Abstract The treatment of hyperlipidemia has been established to reduce the development and progression of atheroma and thereby reduce atherosclerotic cardiovascular disease events. Low-density lipoprotein cholesterol (LDL-C) is the primary target for treatment, and the LDL-C treatment goals should be determined by the overall cardiovascular risk. Guidelines and consensus statements all recommend statins as the first-line medication to reduce LDL-C following appropriate lifestyle modification. Statins are safe and well-tolerated when used in appropriate doses, but muscle symptoms sometimes limit their use. Drug interactions with some statins may result in severe muscle toxicity. If LDL-C targets are not achieved with high-intensity statin treatment, ezetimibe should be added. If that is insufficient to reach the LDL-C target, adding or substituting a proprotein convertase subtilisin/kexin type 9 inhibitor or bempedoic acid should be considered, depending on cost, availability, and patient preference. The combination of two or three medications should be sufficient for the majority of patients with preserved LDL receptor function to reach the LDL-C goal. However, observational studies often find that LDL-C targets are not attained, which may be related to poor adherence to therapy or failure to use appropriate combination therapy. Severe elevation of triglycerides is a risk for acute pancreatitis and should be treated with fibrates and/or omega-3 fatty acids along with a low-fat diet. Milder degrees of hypertriglyceridemia contribute to cardiovascular risk, which can be evaluated by non-high-density lipoprotein cholesterol or apolipoprotein B levels, and these may represent better markers of atherogenic burden than LDL-C. Treatment with icosapent ethyl or a fibrate should be considered if triglycerides remain elevated despite achieving LDL-C targets. Treatments for the very rare conditions of homozygous familial hypercholesterolemia with lomitapide or evinacumab and familial chylomicronemia syndrome with apolipoprotein C3 inhibitors have been developed but may not be readily available everywhere.
Brian Tomlinson (Mon,) studied this question.