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................................................................................... Convincing evidence of the causal association between diet and ASCVD risk is, nevertheless, available indirectly from randomized ‘metabolic ward’ studies showing that high saturated fat intake causes increased LDL-C concentrations, and from cohort studies, genetic epidemiological studies, and randomized trials showing that higher LDL-C levels cause ASCVD.

The lack of concordance between studies is due both to methodological problems (particularly inadequate sample sizes or short study durations) and the difficulties of evaluating the impact of a single dietary factor independently of any other changes in the diet.130 In fact, as foods are mixtures of different nutrients and other components, it is not appropriate to attribute the health effects of a food to only one of its components. Moreover, if energy intake must be kept constant, eating less of one macronutrient implies necessarily eating more of others. The quality of the replacement (for instance, unsaturated fat vs. highly refined grains) can influence the effect observed, significantly modifying the impact on health of the nutrient replaced. These limitations suggest caution in interpreting the results of RCTs or even meta-analyses of RCTs in relation to the effect of a single dietary change on ASCVD.130 To overcome, at least in part, these problems, in recent years nutrition research has focused on the relationship between ASCVD on the one hand, and foods and dietary patterns—rather than single nutrients—on the other. Consistent evidence from epidemiological studies indicates that higher consumption of fruit, non-starchy vegetables, nuts, legumes, fish, vegetable oils, yoghurt, and wholegrains, along with a lower intake of red and processed meats, foods higher in refined carbohydrates, and salt, is associated with a lower incidence of CV events.131 Moreover, it indicates that the replacement of animal fats, including dairy fat, with vegetable sources of fats and polyunsaturated fatty acids (PUFAs) may decrease the risk of CVD.132

Dietary patterns that have been more extensively evaluated are the Dietary Approaches to Stop Hypertension (DASH) diet—particularly in relation to BP control—and the Mediterranean diet; both have proved to be effective in reducing CV risk factors and, possibly, to contribute to ASCVD prevention.133 The most relevant difference between the Mediterranean and the DASH diet is the emphasis of the former on extra-virgin olive oil. The Mediterranean diet is associated with a reduced incidence of CV and other non-communicable diseases in epidemiological studies,134,135 and has been proved in RCTs to be effective in reducing CV events in primary and secondary prevention.136 In particular, the Prevencion con Dieta Mediterranea (PREDIMED) trial indicated that participants allocated to a Mediterranean-type diet, supplemented with extra-virgin olive oil or nuts, had a significantly lower (around 30%) incidence of major CV events compared with those who were on a low-fat diet.137 In summary, despite the results of PREDIMED and a few other intervention studies with ASCVD endpoints that support a healthy lifestyle for ASCVD prevention, RCTs cannot represent the sole grounds on which dietary recommendations should rely. They also need to be based on the combination of large observational cohort studies and relatively short-term randomized trials having intermediate risk factors (such as blood lipids) as outcomes.

Table 7 Treatment targets and goals for cardiovascular disease prevention

Smoking No exposure to tobacco in any form. Diet Healthy diet low in saturated fat with a focus on wholegrain products, vegetables, fruit, and fish. Physical activity 3.57 h moderately vigorous physical activity per week or 3060 min most days. Body weight BMI 2025 kg/m2, and waist circumference <94 cm (men) and <80 cm (women). Blood pressure <140/90 mmHg.a LDL-C Very-high risk in primary or secondary prevention:

A therapeutic regimen that achieves >_50% LDL-C reduction from baselineb and an LDL-C goal of <1.4 mmol/L (<55 mg/dL). No current statin use: this is likely to require high-intensity LDL-lowering therapy. Current LDL-lowering treatment: an increased treatment intensity is required. High risk: A therapeutic regimen that achieves >_50% LDL-C reduction from baselineb and an LDL-C goal of <1.8 mmol/L (<70 mg/dL). Moderate risk: A goal of <2.6 mmol/L (<100 mg/dL). Low risk: A goal of <3.0 mmol/L (<116 mg/dL).

Non-HDL-C Non-HDL-C secondary goals are <2.2, 2.6, and 3.4 mmol/L (<85, 100, and 130 mg/dL) for very-high-, high-, and moderate-risk

people, respectively.

ApoB ApoB secondary goals are <65, 80, and 100 mg/dL for very-high-, high-, and moderate-risk people, respectively. Triglycerides No goal, but <1.7 mmol/L (<150 mg/dL) indicates lower risk and higher levels indicate a need to look for other risk factors. Diabetes HbA1c: <7% (<53 mmol/mol). Apo = apolipoprotein; BMI = body mass index; HbA1c = glycated haemoglobin; HDL-C = high-density lipoprotein cholesterol; LDL-C = low-density lipoprotein cholesterol. aLower treatment targets are recommended for most treated hypertensive patients, provided that the treatment is well tolerated.118 bThe term ‘baseline’ refers to the LDL-C level in a person not taking any lipid-lowering medication, or to the extrapolated baseline value for those who are on current treatment. Downloaded from academic.oup.com/eurheartj/article/41/1/111/5556353 by guest on 07 October 2026