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..................................... of family history applied and that conventional ASCVD risk factors largely explain the impact of family history.

A family history of premature CVD is simple, inexpensive information that can trigger comprehensive risk assessment in individuals with a family history of premature CVD.136

3.3.6. Genetics The aetiology of ASCVD has a genetic component, but this information is not currently used in preventive approaches.142 Advances on polygenic risk scores for risk stratification could increase the use of genetics in prevention.143145 For ASCVD, there is, however, a lack of consensus regarding which genes and corresponding single nucleotide polymorphisms should be included, and whether to use risk factor-specific or outcome-specific polygenic risk scores.146 Polygenic risk scoring has shown some potential to improve ASCVD risk prediction for primary prevention,147149 but the incremental prediction accuracy is relatively modest and needs further evaluation in both men and women.150,151 Additional evidence is also needed to evaluate the clinical utility of polygenic risk scores in other clinical settings, such as in patients with pre-existing ASCVD.152

3.3.7. Socioeconomic determinants Low socioeconomic status and work stress are independently associated with ASCVD development and prognosis in both sexes.153,154 The strongest association has been found between low income and CVD mortality, with a RR of 1.76 [95% confidence interval (CI) 1.452.14].155 Work stress is determined by job strain (i.e. the combination of high demands and low control at work) and effort-reward imbalance. There is preliminary evidence that the detrimental impact of work stress on ASCVD health is independent of conventional risk factors and their treatment.156

3.3.8. Environmental exposure Environmental exposures with CVD risk modifying potential include air and soil pollution as well as above-threshold noise levels. Evaluating individual cumulative exposure to pollutants and noise remains challenging, but when available, might impact on individual risk assessment. Components of outdoor air pollution include airborne particulate matter [PM; ranging in size from coarse particles 2.510 mm in diameter, to fine (<2.5 mm; PM2.5), and ultrafine (<0.1 mm)] and gaseous pollutants (e.g. ozone, nitrogen dioxide, volatile organic compounds, carbon monoxide, sulphur dioxide), produced primarily by combustion of fossil fuels. Soil and water pollutions are also CVD risk modifiers; increased exposure to lead, arsenic, and cadmium is associated with multiple CVD outcomes including hypertension, coronary heart disease (CHD), stroke, and CVD mortality.157 Ambient PM pollution recently ranked as a leading modifiable mortality risk factor and also responsible for attributable disability adjusted life-years at the global level.158 A recent model estimated that loss of life expectancy due to ambient air pollution is similar to, if not exceeding, that due to tobacco smoking, and accounts for a global excess mortality estimated at 8.8 million/year.159 The short-term attributable effects on mortality are linked primarily to exposure to PM, nitrogen dioxide, and ozone, with an average 1.0% increase of all-cause mortality for an increment of 10 lg/m3 in exposure to PM2.5; the long-term effects are associated mainly with PM2.5. The evidence linking exposure to PM and CVD events is based on large-scale epidemiological studies and experimental studies. Associations with ASCVD mortality vary, but the majority of cohort studies link long-term air pollution with an increased risk of fatal or non-fatal CAD, and with subclinical atherosclerosis. Evidence suggests that reduction of PM2.5 is associated with improvements in inflammation, thrombosis, and oxidative stress, and a decrease in death from ischaemic heart disease.38,160,161 As sufficiently precise individual exposure estimates are hard to obtain, formal risk reclassification is difficult to quantify at present.

3.3.9. Biomarkers in blood or urine Many biomarkers have been suggested to improve risk stratification. Some may be causal [e.g. lipoprotein(a), reflecting a pathogenic lipid fraction], whereas others may reflect underlying mechanisms (e.g. Creactive protein reflecting inflammation) or indicate early cardiac damage (e.g. natriuretic peptides or high-sensitivity cardiac troponin). In the 2016 Guidelines,2 we recommended against the routine use of biomarkers because most do not improve risk prediction, and publication bias seriously distorts the evidence.106,162 New studies confirm that C-reactive protein has limited additional value.103 There is renewed interest in lipoprotein(a), but it too provides limited additional value in terms of reclassification potential.163,164 Cardiac biomarkers are promising,165,166 but further work is needed.

3.3.10. Body composition Worldwide, BMI has increased substantially in recent decades, in children, adolescents, and adults.43 In observational studies, all-cause mortality is minimal at a BMI of 20 - 25 kg/m2, with a J- or U-shaped relation in current smokers.45,46 Mendelian randomization analyses suggest a linear relation between BMI and mortality in never-smokers and a J-shaped relation in ever-smokers.44 A meta-analysis concluded that both BMI and waist circumference are similarly strongly and continuously associated with ASCVD in the elderly and the young and in men and women.47 Among those with established ASCVD, the evidence is contradictory. Systematic reviews of patients with ACS or HF have suggested an ‘obesity paradox’ whereby obesity appears protective.167,168 169 However, this evidence should be interpreted with caution as reverse causality and other biases may be operating.45

Recommendations for cardiovascular disease risk related to air pollution

Recommendations Classa Levelb

Patients at (very) high risk for CVD may be encouraged to try to avoid long-term exposure to regions with high air pollution. IIb C In regions where people have long-term exposure to high levels of air pollution, (opportunistic) CVD risk screening programmes may be considered. IIb C

CVD = cardiovascular disease. aClass of recommendation. bLevel of evidence.

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