Search

Background Coronary atherosclerosis detected by imaging is a marker of elevated cardiovascular risk. However, imaging involves large resources and exposure to radiation. The aim was, therefore, to test whether nonimaging data, specifically data that can be self‐reported, could be used to identify individuals with moderate to severe coronary atherosclerosis. Methods and Results We used data from the population‐based SCAPIS (Swedish CardioPulmonary BioImage Study) in individuals with coronary computed tomography angiography (n=25 182) and coronary artery calcification score (n=28 701), aged 50 to 64 years without previous ischemic heart disease. We developed a risk prediction tool using variables that could be assessed from home (self‐report tool). For comparison, we also developed a tool using variables from laboratory tests, physical examinations, and self‐report (clinical tool) and evaluated both models using receiver operating characteristic curve analysis, external validation, and benchmarked against factors in the pooled cohort equation. The self‐report tool (n=14 variables) and the clinical tool (n=23 variables) showed high‐to‐excellent discriminative ability to identify a segment involvement score ≥4 (area under the curve 0.79 and 0.80, respectively) and significantly better than the pooled cohort equation (area under the curve 0.76, P

Abstract Background Factors associated with severe COVID-19 and death among young adults are not fully understood, including differences between the sexes. The aim of this study was to identify factors associated with severe COVID-19 requiring intensive care and 90-day mortality among women and men below 50 years of age. Methods A register-based study using data from mandatory national registers, where patients with severe COVID-19 admitted to the ICU with need for mechanical ventilation (cases) between March 2020 and June 2021 were matched regarding age, sex, and district of residence with 10 population-based controls. Both the study population and the controls were divided into groups based on age (

Abstract Objective Emergency department length of stay (EDLOS) is linked to crowding and patient outcomes whereas worse prognosis in low socioeconomic status remains poorly understood. We studied whether income was associated with ED process times among patients with chest pain. Methods This was a registry‐based cohort study on 124,980 patients arriving at 14 Swedish EDs between 2015 and 2019 with chest pain as their chief complaint. Individual‐level sociodemographic and clinical data were linked from multiple national registries. The associations between disposable income quintiles, whether the time to physician assessment exceeded triage priority recommendations as well as EDLOS were evaluated using crude and multivariable regression models adjusted for age, gender, sociodemographic variables, and ED‐management circumstances. Results Patients with the lowest income were more likely to be assessed by physician later than triage recommendations (crude odds ratio [OR] 1.25 (95% confidence interval [CI] 1.20–1.29) and have an EDLOS exceeding 6 h (crude OR 1.22 (95% CI 1.17–1.27). Among patients subsequently diagnosed with major adverse cardiac events, patients with the lowest income were more likely to be assessed by a physician later than triage recommendations, crude OR 1.19 (95% CI 1.02–1.40). In the fully adjusted model, the average EDLOS was 13 min (5.6%) longer among patients in the lowest income quintile, 4:11 [h:min], (95% CI 4:08–4:13), compared to patients in the highest income quintile, 3:58 (95% CI 3:56–4:00). Conclusions Among ED chest pain patients, low income was associated with longer time to physician than recommended by triage and longer EDLOS. Longer process times may have a negative impact due to crowding in the ED and delay diagnosis and timely treatment of the individual patient.

Abstract To determine whether immigrant background and socioeconomic status were associated with increased risk to develop severe Coronavirus disease 2019 (COVID-19) requiring mechanical ventilation at the intensive care unit and to study their effects on 90-day mortality. Nationwide case–control study with personal-level data from the Swedish Intensive Care register linked with socioeconomic data from Statistics Sweden and comorbidity data from the national patient register. For each case of COVID-19 treated with mechanical ventilation at the intensive care unit (outcome), 10 population controls were matched for age, sex and area of residence. Logistic and Cox regression were used to study the association between the exposure (immigrant background, income and educational level) and 90-day mortality. In total, 4 921 cases and 49 210 controls were matched. In the adjusted model, the risk of severe COVID-19 was highest in individuals born in Asia (Odds ratio [OR] = 2.44, 95% confidence interval [CI] = 2.20–2.69), South America (OR = 2.34, 95% CI = 1.82–2.98) and Africa (OR = 2.11, 95% CI = 1.76–2.50). Post-secondary education was associated with a lower risk of severe COVID-19 (OR = 0.75, CI = 0.69–0.82) as was the highest (vs. lowest) income quintile (OR = 0.87, CI = 0.77–0.97). In the fully adjusted Cox-regression analysis birth region of Africa (OR 1.38, CI = 1.03–1.86) and high income (OR 0.75, CI 0.63–0.89) were associated with 90-day mortality. Immigrant background, educational level and income were independently associated with acquiring severe COVID-19 with need for mechanical ventilation.

Abstract Aims The HERMES (HEart failure Molecular Epidemiology for Therapeutic targetS) consortium aims to identify the genomic and molecular basis of heart failure. Methods and results The consortium currently includes 51 studies from 11 countries, including 68 157 heart failure cases and 949 888 controls, with data on heart failure events and prognosis. All studies collected biological samples and performed genome‐wide genotyping of common genetic variants. The enrolment of subjects into participating studies ranged from 1948 to the present day, and the median follow‐up following heart failure diagnosis ranged from 2 to 116 months. Forty‐nine of 51 individual studies enrolled participants of both sexes; in these studies, participants with heart failure were predominantly male (34–90%). The mean age at diagnosis or ascertainment across all studies ranged from 54 to 84 years. Based on the aggregate sample, we estimated 80% power to genetic variant associations with risk of heart failure with an odds ratio of ≥1.10 for common variants (allele frequency ≥ 0.05) and ≥1.20 for low‐frequency variants (allele frequency 0.01–0.05) at P

Heart failure is a complex syndrome that is associated with many different underlying risk factors. Here, to increase power, the authors jointly analyse cases of heart failure of different aetiologies in a genome-wide association study and identify 11 loci of which ten had not been previously reported.

Background Family history of atherosclerotic cardiovascular disease (ASCVD) is easily accessible and captures genetic cardiovascular risk, but its prognostic value in secondary prevention is unknown. Methods and Results We followed 25 615 patients registered in SWEDEHEART (Swedish Web‐System for Enhancement and Development of Evidence‐Based Care in Heart Disease Evaluated According to Recommended Therapies) from their 1‐year revisit after a first‐time myocardial infarction during 2005 to 2013, until December 31, 2018. Data on relatives, diagnoses and socioeconomics were extracted from national registers. The association between family history and recurrent ASCVD was studied with Cox proportional‐hazard regression, adjusting for risk factors and socioeconomics. A family history of ASCVD was defined as hospitalization due to myocardial infarction, angina with coronary revascularization, stroke, or cardiovascular death in ≥1 parent or full sibling, with early‐onset defined as disease‐onset before 55 years in men and 65 in women. The additional discriminatory value of family history to Thrombolysis in Myocardial Infarction Risk Score for Secondary Prevention was assessed with Harrell’s C‐index difference and reclassification was studied with continuous net reclassification improvement. Family history of early‐onset ASCVD in ≥1 first‐degree relative was present in 2.3% and was associated with recurrent ASCVD (hazard ratio [HR] 1.31; 95% CI, 1.17–1.47), fully adjusted for risk factors (HR, 1.22; 95% CI, 1.05–1.42). Early‐onset family history improved the discriminatory ability of the Thrombolysis in Myocardial Infarction Risk Score for Secondary Prevention, with Harrell’s C improving 0.003 points (95% CI, 0.001–0.005) from initial 0.587 (95% CI, 0.576–0.595) and improved reclassification (continuous net reclassification improvement 2.1%, P

Abstract Aims We aimed to investigate whether metabolomic profiling of blood can lead to novel insights into heart failure pathogenesis or improved risk prediction. Methods and results Mass spectrometry‐based metabolomic profiling was performed in plasma or serum samples from three community‐based cohorts without heart failure at baseline (total n = 3924; 341 incident heart failure events; median follow‐up ranging from 4.6 to 13.9 years). Cox proportional hazard models were applied to assess the association of each of the 206 identified metabolites with incident heart failure in the discovery cohorts Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) (n = 920) and Uppsala Longitudinal Study of Adult Men (ULSAM) (n = 1121). Replication was undertaken in the independent cohort TwinGene (n = 1797). We also assessed whether metabolites could improve the prediction of heart failure beyond established risk factors (age, sex, body mass index, low‐density and high‐density lipoprotein cholesterol, triglycerides, lipid medication, diabetes, systolic and diastolic blood pressure, blood pressure medication, glomerular filtration rate, smoking status, and myocardial infarction prior to or during follow‐up). Higher circulating urobilin and lower sphingomyelin (30:1) were associated with incident heart failure in age‐adjusted and sex‐adjusted models in the discovery and replication sample. The hazard ratio for urobilin in the replication cohort was estimated to 1.29 per standard deviation unit, 95% confidence interval (CI 1.03–1.63), and for sphingomyelin (30:1) to 0.72 (95% CI 0.58–0.89). Results remained similar after further adjustment for established heart failure risk factors in meta‐analyses of all three cohorts. Urobilin concentrations were inversely associated with left ventricular ejection fraction at baseline in the PIVUS cohort (β = −0.70, 95% CI −1.03 to −0.38). No major improvement in risk prediction was observed when adding the top 2 metabolites (C‐index 0.787, 95% CI 0.752–0.823) or nine Lasso‐selected metabolites (0.790, 95% CI 0.754–0.826) to a modified Atherosclerosis Risk in Communities heart failure risk score model (0.780, 95% CI 0.745–0.816). Conclusions Our metabolomic profiling of three community‐based cohorts study identified associations of circulating levels of the haem breakdown product urobilin, and sphingomyelin (30:1), a cell membrane component involved in signal transduction and apoptosis, with incident heart failure.

Background: Office blood pressure (OBP) is used for diagnosing and treating hypertension but ambulatory blood pressure measurement (ABPM) associates more accurately with patient outcome. BP control is important in secondary prevention but it is unknown whether the use of APBM improves BP-control in this setting. Our objective was to investigate whether physician awareness of ABP after percutaneous coronary intervention (PCI) improved BP-control. Methods: A total of 200 patients performed ABPM before and after their PCI follow-up visit. Patients were randomized to open (O) or concealed (C) ABPM results for the physician at the follow-up visit. The change in ABP and antihypertensive medication in relation to baseline ABP was compared between the two groups. Results: The average OBP (O and C: 128/76 mmHg) and ABP (O: 123/73 mmHg, C: 127/74 mmHg) was well controlled and did not change between the first and second measurement. A slight increase in systolic ABP during night time was observed in the open arm compared to the concealed arm. Among patients with high ABP (>130/80 mm Hg) at baseline more patients in the C compared to O group remained with a high ABP at the end of study 34/44 (77%) vs 19/34 (56%), p = 0.045. There was a positive correlation between baseline systolic ABP and ABP change in both the O (r = 0.41, p

Aims The risks associated with diabetes, obesity and hypertension for severe COVID-19 may be confounded and differ by sociodemographic background. We assessed the risks associated with cardiometabolic factors for severe COVID-19 when accounting for socioeconomic factors and in subgroups by age, sex and region of birth.Methods and results In this nationwide case–control study, 1.086 patients admitted to intensive care with COVID-19 requiring mechanical ventilation (cases), and 10.860 population-based controls matched for age, sex and district of residency were included from mandatory national registries. ORs with 95% CIs for associations between severe COVID-19 and exposures with adjustment for confounders were estimated using logistic regression. The median age was 62 years (IQR 52–70), and 3003 (24.9%) were women. Type 2 diabetes (OR, 2.3 (95% CI 1.9 to 2.7)), hypertension (OR, 1.7 (95% CI 1.5 to 2.0)), obesity (OR, 3.1 (95% CI 2.4 to 4.0)) and chronic kidney disease (OR, 2.5 (95% CI 1.7 to 3.7)) were all associated with severe COVID-19. In the younger subgroup (below 57 years), ORs were significantly higher for all cardiometabolic risk factors. The risk associated with type 2 diabetes was higher in women (p=0.001) and in patients with a region of birth outside European Union(EU) (p=0.004).Conclusion Diabetes, obesity and hypertension were all independently associated with severe COVID-19 with stronger associations in the younger population. Type 2 diabetes implied a greater risk among women and in non-EU immigrants. These findings, originating from high-quality Swedish registries, may be important to direct preventive measures such as vaccination to susceptible patient groups.Trial registration number Clinicaltrial.gov (NCT04426084).

Background Patients with rheumatoid arthritis (RA) are, on average, at increased risk of acute coronary syndrome (ACS) compared to the general population, but it remains unknown whether RA remains an ACS risk factor also in settings where the ACS risk is already high elevated, such as among individuals presenting to the emergency department (ED) with chest pain.Methods and results We included 49 283 individuals (514 (1.0%) had RA) presenting with chest pain at the four hospital EDs in Stockholm, Sweden, 2013–2016 in a cohort study. Information on exposure (RA), outcome (ACS) and comorbidities was provided through national registers. The association between RA and ACS was assessed, overall and by levels of high-sensitivity cardiac troponin T (hs-cTnT) and number of ACS risk factors, using logistic regression models adjusted for age, sex, hospital, calendar year and cardiovascular risk factors. ACS was more common in patients with (8.2%) than without (4.6%) RA, adjusted OR =1.4, 95% CI 1.0 to 2.0. This association was particularly strong in individuals with initial hs-cTnT levels between 5 and 14 ng/L, or no additional ACS risk factors (adjusted ORs above 2), but no longer detectable in those with hs-cTnT >14 ng/L or with three or more additional ACS risk factors.Conclusion RA is a risk factor for ACS also among patients at the ED with chest pain. This association is not explained by traditional ACS risk factors, and most pronounced in patients with normal hs-cTnT and few other ACS risk factors, prompting particular ACS vigilance in this RA patient group.

BackgroundThe variation and covariation for many cardiometabolic traits have been decomposed into genetic and environmental fractions, by using twin or single‐nucleotide polymorphism (SNP) models. However, differences in population, age, sex, and other factors hamper the comparison between twin‐ and SNP‐based estimates. Methods and ResultsTwenty‐four cardiometabolic traits and 700,000 genotyped SNPs were available in the study base of 10 682 twins from TwinGene cohort. For the 27 highly correlated pairs (absolute phenotypic correlation coefficient ≥0.40), twin‐based bivariate structural equation models were performed in 3870 complete twin pairs, and SNP‐based bivariate genomic relatedness matrix restricted maximum likelihood methods were performed in 5779 unrelated individuals. In twin models, the model including additive genetic variance and unique/nonshared environmental variance was the best‐fitted model for 7 pairs (5 of them were between blood pressure traits); the model including additive genetic variance, common/shared environmental variance, and unique/nonshared environmental variance components was best fitted for 4 pairs, but estimates of shared environment were close to zero; and the model including additive genetic variance, dominant genetic variance, and unique/nonshared environmental variance was best fitted for 16 pairs, in which significant dominant genetic effects were identified for 13 pairs (including all 9 obesity‐related pairs). However, SNP models did not identify significant estimates of dominant genetic effects for any pairs. In the paired t test, twin‐ and SNP‐based estimates of additive genetic correlation were not significantly different (both were 0.67 on average), whereas the nonshared environmental correlations from these 2 models differed slightly from each other (on average, twin‐based estimate=0.64 and SNP‐based estimate=0.68). ConclusionsBeside additive genetic effects and nonshared environment, nonadditive genetic effects (dominance) also contribute to the covariation between certain cardiometabolic traits (especially for obesity‐related pairs); contributions from the shared environment seem to be weak for their covariation in TwinGene samples.

BackgroundCystatin C is associated with both renal function and atherosclerotic cardiovascular disease (ASCVD). We have previously shown a genetic correlation between cystatin C and prevalent ASCVD. The objective of this article is to study whether variation in cystatin C or creatinine predicts incident ASCVD when controlled for genetic factors. Methods and ResultsThe predictive value of cystatin C and creatinine for incident ASCVD was studied in 11 402 Swedish twins, free of CVD at baseline, in an adjusted Cox‐regression model during a median follow‐up of 71 months. Twin pairs discordant for incident stroke, myocardial infarction and ASCVD during follow‐up were identified and within‐pair comparisons regarding cystatin C and creatinine levels were performed. We also investigated whether contact frequency and degree of shared environment influences were associated with similarity in cystatin C levels. In univariate analysis, cystatin C predicted incident ASCVD hazard ratio 1.57, 95% CI 1.47–1.67. When adjusted for traditional Framingham risk factors as covariates, cystatin C remained a predictor of incident stroke hazard ratio 1.45, 95% CI (1.25–1.70), ASCVD hazard ratio 1.26, 95% CI (1.13–1.41), and myocardial infarction hazard ratio 1.16, 95% CI (1.01–1.33). In twins discordant for incident stroke, cystatin C at baseline was higher in the twin who experienced a stroke compared to the healthy co‐twin (1.11±0.3 mg/L versus 1.06±0.3 mg/L), whereas creatinine was lower in the twin who developed CVD compared to their healthy co‐twins (76.1±16.9 μmol/L versus 79.4±20.3 μmol/L). ConclusionsVariation in cystatin C relates to incident ASCVD and to stroke when adjusted for genetic confounding. In identical twins, cystatin C may be a sensitive marker of early hypertensive end‐organ damage and small‐vessel disease, whereas creatinine level may reflect nutritional status. The findings in disease‐discordant monozygotic twins indicate that unique, possibly preventable, environmental factors are important.

In-depth interviews were conducted with the life skills coordinators of 9 of 21 institutions identified as being “dedicated” to service (Andrassy & Bruening, 2011). As a result of service being one portion of CHAMPS/Life Skills programming, we expanded our investigation to include all aspects of this student development program. In particular, we focused our inquiry on organizational capacity and its role in student involvement. Findings indicate these ‘dedicated’ athletic departments were characterized by strong organizational capacity for engaging student-athletes in meaningful service efforts. The critical role of coaches and mutual values among internal stakeholders emerged as the primary strengths of department’s human resources capacity. Despite the limited financial capacity, departments were able to creatively secure some funding for development programs. The ability to leverage external relationships, an organizational culture promoting participative decision-making and student-athlete development, and on-going efforts to improve service and life skills opportunities for student-athletes indicated strong structural capacity.