mortality and an important cause of morbidity in Malaysiafor several years. To reduce global cardiovascular (CV) riskin the population, primary preventive strategies need to beimplemented. Hypercholesterolaemia is one of the majorrisk factors for CVD. This paper is an expert review on themanagement of hypercholesterolemia focusing on high andvery high risk individuals. In low and Intermediate riskindividuals, therapeutic lifestyle changes (TLC) and ahealthy lifestyle alone may suffice. In high and very high riskindividuals, drug therapy in conjunction with TLC arenecessary to achieve the target LDL-C levels which havebeen shown to slow down progression and sometimes evenresult in regression of atherosclerotic plaques. Statins arefirst-line drugs because they have been shown in numerousrandomized controlled trials to be effective in reducing CVevents and to be safe. In some high risk individuals, despitemaximally tolerated statin therapy, target Low DensityLipoprotein Cholesterol (LDL-C) levels are not achieved.These include those with familial hypercholesterolaemia andstatin intolerance. This paper discusses non-statintherapies, such as ezetimibe and the newer Proproteinconvertase subtilisin/kexin type 9 Inhibitors (PCSK9-i).

Myocardial infarction (MI) in the young adults are more common among the Asians compared to the Caucasians. It is of great interest to investigate the genetic risks that increase the susceptibility of MI in young patients with no family history. We conducted a genetic analysis on a young adult diagnosed with acute MI. The coronary angiogram showed acute complete occlusion of the left anterior descending artery with 40% left ventricular ejection fraction (LVEF). Patient’s DNA was subjected to genotyping using Infinium Asian Screening Array. The genotypes were annotated and associated with risks of cardiovascular diseases catalogued in GWAS database. Ninety-four genetic variants were detected. Patient has more than half of the genetic variants being homozygous risk genotypes for coronary artery and coronary heart diseases. Identifying the potential genetic modifiers associated with MI in young patients is of great interest to help the clinician make informed decisions to implement preventive and personalised medicine for this patient.