriers, workload pressures and insufficiently adapted tools. The 2025 European consensus emphasizes the need for multidisciplinary teamwork, digital innovation and equity-focused strategies to strengthen prevention across diverse healthcare systems. Translating these recommendations into actionable, context-specific approaches is essential to close the evidence-practice gap and improve population cardiovascular outcomes.
Objectives Female sex and anticitrullinated protein antibodies (ACPA) are associated with higher disease activity in rheumatoid arthritis (RA). Since disease-related inflammation is linked to cardiovascular risk, we explored whether sex and ACPA influenced the association between disease activity at study entry and cardiovascular risk in established RA.Methods We evaluated 4008 patients with prevalent RA from an international observational cohort enrolled between 1985 and 2012. Outcomes included major adverse cardiovascular events (MACE: cardiovascular death, myocardial infarction and stroke) and ischaemic cardiovascular events (iCVE: MACE, angina, revascularisation, transient ischaemic attack and peripheral arterial disease). Follow-up accrued from enrolment until the first event or censoring. Multivariable Cox models stratified by centre risk evaluated disease activity, sex, ACPA and their interactions.Results We documented 193 MACE and 299 iCVE. Disease activity and sex were associated with MACE (all p≤0.017) and iCVE (p≤0.005) but ACPA was only associated with MACE (p=0.043). A three-way interaction on MACE (p=0.034) but not iCVE was noted. Among ACPA-negative patients, disease activity was associated with MACE in males (HR 1.57 (95% CI 1.14 to 2.16)) but not females (p-for-interaction=0.022). Among ACPA-positive patients, neither the disease activity x sex interaction (p=0.929), nor main effect of disease activity on MACE (p=0.124) was significant, but male sex was (HR 1.61 (95% CI 1.15 to 2.27)). Among females, neither disease activity x ACPA interaction (p=0.523) nor disease activity (p=0.319) was significant for MACE, but ACPA was (HR 1.57 (95% CI 1.02 to 2.42)).Conclusions The effect of disease activity at enrolment on cardiovascular risk in prevalent RA varies across patient groups with different sex and ACPA characteristics.
ObjectiveDetermine the association between antecedent pharyngitis or tonsillitis and subsequent rheumatic disease.MethodsThis population-based, case-control study identified all incident, criteria-confirmed individuals with rheumatic diseases from 2002-2014, matched to controls 3:1 on age, sex, and length of preceding electronic health record. The primary exposure was pharyngitis or tonsillitis, defined by diagnostic codes (positive predictive value 89% and 70% respectively). We calculated odds ratios (OR) with 95% confidence intervals (CI) for each disease and disease group using logistic regression models adjusting for confounders. Sensitivity analyses studied these associations by time between exposure and incident rheumatic disease (>1-5, >5-10, >10 years), number of codes (1-3, 4-6, 7+), and smoking status.ResultsWe identified 1,427 individuals with incident rheumatic disease matched to 4,281 controls (mean age 61, 67% female). Prior pharyngitis occurred in 25% of cases and 27% of controls, corresponding to decreased odds of any rheumatic disease (OR 0.86, 95% CI 0.74-1.00), rheumatoid arthritis (RA, OR 0.79, 95% CI 0.65-0.98), and lupus (unadjusted OR 0.26, 95% CI 0.11-0.62). Statistically significant lower odds of rheumatic disease were associated with acute pharyngitis, first pharyngitis exposure >10 years prior to index date, and 1-3 pharyngitis codes. Associations between pharyngitis and smoking status also followed these trends. Tonsillitis occurred in only 2% of cases and 1% of controls and was not associated with incident rheumatic disease (OR 1.26, 95% CI 0.77-2.07).ConclusionPreceding pharyngitis was associated with decreased odds of developing rheumatic disease, including lupus and RA. Future studies should replicate these results.
Despite recent advances in cardiovascular pharmacotherapy, prevention and treatment of many cardiovascular diseases remain limited with a clear need for more effective and safer pharmacological strategies. Here, we summarize the most relevant advances in cardiovascular pharmacotherapy in 2025, including the approval of four new drugs (aficamten, etripamil, lerodalcibep, and plozasiran), the label expansions for five already approved drugs, and the results of major randomized clinical trials with already approved drugs, including those that met the prespecified primary endpoints (positive trials) representing new pharmacological options for cardiovascular diseases, those with neutral or negative results, which did not confirm the primary endpoints and the withdrawal from the US market of Andexanet-alfa for safety concerns. Finally, we present the most promising experimental cardiovascular drugs currently being investigated in ongoing Phase 2 and 3 clinical trials.
Background: Rheumatoid arthritis (RA) is a chronic, inflammatory rheumatic disease with the potential to induce significant disability. Patients with RA are at increased risk of cardiovascular diseases (CVD). Smokers with RA tend to experience more pain and fatigue, higher disease activity, more erosive joint destruction, and a lower health-related quality of life (HR-QoL) than non-smokers. It remains to be determined whether these effects can be reduced by smoking cessation intervention (SCI). Objectives: The primary objective was to compare the effect of an intensive SCI, relative to treatment-as-usual, on smoking cessation and achievement of EULAR clinical response on disease activity 3 months post-intervention, in patients with RA. Methods: The randomised 'REU-stop' study was designed as a multicentre, open label, two arm, parallel group, randomised controlled trial, including 150 daily smokers with RA, being in remission or having low-to-moderate disease activity (DAS28 ≤ 5.1) [1]. The intensive SCI consisted of five individual counselling sessions (during 6 weeks) with a smoking cessation counsellor, plus free nicotine replacement therapy. Smoking cessation was self-reported and validated using exhaled carbon monoxide. Patients were followed over 58 weeks from baseline (i.e., 12 months post intervention period), with outcome assessments at 3, 6, and 12, months post intervention. The co-primary endpoints were analysed 3 months post intervention according to the intention-to-treat population, using logistic regression with missing data handled by a simplistic imputation assuming trial failure. Results: In total, 94 individuals underwent randomisation, with 49 and 45 patients allocated to smoking cessation and control, respectively. The mean age was 58.4 years (SD 9.9) and 64 (68%) were women. Baseline disease activity score of 28 joints was 2.95 (SD 1.29). At 3 months after the intervention, 9 (18%) intervention and 2 (4%) control patients achieved self-reported smoking cessation (co-primary endpoint), OR=4.84 [95%CI 0.99 to 23.76]) validated by exhaled carbon monoxide. Six (12%) intervention and 9 (20%) control patients had a EULAR clinical response (co-primary endpoint) OR=0.56 [0.18 to 1.72]) (Figure 1). Among the secondary outcomes, DAS28, number of tender joints and CRP improved more in the control group than in the cessation group, while the remaining secondary outcomes did not differ across groups (Table 1). Conclusion: In this randomised trial, intensive SCI had no significant effect on the primary co-outcomes (smoking cessation and EULAR clinical response), while three of the secondary core outcomes showed significantly higher disease activity scores compared to the control group. Trial Registration: ClinicalTrials.gov, identifier: NCT02901886. REFERENCES: [1] Roelsgaard, I. K., Thomsen, T., Østergaard, M., Christensen, R., Hetland, M. L., Jacobsen, S., Andersen, L., Tønnesen, H., Rollefstad, S., Semb, A. G., & Esbensen, B. A. (2017). The effect of an intensive smoking cessation intervention on disease activity in patients with rheumatoid arthritis: Study protocol for a randomised controlled trial. Trials, 18(1). https://doi.org/10.1186/s13063-017-2309-5. Acknowledgements: NIL. Disclosure of Interests: Bente Appel Esbensen: None declared, Thordis Thomsen: None declared, Ida Kristiane Roelsgaard: None declared, Mikkel Østergaard: None declared, Merete Lund Hetland Speaker for Pfizer, Medac, Sandoz (no personal income, institution), Research grants (institution) from Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Nordforsk, Anne Grete Semb: None declared, Hanne Tønnesen: None declared, Lena Andersen: None declared, Robin Christensen: None declared.
Objectives Rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPA) are linked to disease activity, severity and cardiovascular risk in rheumatoid arthritis (RA). Since RA-related inflammation associates with cardiovascular disease, we investigated whether RF and ACPA status influence the relationship between RA activity and event risk.Methods We assessed 3952 cardiovascular disease-free patients with prevalent RA registered in an international observational consortium between 1985 and 2012. Main outcome was a first major adverse cardiovascular event (MACE) including myocardial infarction, stroke and cardiovascular death. Follow-up accrued from enrolment until first MACE or censoring. Multivariable Cox models stratified by centre risk evaluated disease activity, RF, ACPA and their interactions.Results We recorded 184 first MACE events over 22 981 patient-years. Disease activity associated with MACE (HR 1.18 (95% CI 1.03 to 1.35)), whereas RF (HR 1.26 (0.82 to 1.94)) and ACPA (HR 1.25 (0.85 to 1.83)) did not reach statistical significance, though CIs were wide and a clinically meaningful association cannot be excluded. A three-way interaction between disease activity, RF and ACPA on MACE (p for interaction=0.044) was observed. RA activity associated with MACE in seronegative and double seropositive (p≤0.047), but not single RF-positive or ACPA-positive patients. Among RF-negative participants, RA activity was linked to MACE in ACPA-negative but not positive ones (p for interaction=0.003). Among ACPA-positive patients, disease activity was linked to MACE in RF-positive but not RF-negative ones (p for interaction=0.040).Conclusions Disease activity may better discriminate inflammation-driven cardiovascular risk in seronegative and double seropositive than single RF-positive or ACPA-positive patients. Risk protection through lowering disease activity may be serostatus dependent.
Heart failure (HF) and atrial fibrillation (AF) are major global health challenges with rising prevalence and significant morbidity, mortality, and healthcare burden. Despite advances in HF management, AF remains a critical comorbidity that worsens outcomes and requires ad hoc treatment strategies, increasing the risk of non-adherence and side effects. While rhythm control strategies in AF have gained attention for their prognostic benefits in HF, the pharmacological treatment of HF in patients with AF, including the benefit of rhythm versus rate control, remains underexplored. The relationship between HF and AF lacks sufficient evidence and targeted research to assess the optimal treatment strategies. This narrative review critically examines current HF pharmacotherapy in the context of AF, focusing on the four cornerstone treatments and modifiers of prognosis for HF with reduced ejection fraction: beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/sacubitril-valsartan, aldosterone antagonists, and sodium–glucose co-transporter 2 inhibitors. Although these therapies are well-established in HF patients, their efficacy in patients with concomitant AF requires further prospective investigation. The unique challenges posed by AF, including arrhythmia-induced remodelling and cardiomyopathy, necessitate a more individually tailored treatment. We also highlight critical knowledge gaps and the need for dedicated clinical trials specifically assessing HF therapies in AF subgroups, such as paroxysmal, long-standing persistent and permanent AF, and the benefit of heart rate and rhythm control strategies. The future of precision medicine in HF-AF management lies in bridging these evidence gaps through targeted research and interdisciplinary collaboration.
This review aims to examine the evidence on the benefits and risks of lipid-lowering drugs in patients with liver disease. Elevated liver enzyme levels often lead to cautious discontinuation of these drugs, potentially withholding from patients their benefit in reducing cardiovascular disease morbidity and mortality. Using a literature search of PubMed, we examine the efficacy and safety profiles of various lipid-lowering agents, including statins, ezetimibe, bempedoic acid, PCSK9 inhibitors, fibrates, and icosapent ethyl, focusing particularly on their potential side effects related to liver health. A major challenge in the assessment of drug-induced hepatotoxicity is the fact that it relies heavily on case reports rather than real-world evidence. There is currently a lack of robust evidence on lipid-lowering therapy in people with pre-existing liver disease. Nevertheless, we have attempted to summarize the available data for all the drugs mentioned in order to provide guidance for the treatment of patients with liver dysfunction. This review highlights the need for further research to optimize treatment strategies for patients with coexisting liver and cardiovascular disease.
BACKGROUND:The European Alliance of Associations for Rheumatology recommendations for cardiovascular risk management highlighted the importance of traditional cardiovascular risk factor control in antiphospholipid syndrome (APS). However, cardiovascular risk factor target attainment in APS and differences between primary APS and systemic lupus erythematosus (SLE)-related APS remain uncertain. METHODS:Cardiovascular risk factor data were collected from medical records of patients in 17 centres from 11 countries between Jan 1, 2015, and Jan 1, 2020 (extended to 2022 for some centres unable to complete the survey by the end of 2020 due to the COVID-19 pandemic), and analysed cross-sectionally. Included patients were 18 years or older and met the revised Sapporo APS classification criteria. Patients who also met the 2012 Systemic Lupus International Collaborating Clinics (SLICC) classification criteria for SLE were classified as having SLE-related APS. Patients with APS in association with systemic autoimmune diseases other than SLE were excluded. Cardiovascular risk was estimated using the Systematic Coronary Risk Evaluation algorithm, and cardiovascular risk factor target attainment was assessed using European Society of Cardiology guidelines. Unadjusted and adjusted mixed effects logistic regression models were fitted. People with lived experience were not involved in the study design. FINDINGS:In total, 1003 patients with APS were included (779 [78%] women and 224 [22%] men; 662 [66%] of 1000 were White), with a median age of 47·0 years (IQR 38·0-57·0) and a median disease duration of 11·0 years (5·0-18·0). 539 (54%) patients had primary APS and 464 (46%) had SLE-related APS. We found a high prevalence of cardiovascular risk factors (hypertension, 411 [41%] of 1003; hyperlipidaemia, 344 [34%] of 1003; obesity, 295 [32%] of 919; current smoking, 186 [19%] of 963) and inadequate individual (blood pressure less than 130/80 mm Hg, BMI, and lipids) and composite cardiovascular risk factor control in all patients. A higher prevalence of hypertension (234 [50%] of 464 vs 177 [33%] of 539; p<0·0001) and hyperlipidaemia (184 [40%] of 464 vs 160 [30%] of 539; p=0·0009) was observed in SLE-related APS versus primary APS, but a lower prevalence of current smoking (72 [16%] of 452 vs 114 [22%] of 511; p=0·012). Patients with primary APS had worse target attainment for smoking cessation (397 [78%] of 511 vs 380 [84%] of 452; p=0·012), blood pressure less than 130/80 mm Hg (246 [48%] of 514 vs 258 [57%] of 456; p=0·0067), and two or more cardiovascular risk factor targets (of smoking, BMI, blood pressure, LDL) than patients with SLE-related APS in the entire group, as well as worse target attainment for smoking cessation, blood pressure less than 130/80 mmHg, BMI, LDL, triglycerides, two or more and three or more targets in the high and very high cardiovascular risk subgroup. Age and arterial thrombosis history were associated with lower odds of attaining three or more or all four cardiovascular risk factor targets. INTERPRETATION:In this large real-world study, high prevalence and suboptimal cardiovascular risk factor control were observed in patients with APS, highlighting the need for increased cardiovascular risk awareness, especially in those with primary APS, whose cardiovascular risk is often overlooked. FUNDING:None.
This scientific statement explores the challenges and opportunities associated with implementing cardiovascular disease (CVD) prevention guidelines in primary healthcare across Europe. It identifies key barriers to adherence, including limited resources, diagnostic complexity, and inconsistencies in care delivery. Emphasis is placed on the use of practical tools such as risk assessment instruments, shared decision-making, and integrated information technology systems to support effective implementation. Particular focus is given to vulnerable populations, including individuals with multi-morbidity, to promote equitable access to prevention and care. As CVD remains the leading global cause of death, a proactive and structured preventive approach in primary care is essential to reduce its burden. Evidence-based interventions-including health monitoring, lifestyle counselling, and pharmacotherapy-play a central role in improving outcomes. While patients at high cardiovascular risk are a major focus, strategies for those at lower risk but without established disease are also needed. Promoting long-term adherence to healthy behaviours from early stages may significantly delay disease onset. However, many patients in Europe still fail to meet key prevention targets, such as optimal levels of cholesterol, blood pressure, and glucose control. Variability in implementation across regions, especially in lower-income countries, underscores the need for practical, user-friendly, and context-adapted guidelines. Coordinated care models involving multiple disciplines and sectors, supported by leadership and digital tools, are critical. The statement also highlights three specific areas of interest for improving CVD prevention in primary care: chronic venous disease, lipoprotein(a) management, and cardiovascular risk in patients with inflammatory rheumatic diseases.