Statins remain the cornerstone of hypolipidaemic drug treatment. The recent American College of Cardiology
(ACC)/American Heart Association (AHA) lipid guidelines suggest using percent reductions of low density lipoprotein cholesterol
(LDL-C), according to cardiovascular disease (CVD) risk, rather than specific LDL-C targets. These guidelines raised concerns and other
Societies (US, International, European) have not endorsed them. The implementation of previous guidelines in clinical practice is suboptimal
due to attitudes of physicians and restrictions in health care systems. Monoclonal antibodies that inhibit proprotein convertase subtilisin/
kexin type 9 (PCSK9), which degrades the LDL receptor, like alirocumab and evolocumab, are in phase 3 trials. These drugs are
suitable for statin intolerant or resistant patients, heterozygous familial hypercholesterolaemia (HeFH) and some forms of homozygous
FH (HoFH). Mipomersen (antisense oligonucleotide against apolipoprotein B) and lomitapide (microsomal triglyceride transfer protein
blocker) have already been approved for HoFH. Eventually, silencing micro-RNA oligonucleotides may also become available. The repair
or silencing of genes implicated in hyperlipidaemia and/or atherosclerosis is also on the horizon. If the new therapeutic options mentioned
above prove to be effective and safe then by combining them with statins and/or ezetimibe we should be able to effectively control
acquired or hereditary dyslipidaemias and substantially further reduce CVD morbidity and mortality.
Keywords: Statins, ACC/AHA guidelines, proprotein convertase subtilisin/kexin type 9, anti-micro-RNA oligonucleotides, gene repair or
silencing, familial hypercholesterolaemia.
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