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......................................................................................................................................................................... Another important risk factor is adiposity, which increases CVD risk via both major conventional risk factors and other mechanisms. In addition to these, there are many other relevant risk factors, modifiers, and clinical conditions, which are addressed under risk modifiers and clinical conditions (sections 3.3 and 3.4). 3.2.1.1 Cholesterol The causal role of LDL-C, and other apo-B-containing lipoproteins, in the development of ASCVD is demonstrated beyond any doubt by genetic, observational, and interventional studies.20 The key attributes of LDL-C as a risk factor for ASCVD are: • Prolonged lower LDL-C is associated with lower risk of ASCVD throughout the range studied, and the results of randomized controlled trials (RCTs) indicate that lowering LDL-C safely reduces CVD risk even at low LDL-C levels [e.g. LDL-C <1.4 mmol/L (55 mg/dL)].20 • The relative reduction in CVD risk is proportional to the absolute size of the change in LDL-C, irrespective of the drug(s) used to achieve such change.21 • The absolute benefit of lowering LDL-C depends on the absolute risk of ASCVD and the absolute reduction in LDL-C, so even a small absolute reduction in LDL-C may be beneficial in a high- or very-high-risk patient.22 • Non-high-density lipoprotein cholesterol (HDL-C) encompasses all atherogenic (apo-B-containing) lipoproteins, and is calculated as: total cholesterol HDL-C = non-HDL-C. The relationship between non-HDL-C and CV risk is at least as strong as the relationship with LDL-C. Non-HDL-C levels contain, in essence, the same information as a measurement of apo- B plasma concentration.23,24 Non-HDL-C is used as an input in the Systemic Coronary Risk Estimation 2 (SCORE2) and SCORE2-Older Persons (SCORE2-OP) risk algorithms. HDL-C is inversely associated with CVD risk. Very high HDL-C levels may signal an increased CVD risk. There is, however, no evidence from Mendelian randomization studies, or randomized trials of cholesteryl ester transfer protein inhibitors, that raising plasma HDL-C reduces CVD risk.2528 HDL-C is nonetheless a useful biomarker to refine risk estimation using the SCORE2 algorithms. The SCORE2 algorithm cannot be used for patients with a genetic lipid disorder, such as familial hypercholesterolaemia (FH). Specific LDL-C thresholds and targets are recommended irrespective of estimated CV risk for patients with FH or other rare/genetic lipid disorders. 3.2.1.2 Blood pressure Longitudinal studies, genetic epidemiological studies, and RCTs have shown that raised BP is a major cause of both ASCVD and nonatherosclerotic CVD [particularly heart failure (HF)], accounting for 9.4 million deaths and 7% of global disability adjusted life-years.29 Elevated BP is a risk factor for the development of coronary artery disease (CAD), HF, cerebrovascular disease, lower extremity arterial disease (LEAD), chronic kidney disease (CKD), and atrial fibrillation (AF). The risk of death from either CAD or stroke increases linearly from BP levels as low as 90 mmHg systolic and 75 mmHg diastolic upwards.30,31 The absolute benefit of reducing systolic BP (SBP) depends on absolute risk and the absolute reduction in SBP, except that lower limits of SBP are imposed by tolerability and safety considerations. Management is determined by the category of hypertension (optimal, normal, high-normal, stages 1 to 3, and isolated systolic hypertension), defined according to seated office BP, ambulatory BP monitoring (ABPM), or home BP average values (see section 4.7). Evidence suggests that lifetime BP evolution differs in women compared to men, potentially resulting in an increased CVD risk at lower BP thresholds.3234 The SCORE2 algorithm cannot be used for patients with secondary causes and rarer forms of hypertension, such as primary hyperaldosteronism. 3.2.1.3 Cigarette smoking Cigarette smoking is responsible for 50% of all avoidable deaths in smokers, with half of these due to ASCVD. A lifetime smoker has a 50% probability of dying due to smoking, and on average will lose 10 years of life.35 The CVD risk in smokers <50 years of age is five-fold higher than in non-smokers.36 Prolonged smoking is more hazardous for women than for men.37 Worldwide, after high SBP, smoking is the leading risk factor for disability adjusted life-years.38 Second-hand smoke is associated with an increase in CVD risk.39 Some smokeless tobacco is also associated with increased risk of CVD.40 Recommendations for CVD risk assessment Recommendations Classa Levelb Systematic global CVD risk assessment is recommended in individuals with any major vascular risk factor (i.e. family history of premature CVD, FH, CVD risk factors such as smoking, arterial hypertension, DM, raised lipid level, obesity, or comorbidities increasing CVD risk). I C Systematic or opportunistic CV risk assessment in the general population in men >40 years of age and in women >50 years of age or postmenopausal with no known ASCVD risk factors may be considered.9 IIb C In those individuals who have undergone CVD risk assessment in the context of opportunistic screening, a repetition of screening after 5 years (or sooner if risk was close to treatment thresholds) may be considered. IIb C Opportunistic screening of BP in adults at risk for the development of hypertension, such as those who are overweight or with a known family history of hypertension, should be considered.19 IIa B Systematic CVD risk assessment in men <40 years of age and women <50 years of age with no known CV risk factors is not recommended.9 III C ASCVD = atherosclerotic cardiovascular disease; BP = blood pressure; CV = cardiovascular; CVD = cardiovascular disease; DM = diabetes mellitus; FH = familial hypercholesterolaemia. aClass of recommendation. bLevel of evidence. 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