European journal of preventive cardiology最新文献

Background: Epidemiology links noise to increased risk of metabolic diseases like diabetes and obesity. Translational studies in humans and experimental animals showed that noise causes reactive oxygen species (ROS)-mediated cardiovascular damage. The interaction between noise and diabetes, specifically potential additive adverse effects, remains to be determined.

Methods and results: C57BL/6 mice were treated with streptozotocin (i.p. injections, 50 mg/kg/d for 5d) to induce type-1 diabetes, with S961 (subcutaneous osmotic minipumps, 0.57 mg/kg/d for 7d) or fed a high-fat diet (HFD, 20 weeks) to induce type-2 diabetes. Control and diabetic mice were exposed to aircraft noise to an average sound pressure level of 72 dB(A) for 4d. While body weight was unaffected, noise reduced insulin production in all diabetes models. The oral glucose tolerance test showed only an additive aggravation by noise in the HFD model. Noise increased blood pressure and aggravated diabetes-induced aortic, mesenteric, and cerebral arterioles endothelial dysfunction. ROS formation in cerebral arterioles, the aorta, the heart, and isolated mitochondria was consistently increased by noise in all models of diabetes. Mitochondrial respiration was impaired by diabetes and noise, however without additive effects. Noise increased ROS and caused inflammation in adipose tissue in the HFD model. RNA sequencing data and alteration of gene pathway clusters also supported additive damage by noise in the setting of diabetes.

Conclusion: In all three models of diabetes, aircraft noise exacerbates oxidative stress, inflammation, and endothelial dysfunction in mice with pre-existing diabetes. Thus, noise may potentiate the already increased cardiovascular risk in diabetic patients.

Aims: The effects of obesity on Fontan hemodynamics are poorly understood. Accordingly, we assessed its impact on exercise invasive hemodynamics and exercise capacity.

Methods: Seventy-seven adults post-Fontan undergoing exercise cardiac catheterization (supine cycle protocol) were retrospectively identified using an institutional database and categorized according to the presence of obesity (body mass index [BMI] >30 kg/m2) and overweight/normal BMI (BMI≤30 kg/m2).

Results: There were 18 individuals with obesity (BMI 36.4±3 kg/m2) and 59 (BMI 24.1±3.6 kg/m2) with overweight/normal BMI. Peak oxygen consumption (VO2) on noninvasive cardiopulmonary exercise testing was lower in patients with obesity (15.6±3.5 vs 19.6±5.8 ml/kg/min, p=0.04). At rest, systemic flow (Qs) (7.0 [4.8; 8.3] vs 4.8 [3.9; 5.8] l/min, p=0.001), pulmonary artery (PA) pressure (16.3±3.5 vs 13.1±3.5 mmHg, p=0.002), and PA wedge pressure (PAWP) (11.7±4.4 vs 8.9±3.1 mmHg, p=0.01) were higher, while arterial O2 saturation was lower (89.5% [86.5; 92.3] vs 93% [90; 95]) in obesity compared to overweight/normal BMI. Similarly, patients with obesity had higher exercise PA pressure (29.7±6.5 vs 24.7±6.8 mmHg, p=0.01) and PAWP (23.0±6.5 vs 19.8±7.3 mmHg, p=0.047), but lower arterial O2 saturation (82.4±7.0% vs 89% [85; 92], p=0.003).

Conclusion: Adults post-Fontan with obesity have worse aerobic capacity, increased Qs, higher filling pressures, and decreased arterial O2 saturation compared to those with overweight/normal BMI, both at rest and during exercise, mirroring the findings observed in the obesity phenotype of heart failure with preserved ejection fraction. Whether treating obesity and its cardiometabolic sequelae in Fontan patients will improve hemodynamics and outcomes requires further study.

Aims: Incidental physical activity as part of daily living may offer feasibility advantages over traditional exercise. We examined the joint associations of incidental physical activity and sedentary behaviour with major adverse cardiovascular events (MACE) risk.

Methods: Analyses included 22,368 non-exercising adults from the UK Biobank accelerometry sub-study (Median age [IQR]: 62.9 [11.6] years; 41.8% male). Physical activity and sedentary behaviour exposures were derived using a machine learning-based intensity and posture classification schema. We assessed the tertile-based joint associations of sedentary behaviour and: a) incidental vigorous (VPA), b) incidental moderate to vigorous (MVPA), c) vigorous intermittent lifestyle physical activity (VILPA; bouts lasting up to 1 minute), and d) moderate to vigorous intermittent lifestyle physical activity (MV-ILPA; bouts lasting up to 3 minutes) with MACE risk.

Results: Over an 8.0-year median follow-up, 819 MACE events occurred. Compared to the highest physical activity and lowest sedentary time, high sedentary behaviour (>11.4 hours/day) with low incidental VPA (<2.1 minutes/day) had an HR of 1.34 (95% CI: 0.98, 1.84) and low incidental MVPA (<21.8 minutes/day) had a 1.89 HR (95% CI: 1.42, 2.52) for MACE. Sedentary behaviour was not associated with MACE at medium and high levels of VPA or VILPA. Completing 4.1 minutes/day of VPA or VILPA may offset the MACE risk associated with high sedentary behaviour. Conversely, 31-65 minutes of incidental MVPA or 26-52 minutes of MV-ILPA per day largely attenuated the associations with MACE.

Conclusion: Brief intermittent bursts of vigorous incidental physical activity may offset cardiovascular risks from high sedentary behaviour.

Aim: Chronotropic incompetence and impaired heart rate (HR) recovery are related to mortality. Guidelines lack specific reference values for HR recovery. We defined normal values and studied blunted HR response and recovery, and mortality risk.

Methods: We included 9,917 subjects (45% females) aged 18-85 years who performed a cycle exercise test. We defined normal values for peak HR, HR reserve, and HR recovery at 1 and 2 minutes (HRR1 and HRR2) based on individuals apparently healthy (N=2,242). Associations between blunted HR indices (<5th percentile) and mortality over a median follow-up of 8.6 years were analysed using Cox regression and competing risk analysis.

Results: All HR indices were age-dependent and independent predictors of all-cause and CV mortality. The 5th percentiles of HR reserve, HRR1, and HRR2 correlated weakly with existing reference values. HR recovery variables were the strongest predictors of all-cause mortality (HRR1, hazard ratio 1.70 [95% confidence interval, 1.49-1.94] and HRR2, 1.57 [1.37-1.79]), including in subjects with normal exercise capacity (HRR1, 1.96 [1.61-2.39] and HRR2, 1.76 [1.46-2.12]). Combining HR indices appeared to increase the risk of all-cause (HRR1 and HRR2, 1.96 [1.68-2.29] and peak HR and HRR1, 1.87 [1.56-2.23]) and CV mortality, although no specific combination was superior for predicting CV mortality.

Conclusions: All HR variables were age-dependent and associated with all-cause and CV mortality. Blunted HR recovery variables were the strongest predictors of all-cause mortality, even in subjects with normal exercise capacity. Combined blunted HR indices appeared to add prognostic value.

Background: Circadian heart rate (HR) fluctuations are associated with cardiovascular health. We examined their relationship with microvascular disease and long-term survival in patients with diabetes.

Methods: In this secondary analysis from the CHAMP1ON cohort of 497 adults with metabolic disease, 349 participants who had type 1 or type 2 diabetes, baseline 24h ambulatory blood pressure and HR monitoring (ABPM), and survival data over a 21-year observational follow-up were included. Clinical features, microvascular complications, and mortality rates were examined in participants with low circadian HR fluctuations (24h-HR SD below the median of 30.4) and blunted nocturnal HR dip (<10%).

Results: Low 24h-HR SD and blunted nocturnal HR dip were associated with an adverse cardiometabolic risk profile and 12-23% higher prevalence of cardiac autonomic neuropathy and nephropathy. After 6,251 person-years follow-up (21.0 [14.0-21.0] years), a total of 136 (39%) deaths occurred, of which 100 (68%) of cardiovascular cause. The low 24h-HR SD group had a higher risk for both cardiovascular (adjusted hazard ratio [aHR] 2.00, 95%CI 1.30-3.08, p=0.002) and all-cause mortality (aHR 1.61, 95%CI 1.13-2.29, p=0.009), compared with high 24h-HR SD. Similarly, patients with blunted nocturnal HR dip had a higher risk for cardiovascular (aHR 1.63, 95%CI 1.08-2.46, p=0.019) and all-cause mortality (aHR 1.69, 95%CI 1.20-2.38, p=0.003), compared with those with preserved nocturnal HR dip.

Conclusions: Impaired circadian HR fluctuations are associated with microvascular disease and long-term cardiovascular and all-cause mortality in diabetes. ABPM-derived HR measures may provide a widely available and inexpensive risk stratification tool in this high-risk population.

Aims: The Future Innovations in Novel Detection of Atrial Fibrillation (FIND-AF) longitudinal cohort study is a multi-centre prospective cohort study of patients identified at risk of atrial fibrillation (AF). The aim of the FIND-AF longitudinal cohort study is to provide multi-modal phenotypic characterisation of these patients.

Methods and results: 1955 participants identified as at risk of AF by the FIND-AF algorithm from primary care electronic health (EHR) data, aged 30 years and above and eligible for oral anticoagulation, will be be recruited between October 2023 and November 2024 to receive home-based intermittent ECG monitoring. About 500 participants without diagnosed AF will then undergo cross-sectional phenotypic characterisation including physical examination, symptoms assessment, serum blood biomarkers and echocardiography, and non-stress cardiac magnetic resonance imaging. Longitudinal information about cardio-renal-metabolic-pulmonary outcomes will be ascertained from linkages to EHR data. The study is funded by the British Heart Foundation (CC/22/250026). The study has ethical approval (North West - Greater Manchester South Research Ethics Committee reference 23/NW/0180). Findings will be announced at relevant conferences and published in peer-reviewed journals in line with the Funder's open access policy.

Conclusions: The FIND-AF multi-centre prospective longitudinal cohort study aims to (i) provide evidence for the impact of comorbidities on AF genesis (ii) uncover actionable targets to prevent AF, and (iii) act as a platform for cohort randomised clinical trials that investigate enhanced detection and prevention of AF.

Aims: Diagnosis of atrial fibrillation (AF) provides opportunities to reduce stroke risk. This study aimed to compare AF diagnosis rates, participant satisfaction and feasibility of an electrocardiogram (ECG) self-screening virtual care system with usual care.

Methods: This randomised controlled implementation study involving community-dwelling people aged ≥75 years was conducted from May 2021 to June 2023. Participants were given a handheld single-lead ECG device and trained to self-record ECGs once daily on weekdays for 12 months. The control group received usual care with their general practitioners in the first 6 months and participated in the subsequent 6 months. AF diagnosis and participant satisfaction were assessed at 6 months.

Results: 200 participants (mean age 79.0±3.4 years; 54.0% female; 72.5% urban). AF was diagnosed in 10/97 (10.3%) intervention participants and 2/100 (2.0%) in the control group (Odds Ratio 5.6, 95% CI 1.4-37.3, p=0.03). In the intervention, 80% of AF cases were diagnosed within 3 months. 91/93 (97.9%) intervention participants and 55/93 (59.1%) control-waitlisted participants (p<0.001) were satisfied with AF screening. Of the expected 20 days per month, the overall monthly median number of days participants self-recorded ECGs was 20 (interquartile range 17-22). Participants were confident using the device (93%), reported it was easy to use (98%) and found screening efficient (96%).

Conclusions: Patient-led AF self-screening using single-lead ECG devices with a remote central monitoring system was feasible, acceptable, and effective in diagnosing AF among older people. This screening model could be adapted for implementation, interfacing with integrated care models within existing health systems.