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........................................................................................................................................................ outcomes.354 Recently, the REDUCE-IT trial194 demonstrated that in statin-treated patients with high CV risk with fasting TG levels between 135499 mg/dL (1.521.63 mmol/L), high-dose icosapent ethyl, a highly purified and stable EPA (2 g) taken b.i.d., significantly reduced the risk of ischaemic events, including CV death, by about one-quarter over a median follow-up of 4.9 years. In addition, the VITAL trial showed that n-3 fatty acids at the lower dose of 1 g/day were not effective for primary prevention of CV or cancer events among healthy middle-aged men and women over 5 years of followup.333 Recommendations for the treatment of HTG are shown below.

9 Management of dyslipidaemias

in different clinical settings

9.1 Familial dyslipidaemias

Plasma lipid levels are, to a very large extent, determined by genetic factors. In its more extreme forms this is manifested as familial dyslipidaemias. A number of monogenic lipid disorders have been identified; among these, FH is the most common and is strongly related to CVD (Table 11). In general, in a patient with dyslipidaemia, the pattern of inheritance commonly does not suggest that there is a major single gene (monogenic) disorder causing the abnormality; rather, it stems from the inheritance of more than one gene variant affecting lipoprotein metabolism that, on its own, might have relatively little effect, but in combination with another or others has a greater influence on TC, TGs, or HDL-C. The pattern of inheritance is polygenic.357 It is common to find that high LDL-C, high TG, or low HDL-C levels affect several family members.

9.1.1 Familial combined hyperlipidaemia Familial combined hyperlipidaemia (FCH) is a highly prevalent mixed dyslipidaemia (1:100200) characterized by elevated levels of LDL- C, TGs, or both, and is an important cause of premature CAD. FCH is a complex disease, and the phenotype is determined by the interaction of multiple susceptibility genes and the environment. It has considerable overlap with the dyslipidaemic phenotypes of T2DM and MetS. Even within a family, the phenotype shows high inter- and intrapersonal variability based on lipid values (TGs, LDL-C, HDL-C, and ApoB). FCH has no monogenic component and is not linked to a single genetic cause, but the phenotype is high LDL-C and/or high TGs.358,359 Therefore, the diagnosis is commonly missed in clinical practice; the combination of ApoB >120 mg/dL and TGs >1.5 mmol/ L (>133 mg/dL) with a family history of premature CVD can be used to identify people who most probably have FCH.360 The concept of mixed dyslipidaemia is also valuable clinically in assessing CV risk. It emphasizes both the importance of considering family history in deciding how rigorously to treat dyslipidaemia and that elevated LDL-C levels portend a higher risk when HTG is also present. Statin treatment decreases CV risk by the same relative amount in people with HTG as in those without. Because the absolute risk is often greater in those with HTG, they may therefore benefit greatly from LDL-lowering therapy.

9.1.2 Familial hypercholesterolaemia 9.1.2.1 Heterozygous familial hypercholesterolaemia. FH is a common codominant monogenic dyslipidaemia causing premature CVD due to lifelong elevation of plasma levels of LDL-C. If left untreated, men and women with HeFH typically develop early CAD before the ages of 55 and 60 years respectively. The risk of CHD among individuals with definite or probable HeFH is estimated to be increased at least 10-fold. However, early diagnosis and appropriate treatment can dramatically reduce the risk for CAD. The prevalence of HeFH in the population is estimated to be 1/200250,361 translating to a total number of cases between 1434 million worldwide.362,363 Only a minor fraction of these cases is identified and properly treated.

Recommendations for drug treatment of patients with hypertriglyceridaemia

Recommendations Classa Levelb

Statin treatment is recommended as the first drug of choice to reduce CVD risk in high-risk individuals with hypertriglyceridaemia [TG levels >2.3 mmol/L (>200 mg/dL)].355 I B In high-risk (or above) patients with TG levels between 1.55.6 mmol/L (135499 mg/dL) despite statin treatment, n-3 PUFAs (icosapent ethyl 22 g/day) should be considered in combination with a statin.194 IIa B In primary prevention patients who are at LDL-C goal with TG levels >2.3 mmol/L (>200 mg/dL), fenofibrate or bezafibrate may be considered in combination with statins.305307,356 IIb B In high-risk patients who are at LDL-C goal with TG levels >2.3 mmol/L (>200 mg/dL), fenofibrate or bezafibrate may be considered in combination with statins.305307,356 IIb C

CVD = cardiovascular disease; LDL-C = low-density lipoprotein cholesterol; PUFA = polyunsaturated fatty acids; TG = triglyceride. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/41/1/111/5556353 by guest on 07 October 2026