Global association of air pollution and heart failure:a systematic review and meta-analysis

BACKGROUND: Acute exposure to air pollution has been linked to myocardial infarction, but its effect on heart failure is uncertain. We did a systematic review and meta-analysis to assess the association between air pollution and acute decompensated heart failure including hospitalisation and heart failure mortality. METHODS: Five databases were searched for studies investigating the association between daily increases in gaseous (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate (diameter <2·5 μm [PM(2·5)] or <10 μm [PM(10)]) air pollutants, and heart failure hospitalisations or heart failure mortality. We used a random-effects model to derive overall risk estimates per pollutant. FINDINGS: Of 1146 identified articles, 195 were reviewed in-depth with 35 satisfying inclusion criteria. Heart failure hospitalisation or death was associated with increases in carbon monoxide (3·52% per 1 part per million; 95% CI 2·52–4·54), sulphur dioxide (2·36% per 10 parts per billion; 1·35–3·38), and nitrogen dioxide (1·70% per 10 parts per billion; 1·25–2·16), but not ozone (0·46% per 10 parts per billion; −0·10 to 1·02) concentrations. Increases in particulate matter concentration were associated with heart failure hospitalisation or death (PM(2·5) 2·12% per 10 μg/m(3), 95% CI 1·42–2·82; PM(10) 1·63% per 10 μg/m(3), 95% CI 1·20–2·07). Strongest associations were seen on the day of exposure, with more persistent effects for PM(2·5). In the USA, we estimate that a mean reduction in PM(2·5) of 3·9 μg/m(3) would prevent 7978 heart failure hospitalisations and save a third of a billion US dollars a year. INTERPRETATION: Air pollution has a close temporal association with heart failure hospitalisation and heart failure mortality. Although more studies from developing nations are required, air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy. FUNDING: British Heart Foundation

Sex-differences in oral anticoagulation therapy in patients hospitalized with atrial fibrillation:a nationwide cohort study

Background Important disparities in the treatment and outcomes of women and men with atrial fibrillation (AF) are well recognized. Whether introduction of direct oral anticoagulants has reduced disparities in treatment is uncertain. Methods and Results All patients who had an incident hospitalization from 2010 to 2019 with nonvalvular AF in Scotland were included in the present cohort study. Community drug dispensing data were used to determine prescribed oral anticoagulation therapy and comorbidity status. Logistic regression modeling was used to evaluate patient factors associated with treatment with vitamin K antagonists and direct oral anticoagulants. A total of 172 989 patients (48% women [82 833 of 172 989]) had an incident hospitalization with nonvalvular AF in Scotland between 2010 and 2019. By 2019, factor Xa inhibitors accounted for 83.6% of all oral anticoagulants prescribed, while treatment with vitamin K antagonists and direct thrombin inhibitors declined to 15.9% and 0.6%, respectively. Women were less likely to be prescribed any oral anticoagulation therapy compared with men (adjusted odds ratio [aOR], 0.68 [95% CI, 0.67–0.70]). This disparity was mainly attributed to vitamin K antagonists (aOR, 0.68 [95% CI, 0.66–0.70]), while there was less disparity in the use of factor Xa inhibitors between women and men (aOR, 0.92 [95% CI, 0.90–0.95]). Conclusions Women with nonvalvular AF were significantly less likely to be prescribed vitamin K antagonists compared with men. Most patients admitted to the hospital in Scotland with incident nonvalvular AF are now treated with factor Xa inhibitors and this is associated with fewer treatment disparities between women and men

Implications of lowering threshold of plasma troponin concentration in diagnosis of myocardial infarction: cohort study

Objective To assess the relation between troponin concentration, assay precision, and clinical outcomes in patients with suspected acute coronary syndrome

Cardiac Troponin T and Troponin I in the General Population: Comparing and Contrasting Their Genetic Determinants and Associations With Outcomes

Background: There is great interest in widening the use of high sensitivity cardiac troponins for population cardiovascular disease (CVD) and heart failure screening. However, it is not clear whether cardiac troponin T (cTnT) and troponin I (cTnI) are equivalent measures of risk in this setting. We aimed to compare and contrast i) the association of cTnT and cTnI with CVD and non-CVD outcomes, and ii) their determinants in a Genome wide association study (GWAS). Methods: High-sensitivity cTnT and cTnI were measured in serum from 19,501 individuals in Generation Scotland Scottish Family Health Study. Median follow-up was 7.8 years (Q1-Q3 7.1-9.2). Associations of each troponin with a composite CVD outcome (1,177 events), CVD death (n=266), non-CVD death (n=374), and heart failure (n=216) were determined using Cox models. A genome-wide association study was conducted using a standard approach developed for the cohort. Results: Both cTnI and cTnT were strongly associated with CVD risk in unadjusted models. After adjusting for classical risk factors, the hazard ratio for a one standard deviation increase in log transformed troponin was 1.24 (95%CI 1.17-1.32) and 1.11 (1.04-1.19) for cTnI and cTnT, respectively; ratio of HRs 1.12 (1.04-1.21). cTnI, but not cTnT, was associated with MI and CHD. Both cTnI and cTnT had strong associations with CVD death and heart failure. By contrast, cTnT, but not cTnI, was associated with non-CVD death; ratio of HRs 0.77 (0.67-0.88). We identified five loci (53 individual SNPs) that had GWAS significant associations with cTnI, and a different set of four loci (4 SNPs) for cTnT. Conclusions: The upstream genetic causes of low grade elevations in cTnI and cTnT appear distinct, and their associations with outcomes also differ. Elevations in cTnI are more strongly associated with some CVD outcomes, whereas cTnT is more strongly associated with the risk of non-CVD death. These findings help inform selection of an optimal troponin assay for future clinical care and research in this setting

Prevalence, determinants, and clinical associations of high-sensitivity cardiac troponin in patients attending emergency departments

Background: High-sensitivity cardiac troponin assays may improve the diagnosis of myocardial infarction but increase the detection of elevated cardiac troponin in patients without acute coronary syndrome. Methods: In a prospective cohort study, we evaluated the prevalence, determinants, and outcome of patients with elevated cardiac troponin attending the emergency department without suspected acute coronary syndrome. We measured high-sensitivity cardiac troponin in 918 consecutive patients attending the emergency department without suspected acute coronary syndrome who had blood sampling performed by the attending clinician. Elevated high-sensitivity cardiac troponin I was defined as concentrations above the sex-specific 99th percentile threshold. Clinical demographics, physiological measures, and all-cause mortality at 1 year associated with elevated high-sensitivity cardiac troponin concentrations were recorded. Results: Elevated cardiac troponin concentration occurred in 114 (12.4%) patients, of whom 2 (0.2%), 3 (0.3%), and 109 (11.9%) were adjudicated as type 1 myocardial infarction, type 2 myocardial infarction, and myocardial injury, respectively. Elevated troponin concentrations were associated with increasing age, worsening renal function, multimorbidity, and adverse physiology. Across a total of 912 patient-years follow-up, cardiac troponin concentration was a strong predictor of death (hazard ratio [HR] 1.26 per 2-fold increase, 95% confidence interval [CI] 1.06 to 1.49) independent of age, sex, multimorbidity, and adverse physiology. Conclusions: High-sensitivity cardiac troponin concentrations were elevated in 1 in 8 consecutive patients without suspected acute coronary syndrome attending the emergency department and were associated with increasing age, multimorbidity, adverse physiology, and death. Elevated cardiac troponin in unselected patients predominantly reflects myocardial injury rather than myocardial infarction