We review all the phase II and III studies carried out with bempedoic acid at the dose of 180mg, alone or in combination with different lipid-lowering drugs and in different subgroups of patients that unequivocally show the efficacy and safety of the drug. We point out some of the potential advantages of its use in clinical practice in patients with statin intolerance and the efficacy in reducing LDL-c when combined with statins, and with statins and ezetimibe, as well as in reducing inflammation markers pending the results of the CV Clear Outcomes trial that will end in 2022.Bempedoic acid acts by inhibiting adenosine triphosphate-citrate lyase (ACL) and consequently cholesterol biosynthesis, leading to increased expression of LDL receptors and increasing low-density lipoproteins (LDL-C) plasma clearence. It is a prodrug for oral administration with intracellular activation. It is activatedin liver cells and to a lesser extent in kidney cells, being absent in adipose tissue and muscle cells. Therefore, unlike statins, its potential myotoxic effect is very limited. It has recently been approved as a lipid-lowering drug in combination with diet, with statins, or with other lipid-lowering drugs in patients with hypercholesterolaemia, mixed dyslipidaemia, statin intolerance, or when these are contraindicated. The marketing of bempedoic acid implies, in clinical practice, having a new family of lipid-lowering drugs.The use of low-density lipoprotein cholesterol (LDLc)-lowering medications has led to a significant reduction of cardiovascular risk in both primary and secondary prevention. Statins represent the cornerstone of lipid-lowering treatment and substantially decreases cardiovascular morbidity and mortality. However, there are still unmet clinical needs in the management of dyslipidaemia. Indeed, it is difficult to achieve LDLc targets in many patients, particularly in those at high/very high cardiovascular risk and in those with very high baseline LDLc concentrations. Moreover, a considerable proportion of patients are unable to tolerate maximum statin doses, mostly due to muscle-related adverse effects. In the present narrative review, a summary is presented on the current knowledge on the effects of the different cholesterol-lowering drugs, including those recently approved by European and American regulatory agencies, on lipid profile, and on cardiovascular risk. Since difficult-to-treat patients may benefit from new combination therapies as a result of the emergence of new drugs with clinical evidence, updates of the clinical guidelines would be recommended.The lack of achieving the LDL-cholesterol goal observed in epidemiological studies, highlights the difficulty of transferring the benefit of the hypolipidaemic treatment noted in clinical trials, to current clinical practice. Although the reasons for not reaching LDL targets are probably multiple, i.e. treatment non-adherence, or therapeutic inertia, or treatment discontinuation as a consequence of statin intolerance, is frequently described. Statins are safe medications. However, 10 to 20% of the population refer to myalgias associated with their use, and 1 to 3% abandon treatment for this cause. In these subjects, it is necessary to change to a different statin, to use lower doses of statins, or to use irregular prescription regimes. If these actions are not useful, emphasis should be placed on the importance of hygienic and dietary recommendations and, when needed and depending on the cholesterol goal to achieve, the need of other lipid lowering treatments, like ezetimibe, bile acid sequestrants, bempedoic acid, or PCSK9i, often in combination.The clinical practice guidelines (CPG) have contributed to the dissemination of scientific information that supports decision-making in different clinical situations. CPGs have become more necessary as scientific information has grown, sometimes offering contradictory data, which makes it difficult for the clinician to easily make the most appropriate decision. In this context, the CPGs summarize and simplify the available scientific information, making it available to the doctor who must make the decisions. The publication of a CPG does not mean that it is applied in practice, much less that it is adopted quickly. In fact, despite the improvement in the quality of the CPGs, it is observed that they have not been fully implemented in a large number of cases, which prevents relevant information from ending up being transferred to clinical practice, with the consequent impact on the quality of care. In this article we will briefly review the strategies adopted to ensure that the scientific recommendations contained in the CPGs end up being transferred to patients and, asa consequence, achieving a reduction in the impact of cardiovascular diseases.This chapter summarises, and updates, lipid metabolism. Both pathways, exogenous metabolisms route via the chylomicrons, and the endogenous pathway of very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL). The reverse cholesterol metabolism will also be mentioned. It also includes the current classification of hyperlipidaemias or hyperlipoproteinaemias, with a reminder of the phenotype classification, and further developments of the aetiological classification. Both parts have updated references, with which knowledge of this vast subject can be expanded.The lipid theory of atherosclerosis dates back more than a century. Despite this, some authors have questioned the relevance of hypercholesterolaemia in its development. Multiple experimental, epidemiological, and clinical evidence underpins this association. https://www.selleckchem.com/products/OSI-906.html Atherosclerotic cardiovascular disease remains as the major cause of mortality in the world. Recent genetic studies of Mendelian randomisation and randomised clinical trials aimed at LDL cholesterol reduction, are summarised in this article. They, unequivocally ratify the aetiological role of LDL cholesterol in the development of atherosclerosis. Thus, LDL cholesterol lowering is the cornerstone of lipid lowering therapy for the reduction of cardiovascular complications of atherosclerosis.